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Alzheimers the cannot remember disease

Sept 22nd 2018

World Alzheimer's Day: Time to deal with the stigma in the Asian community

Dementia is a global health crisis and one of the leading causes of death. 50 million people live with dementia worldwide, with someone developing the condition every three seconds.

There is very little support available and people with dementia are often locked in rooms for whole days at a time and kept away from the wider community. As a result they become lonely, depressed and isolated. In India, some people with dementia are even accused of witchcraft and we know that in other developing countries, people are at risk of violence and attack if they have dementia. This shows how vital it is for us to raise awareness and understanding of the condition.

My uncle had dementia and I saw first-hand the impact it had on him and his family. I have such fond memories of him as a fit and active man who loved watching his grandchildren play football. He would walk to the sports ground to watch them play and he had an incredible knowledge about the game, which was rare for someone of his generation. He also spoke a bit of English, which I envied because my parents and in-laws couldn’t speak English with my children. He was such an intelligent, active member of the community and dementia completely transformed his life.

The first signs of memory loss and confusion were pointed out by my uncle’s daughter-in-law, who was his main carer. In hindsight, she said she should have spoken out sooner and louder because she knew something wasn’t quite right. However, the fear of upsetting her family or being labelled as someone who was finding excuses not to care for her father-in-law held her back.

In my experience, when a woman living in a South Asian community marries and leaves her own family, one of the most important asks from her parents is to be ‘a good daughter-in-law’. It’s not surprising that this sense of overwhelming responsibility prevented her from asking questions or flagging concerns to the rest of the family. The pressure on my uncle’s daughter-in-law only increased as his dementia progressed. We know that women are disproportionately affected by dementia and contribute 58 billion informal care hours (care provided by loved ones). This isn’t sustainable.

Families like my own, who moved to the UK from India, brought these attitudes towards dementia with them. Misinformation prevents people with the condition and their carers seeking help or receiving a diagnosis. So much needs to happen to tackle the stigma and isolation of people living with dementia in South Asian communities in the UK and abroad.

In the UK we have made great strides in becoming dementia friendly – there are over 2.5 million Alzheimer’s Society Dementia Friends and over 330 Dementia Friendly Communities taking action to ensure people with dementia can live a life they want in their community. But action doesn’t stop on our doorstep – Alzheimer’s Society is growing this movement globally and more needs to be done. We urgently need to continue to tackle stigma and injustice – every country in the world needs to become dementia friendly and roll-out Alzheimer’s Society’s Dementia Friends programme, so no one with dementia is left behind.

I recently had the privilege of becoming an ambassador for Alzheimer’s Society, and am also proud to be a Dementia Friends Champion. This World Alzheimer’s Day, I’m calling on global governments and individuals to tackle stigma and uphold the rights of people living with dementia.

I urge everyone to speak out and raise awareness to improve the lives of people living

with dementia not just in South Asian communities, but right across the globe. Together we can and will unite against dementia. 


Sept 7th 2018

Daily exercise reversed Alzheimer's symptoms in mice, study claims

Alzheimer's disease has been reversed in mice with a drug that mimics the benefits of exercise to the brain.

The revolutionary therapy generated new neurons, improving the lab animals' thinking skills by destroying rogue proteins that cause the devastating illness.

It raises the possibility of developing medications that fuel the production of brain cells known as neurogenesis.

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Senior author Professor Rudolph Tanzi, director of the Genetics and Ageing Research Unit at Massachusetts General Hospital, said: 'In our study we showed exercise is one of the best ways to turn on neurogenesis.

'Then, by figuring out the molecular and genetic events involved, we determined how to mimic the beneficial effects of exercise through gene therapy and pharmacological agents.'

The US team say they hope a similar technique may work in humans. Plans to explorethis are already underway. 

Lead author Dr Se Hoon Choi, based at the same lab, said: 'While we do not yet have the means for safely achieving the same effects in patients, we determined the precise protein and gene targets for developing ways to do so in the future.'

Even one 30 minute brisk walk, jog or bike ride pumps extra blood to the brain, delivering the oxygen and nutrients it needs to perform to its best.

This improves mental functions by promoting the birth of neural progenitor cells in the hippocampus, the area of the brain that controls memory.

Experiments in adult mice genetically engineered to develop Alzheimer's like symptoms showed these new neurons could be induced either by exercise or drugs and gene therapy.

At first only exercise worked. This is because physical activity turns on a protein called BDNF which is known to protect brain cells.

Dr Choi explained: 'We found the key difference was that exercise also turned on the production of brain-derived neurotrophic factor or BDNF - known to be important for the growth and survival of neurons - which created a more hospitable brain environment for the new neurons to survive.

'By combining drugs and gene therapy that both induced neurogenesis and increased BDNF production, we were able to successfully mimic the effects of exercise on cognitive function.'

In behaviour tests animals in which neurogenesis had been caused by exercise had improved cognitive performance and reduced levels of beta amyloid.

These are the rogue proteins that form into clumps in the brains of Alzheimer's patients.

The mice in which it had been induced pharmacologically and genetically displayed only limited benefits, until the administration of BDNF.

Tanzi said: 'Although exercise-induced AHN improved cognition in Alzheimer's mice by turning on neurogenesis, trying to achieve that result by using gene therapy and drugs did not help.

'That was because newly born neurons, induced by drugs and gene therapy, were not able to survive in brain regions already ravaged by Alzheimer's pathology, particularly neuroinflammation. So we asked how neurogenesis induced by exercise differs.'

The study published in Science shows those benefits can be blocked by inflammation in the brain of patients with Alzheimer's.

Physical activity can 'clean up' the environment, allowing new nerve cells to survive and thrive and improving cognition in the Alzheimer's mice. 

Tanzi added: 'The lesson learned was it is not enough just to turn on the birth of new nerve cells, you must simultaneously 'clean up' the neighbourhood in which they are being born to make sure the new cells survive and thrive.

'Exercise can achieve that, but we found ways of mimicking those beneficial cognitive effects by the application of drugs and gene therapy that simultaneously turn on neurogenesis and BDNF production.'

The researchers also found blocking neurogenesis in younger mice with Alzheimer's shortly after birth led to more pronounced cognitive deficits later in life.

Tanzi said: 'We will next explore whether safely promoting neurogenesis in Alzheimer's patients will help alleviate the symptoms of the disease and whether doing so in currently healthy individuals earlier in life can help prevent symptoms later on.

'We are very excited to now investigate ways of implementing our new findings to more effectively treat and prevent this terrible disease.'

Sept 3rd 2018

From physical activity to sleep - best ways that can help avoid dementia

One in 14 people over the age of 65 in the UK will develop dementia and while there is no cure, scientific evidence shows there are several ways you can guard against it.

Watch your weight

Among the biggest risk factors for dementia are diabetes and mid-life obesity, which can double your chances of dementia at a later age. Links have also been found between elevated blood pressure, high cholesterol levels and the risk of dementia, although these are not conclusive. Monitoring your weight and cardiovascular health in middle age could greatly reduce your likelihood of dementia.

Don’t smoke

The brain may be affected by the long-term consequences of heavy smoking. Scientists have found smoking to increase the risk of cognitive decline in old age, with one study showing that middle-aged people who smoked more than two packs a day more than doubled their risk of later-life dementia.

Keep active

Numerous studies have shown that regular, vigorous physical activity - and in some cases, even mild exercise such as walking - can preserve your faculties in later life. Staying active is particularly important for the elderly, with studies finding that older individuals who began a regular exercise programme experienced improved cognitive function. However, younger people should avoid sports where they are prone to repeated head traumas, such as boxing or even football. There is growing evidence that even moderate traumas increase the risk of developing certain forms of dementia.

Cognitive training

People with more years of school and university education are known to have a lower risk of dementia, but there is evidence that everyone can reduce their risk of dementia through trying new things as they get older. Taking up new hobbies, learning new skills and partaking in a daily intellectual activity such as doing crossword puzzles are all thought to have neuroprotective effects.

Stay sociable

Maintaining social activities as you get older, such as going to clubs or volunteering, has been found to have a protective effect against dementia. Studies have shown that individuals who maintain a larger social network into old age tend to have better cognitive functions and a reduced risk of cognitive decline.

Adopt the Mediterranean diet

Scientists are still not completely clear on how various nutrients, vitamins and food groups affect your risk of dementia. However, there have been a few studies focusing on the Mediterranean diet – which consists of small amounts of meat, and an emphasis on whole grains, fruits, vegetables, fish, nuts and olive oil – that suggest it can reduce risk of dementia, possibly by preventing high blood pressure.

Keep to normal sleep patterns

Sleep disturbances, for example chronic insomnia, have been linked to increased risk for cognitive decline in later life. Taking steps to deal with any sleep problems could reduce your chances of getting dementia. However scientists still don’t understand exactly how disturbed sleep may contribute to the condition, and whether certain dysfunctional sleep patterns pose more of a risk than others.

Aug 31st 2018

Bill Gates Invests $30M for Affordable Early Alzheimer's Test

There’s currently no way to identify the disease in its early stage.

Billionaire Bill Gates is doubling down on his commitment to Alzheimer’s research.

The Microsoft founder and philanthropist, along with Estée Lauder Companies Inc. chairman emeritus Leonard Lauder, announced this week that they would invest $30 million over three years toward the development of new tests for early Alzheimer’s detection, reports Reuters.

“The process of getting diagnosed with Alzheimer’s today is less than ideal,” Gates wrote in a post to his personal blog, Gates Notes, explaining the current limitations of Alzheimer’s testing.

“It starts with a cognitive test. If you don’t perform well, your doctor needs to rule out all other possible causes for memory loss, like stroke or a nutritional deficiency. Then your doctor can order a spinal tap or PET scan to confirm you have Alzheimer’s. Although these tests are fairly accurate, the only way to diagnose the disease definitively is through an autopsy after death.”

“We need a better way of diagnosing Alzheimer's — like a simple blood test or eye exam — before we're able to slow the progression of the disease," Gates wrote in a statement, reports CNN. “Imagine a world where diagnosing Alzheimer’s disease is as simple as getting your blood tested during your annual physical.”

News of the Diagnostics Accelerator project follows an announcement by Gates in November that he would commit $100 million toward Alzheimer’s disease research, noted TIME. At that time, he also revealed that the disease has touched him personally, as members of his family, including his father, have suffered from it.

Read More: Bill Gates Just Pledged $100,000,000 to Research Dementia

The Alzheimer's Association says the disease is the sixth-leading cause of death in the US, according to the CNN report, killing more than breast and prostate cancer victims combined. Six million Americans are currently living with Alzheimer's and roughly 14 million individuals are expected to be affected by the brain disorder by 2050.

Those figures jump to nearly 50 million people worldwide and are expected to rise to more than 131 million by 2050, according to Alzheimer’s Disease International, reports Reuters.

All stand to benefit from an early diagnosis and potential new treatment therapies funded by Mr Gates.


Aug 23rd 2018

7 lifestyle tests which reveal your risk of developing dementia

Previous studies have suggested that keeping your brain active, maintaining cognitive skills and exercising regularly can help ward of dementia. And now, a new study has revealed the seven health tests that can assess whether you are more at risk of developing dementia.

The study, titled Association of Cardiovascular Health Level in Older Age With Cognitive Decline and Incident Dementia, was published in the journal JAMA and carried out by scientists from the University of Bordeaux in France.

More than 6,000 participants over the age of 65 took part in the study, which sought to examine the connection between cardiovascular health in old age and risk of incident dementia. Seven health tests were used, a method from the American Heart Association, which showed that better heart health was linked to a lower risk of incident dementia.

Among other factors, the researchers suggested that people should stay slim, exercise regularly and not smoke to minimise the risk of developing dementia in older age. See the full list of seven lifestyle choices that have a negative impact below…

7 lifestyle choices that increase risk of dementia

1. Smoking

2. Having a BMI over 25

3. Not exercising regularly

4. Not eating fish twice a week or fruit and vegetables three times a day

5. Having high blood pressure

6. Having high cholesterol

7. Having high blood sugar

The results of the research revealed that people over the age of 65 who suffer from heart problems are more likely to suffer memory and cognitive decline eight years later.

The study authors concluded: “In this cohort of older adults, increased numbers of optimal cardiovascular health metrics and a higher cardiovascular health score were associated with a lower risk of dementia and lower rates of cognitive decline.

“These findings may support the promotion of cardiovascular health to prevent risk factors associated with cognitive decline and dementia.”

However, the study cannot be seen as a compete reflection of the general public as only white, city-dwelling participants were involved in the research.


Aug 19th 2018

As Alzheimer’s drug developers give up on today’s patients, where is the outrage?

When virologists and drug developers were too slow in finding ways to save the lives of people with HIV/AIDS and refused to give patients access to experimental drugs 30 years ago, activists chained themselves to a balcony on the New York Stock Exchange, held demonstrations where scores were arrested, and effectively shut down the Food and Drug Administration for a day.

The lack of progress against Alzheimer’s disease has brought somewhat less outrage. Although the latest analysis of experimental Alzheimer’s drugs finds that literally zero are being tested in late-stage clinical trials to treat moderate to severe Alzheimer’s, no patient advocacy groups uttered a peep in protest.

“We need a Larry Kramer,” said Dr. Sam Gandy, a neurologist and Alzheimer’s expert at Mount Sinai Hospital in New York, referring to the AIDS activist. Instead, he said, patients and their families adopt the fatalistic attitude that dementia is an inevitable consequence of aging, and funders see spending $1 on curing a child as ethically more justified (since it buys more total years of life) than spending $1 on an 80 year old, who’s closer to the grave.

While ageism partly explains why Alzheimer’s patients are being written off, just as gay men were in the 1980s, it’s not the whole story. For more than 20 years drug makers and academic scientists pursued treatments to slow or reverse dementia by targeting amyloid plaques in the brain. Every last one failed. Now companies and investors are instead focused on trying to prevent Alzheimer’s in younger people — potentially a huge, and hugely lucrative, market — or trying to ameliorate agitation and other behavioral symptoms of the disease. Meanwhile, alternative strategies for treating the disease have been largely ignored and underfunded, with little outcry.

“I don’t think most people have really internalized this, or are ready to hear about it,” said chemist Derek Lowe, a longtime pharmaceutical scientist who blogs about drug discovery. “It’s painful, and no one is going to come out and say flatly that people with existing Alzheimer’s damage are probably never going to get any better, and that it would take a major advance just to stop them from getting any worse. It sounds defeatist.”

Not every company has given up on the 5.5 million people in the U.S. who already have Alzheimer’s, all of whose disease will become tragically, mind-robbingly, identity-destroyingly severe if it isn’t already — and if they don’t die first.

“These are the very patients we have to help,” said Dr. Daniel Alkon, president and chief science officer of Neurotrope, which is running a Phase 2 clinical trial of a compound called bryostatin in patients with moderate to severe Alzheimer’s. That makes it literally the only Phase 2 or Phase 3 study of whether a drug can alter the course of disease in patients with severe dementia. “I absolutely do not think it’s hopeless.”

Alkon’s optimism (not shared by most experts) reflects his preclinical research showing that bryostatin boosts two kinds of molecules: those that degrade amyloid and those that increase synapse formation. The first mechanism of action might prevent the formation of synapse-destroying amyloid plaques, while the second might preserve and create synapses, whose destruction underlies the cognitive losses in Alzheimer’s. In lab mice, bryostatin reversed brain damage and improved memory. Neurotrope’s small Phase 2 trial suggests it might do the same for patients with moderate-to-severe Alzheimer’s, but the results still have to be confirmed in a larger trial.

Neurotrope is a complete outlier, however, and even Alkon can understand both the scientific and business case for drug developers’ decision to target mild Alzheimer’s, or even pre-symptomatic but at-risk (i.e. healthy) people.

For more than a decade, drug developers have based their experimental compounds on the amyloid hypothesis, convinced that ridding the brain of sticky amyloid plaques, and preventing new amyloid deposits, was the key to fighting the disease. Trouble was, quite a few drugs did reduce the amyloid burden, “but that didn’t do anything for cognition,” Alkon said. “So the thinking became, plaques are too late, we have to get rid of what causes the plaques,” namely, soluble amyloid molecules called oligomers. By definition, people without amyloid plaques do not have Alzheimer’s disease.

“The scientific rationale was, by the time people get moderate dementia, their brain is pretty filled up with amyloid and they’ve lost neurons and synapses,” said Dr. Howard Fillit, chief science officer of the Alzheimer’s Drug Discovery Foundation. “And what drug developers want is to get a drug to market,” not waste time and money on noble but quixotic causes.

That means that in addition to a scientific justification for targeting earlier disease (or pre-disease), there was a business one. “No one was making any progress in targeting patients with moderate to severe disease,” Alkon said. Eli Lilly alone spent at least $1 billion, analysts estimate, on what turned out to be a failed antibody against amyloid. Such astronomically expensive failures in even moderate Alzheimer’s, he said, “has been the rationale of the entire industry” for why it has basically given up on patients who are losing their memories and their minds and, eventually, their lives.

“The moderate-to-severe patients got completely left in the dust,” said Fillit. “It’s driven by companies’ need for a success.” Given the 200-plus failed clinical trials of experimental Alzheimer’s drugs, the smart money says that is more likely to come from a drug that prevents the development of full-on dementia in people with mild cognitive impairment or even just risk factors (including genetic ones).

“The moderate-to-severe patients got completely left in the dust. It’s driven by companies’ need for a success.”

Not everyone agrees that millions of patients have been abandoned. Nearly three dozen drugs in mid- to late-stage development aim to reduce agitation, sleep disorders, and other behavioral changes that accompany Alzheimer’s. Such drugs, if they work, could make a significant difference in the daily life of patients and caregivers even if they don’t alter the course of the actual disease. Clinical trials for these behavioral symptoms “continue to make up a significant percentage of the total trials,” said Alzheimer’s Association spokesman Niles Frantz.

In addition, federal funding of Alzheimer’s research nearly tripled from $503 million in 2012 to $1.8 billion (if the 2018 congressional appropriation becomes law), partly as a result of advocacy by the Alzheimer’s Association, said Dr. David Knopman of the Mayo Clinic and chair of the group’s Medical and Scientific Advisory Council. Even if those basic biology studies succeed, however, they wouldn’t lead to an effective drug in anything less than a decade.

As for the lack of outrage, “if someone has moderate to severe Alzheimer’s, there is a lot of therapeutic nihilism,” said Fillit. That is, families, caregivers, and even physicians have assimilated the decade-long drumbeat of drug failures. “Most people I see think there’s nothing that can be done and there’s no hope,” said Fillit, who disagrees with that grim assessment. They don’t handcuff themselves to the balcony of the stock exchange because they see no point.

An ethical issue also arises. For the most part, experimental drugs that have shown promise in early clinical trials, before ultimately failing, have merely slowed the rate of cognitive decline. That is, after 18 months on the experimental drug, patients’ scores on standard cognitive tests have fallen 30 percent less than have those of untreated patients. But they’ve still fallen. If a drug that achieves that in a Phase 3 trial (none has) were to win FDA approval, it would be a double-edged sword.

“At the end of 18 months, the patient is still going to be worse” than she was earlier, Fillit said, and it might take expert assessment to even detect that. Many scientists who study Alzheimer’s, as well as clinicians who treat it, therefore wonder if that’s a meaningful outcome, especially since slowing the rate of mental decline almost always means postponing the inevitable and living with a devastating disease for longer.

As for the one outlier in the exodus from drug development for advanced Alzheimer’s, last month Neurotrope said it had begun enrolling what it hopes will be 100 patients in a confirmatory Phase 2 clinical trial of bryostatin. All will have scores on the Mini Mental State Exam of 4 to 15 — moderate to severe Alzheimer’s — and scientists will be looking for signs that patients’ disease doesn’t merely stop worsening but that their cognition and memory improve. The company expects to complete the study around this time next year.


Aug 2nd 2018

People who are teetotal in middle age are at greater risk of developing dementia than those who drink moderate amounts, with benefits particularly apparent in wine drinkers, a new study has found.

Researchers found abstinence was associated with a 45 per cent increase in the chances of getting dementia by early old age, compared to those who drank within recommended limits – up to a bottle and a half of wine a week.

People who drank above the 14 unit guideline were also at increased risk, the team from University College London and French institute for health, Inserm, found. Their risk of developing dementia increased incrementally the more alcoholthey were consuming.


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“We show that both long term alcohol abstinence and excessive alcohol consumption may increase the risk of dementia,” the authors of the study, published in the British Medical Journal, wrote. “Given the number of people living with dementia is expected to triple by 2050 and the absence of a cure, prevention is key.”

Among abstainers, the study also found increased risks of diabetes and cardiovascular disease. These are both conditions which could contribute to dementia, a collective term for the loss of memory, thinking and other cognitive functions, and the leading cause of death in the UK.

Moderate alcohol consumption has previously been shown to help protect against these conditions, by reducing cholesterol and blood pressure levels, and it may be this which is responsible for the dementia protecting benefit.

However the authors said it would be nearly impossible to find a definitive cause without a much larger and impractical trial where participants are randomly allocated to quit drinking or drinking more heavily.

The top 10 countries that drink the most alcohol

10show all

It could also be that people with higher levels of these types of metabolic diseases were more likely to quit drinking, or healthier and more well off people were more likely to be moderate drinkers. The authors said they would not encourage anyone currently abstaining to change their habits.

Of the 9,087 participants, who took part in a British study between 1985 and 1993 and were followed for 23 years on average, there were 397 cases of dementia recorded.

The study found long-term abstainers were at the most extra risk of dementia (67 per cent), compared to those who were abstinent in midlife (45 per cent) and those cutting down (50 per cent).

“The most intriguing finding from this study was the significantly increased risk of dementia among abstainers… and that association was only present in those who abstained from wine,” said Dr Sevil Yasar from John Hopkins School of Medicine in Baltimore, who was not involved in the study

“Wine, in addition to alcohol, contains polyphenolic compounds, which have been associated with neuroprotective effects on both neurodegenerative and vascular pathways, and with cardioprotective effects through inflammation reduction, inhibition of platelet aggregation, and alteration of lipid profile.”

However she added that we should remain cautious about the findings.

Dr Sara Imarisio, head of research at Alzheimer’s Research UK, agreed, adding: “People who completely abstain from alcohol may have a history of heavy drinking and this can make it difficult to interpret the links between drinking and health.

“Future research will need to examine drinking habits across a whole lifetime, and this will help to shed more light on the relationship between alcohol and dementia.”


July 5th 2018

Decorators and cleaners face increased risk of multiple sclerosis

Cleaners, beauticians, decorators and anyone coming into contact with potent solvents in paint thinners and cleaning supplies are 50 per cent more likely more likely to develop multiple sclerosis (MS), a study has found. 

The risk of developing the neurodegenerative disease is seven times higher in people who work with solvents and have a family history of it, according to research published in the journal Neurology.

It was thirty times higher when you added smoking to the mix.

This suggests that constant lung irritation might be activating the immune system in a way that makes it more likely to trigger MS, a disease where immune cells malfunction and attack the body’s nerves.

“It’s possible that exposure to solvents and smoking may both involve lung inflammation and irritation that leads to an immune reaction in the lungs,” said the study’ author Dr Anna Hedström, from the Karolinska Institute in Stockholm, Sweden.

“These are significant interactions where the factors have a much greater effect in combination than they do on their own,” she added.

Independent academics said the findings suggest those working with solvents who have a family history of the disease should aim to cut down their smoking and chemical exposure.

Dr Hedström’s team looked at the health records of 5,000 people, including 2,042 who had recently been diagnosed with MS.

They were asked about their exposure to organic solvents, which are chemicals common in paints and thinners, varnish, nail polish, glues and cleaning products, as well as their smoking history.

To identify MS risk, the researchers used blood tests to look for two variations in genes associated with white blood cells which play a key role when the immune system malfunctions in MS. One variation makes the disease more likely, and one appears to be protective.

These are the best studied genetic traits for the disease, but it is still poorly understood what causes the immune cells to start destroying the outer coat of nerve cells – called the myelin sheath – which allows rapid electrical impulses to be sent.

Vitamin D levels, infection with the Epstein-Barr Virus (mono) and even obesity are all factors that have been considered.

Solvent exposure which can be through the skin, ingestion or inhalation has well-known neurological effects – it can cause temporary euphoria as well as permanent brain damage.

But it appears it is most significant to MS whern in combination with other risks.

From the latest data, the Swedish team identified that a combination of genetic risk factors and exposure to solvents account for up to 60 per cent of a person’s chance of developing the disease. However the researchers say their subjects ability to identify regular solvent exposure may be a limiting factor in the results.

However independent researchers said it was “staggering” that adding smoking into this mix increased the risk of MS 30.3 times.

Dr Gabriele DeLuca, from the University of Oxford, was not involved in the study but in an accompanying editorial in Neurology she said this combined risk warrants further investigation.

“In the meantime, avoidance of cigarette smoke and unnecessary exposure to organic solvents, particularly in combination, would appear reasonable lifestyle modifications to reduce the risk of MS, especially in those with a family history of the disease,” she added.

There will also be services at Westminster Abbey and York Minster to thank staff and patients.

Ethel Armstrong, an 87-year-old former nurse cadet and radiographer - who was working in the NHS on its first day - will be running the @NHS Twitter account.


June 23rd 2018

The magnetic therapy that could recover your memories

Try to recall a conversation without hearing it in your head. It’s difficult, because sound impacts our memory formation. That’s why we forget the milk at the store, and leave without the one thing we came for: we heard the instructions, but we didn’t really listen. 

Maintaining a sound in your mind’s ear—that is, how we imagine it, keep hearing it, and retrieve it after it’s gone—is called auditory working memory.

This cognitive capacity to keep sounds in mind for a short period of time was the focus of a paper published in Neuron by a team at McGill University’s Brain Imaging Centre. The study tested the efficacy of a non-invasive brain therapy called transcranial magnetic stimulation, or TMS. Using a hand-held device placed against the scalp, the researchers positioned the targeted, oscillating pulses (at 5 Hz) into the brain in order to stimulate nerve cells. (The pulses are reportedly not painful.)

The group found some surprising results. TMS seemed to directly improve the working memory of 17 participants in a recall task. Participants were asked to recognize a melody when the order of notes played back was reversed. After TMS treatment, they were able to remember the series of sounds quicker, and more accurately.

“The most exciting aspect is that we found a causal link between brain and behavior,” Philippe Albouy, one of the study’s co-authors, told The Daily Beast. “TMS is easy to control because the stimulation is focused. When you’re targeting a given brain region, you’re sure that you’re hitting that region.”

TMS was recently granted FDA-approval to treat depression, and the treatment is covered by some health insurance plans. The McGill University study focused on theta wave activity in the auditory dorsal stream, a pathway in the brain that helps us process speech. The group also compared the data to the control condition of TMS at 5 Hz with non-rhythmic pulses. The participants’ brain activity was simultaneously tracked with two technologies: a massive, cocoon-like  magnetoencephalography (MEG) scanner, which records the magnetic fields produced by ‘brain waves’; and an electroencephalogram (EEG), a cap-like set of small discs (electrodes) pasted all over the scalp to track the brain’s electrical activity.

“This means that we can use brain activity as a marker for later interventions,” Albouy said. “That’s the interesting part.”

The study’s results suggest broader clinical applications, according to Albouy. TMS, a “relatively painless” tool that doesn’t require anesthesia or hospitalization, has the potential to treat other patients who have deficits in working memory, such as people with Parkinson’s disease or Alzheimer’s disease, or children and adults with ADHD.

“I think you can say that this method could apply to almost everything,” Albouy said. “The only thing is that you have to define a brain marker to a given task. The task can be what you want. It could be attention, visual perception, or memory. Once you have this marker and the region of interest, then you can apply rhythmic stimulation during the task in order to improve performance.”

Though TMS is an emerging, experimental technology, some studies have shown—though at times with mixed results—that the technique has the potential to improve the lives of people with autism and post-traumatic stress disorder (PTSD), and those who struggle with addiction, and chronic pain. A similar study in Science by a team of researchers at the University of Wisconsin-Madison demonstrated that TMS can help us remember: Recent memories can be brought back, and recalled. 

Yet researchers haven’t found a way to help participants sustain their improved working memory. Typically, their performance plummets after leaving the TMS machine behind.

Albouy’s team is working on this problem. He’s currently developing a study with HIV-positive patients who are coping with memory deficits.

“We are trying to see if we can observe any after effects. Then, we will apply it to a clinical population, step by step,” Albouy said. “We’re trying to find some patterns. It’s a promising approach.”

The TMS technique described in the study has the potential to be ready for clinical applications in as soon as a year (next spring), Albouy said. “I’m not sure. I can’t really predict it. We are really in the early stages of this approach, so it’s difficult to predict,” he said.

Another future path for research is how sound impacts long-term, rather than working, memory. Evocative or emotionally-charged sounds can change what we can remember—and what we forget. Sound can take over what we think and how we feel. It’s how a song takes you back. It’s how accents move through families and time zones. It’s anticipating the pause before someone tries to pronounce your last name. (The author's last name, for example, “Beebe,” is pronounced bee-bee, like two insects buzzing.) It’s the lilt in the voice of the person you love, the music of how they talk or laugh or scream or sing.

June 21st 2018

New study supports long-dismissed idea: Herpes viruses could play role in Alzheimer’s

The most detailed molecular analysis of hundreds of brains from people who died with Alzheimer’s disease lends support to an idea that has struggled for funding, been rejected by top journals, and met with ridicule from the Alzheimer’s orthodoxy: that viruses, bacteria, or fungi in the brain play a role in the devastating neurodegenerative disease.

If pathogens either initiate or accelerate Alzheimer’s, then classes of drugs that have never been considered for the disease should be in play. The new study, published Thursday in Neuron, “should bring forward new therapeutic targets and enable the field to predict which drugs out there may be useful,” such as antimicrobials, said Suzana Petanceska of the National Institute on Aging.

A second study, scheduled for publication next month, also points a finger at pathogens. “I wouldn’t say the new studies provide the smoking gun,” said neurobiologist George Perry of the University of Texas at San Antonio and editor-in-chief of the Journal of Alzheimer’s Disease. “But I do think the evidence is continuing to build that infectious agents play a role in this disease.”

During the 14 months that the two studies have been stuck in publication limbo, experimental Alzheimer’s drugs based on the quarter-century-old “amyloid cascade hypothesis” have been flaming out, each more spectacularly than before. (The hypothesis says that production of an aberrant protein called amyloid-beta creates sticky plaques that destroy brain synapses and neurons.) This year alone has brought the demise of the Eli Lilly/AstraZeneca drug lanabecestat; Lilly’s solanezumab; and Merck’s verubecestat. That brings the number of effective Alzheimer’s treatments based on the amyloid cascade hypothesis to … zero, making the need for new ideas more urgent than ever.

For the Neuron paper, scientists led by Joel Dudley, an expert in genomics and bioinformatics at the Icahn School of Medicine at Mount Sinai, examined 622 brains from people who died with Alzheimer’s — the largest number ever analyzed in this detail — and 322 healthy brains. He and his colleagues basically went fishing, looking for genes whose activity changes with Alzheimer’s. While doing that, “we were surprised to see evidence of herpes viruses” in the brains, said co-author Dr. Sam Gandy of Mount Sinai.

They then ran what’s called an unbiased scan, looking not for particular viruses but asking the open-ended question: What non-human genetic material is in the brains?

Using several forms of molecular profiling, from DNA sequencing to proteomics, they got a clear answer: “all sorts, and lots of it.” Especially in brain regions where vast numbers of neurons die in Alzheimer’s, the scientists found that three strains of herpes virus — human herpes virus 6A, 6B, and 7 — were prevalent, reaching levels up to twice that in healthy brains.

In four regions that are ravaged by Alzheimer’s — including the hippocampus, which plays a key role in memory — about one-quarter of the Alzheimer’s brains had evidence of HHV-6A, 22 percent had HHV-6B, and 29 percent had HHV-7. “The fraction of samples that had at least one of these in at least one brain region was substantially higher,” said co-author Ben Readhead of Arizona State University.

“This is the first study to provide strong evidence based on unbiased approaches and large data sets that lends support” to the idea that pathogens are involved in Alzheimer’s, said Dr. Richard Hodes, director of the National Institute on Aging.

Merely finding herpes virus, however, falls well short of demonstrating that it or other microbes cause Alzheimer’s. That idea has been kicking around since at least the 1950s but has never overcome a key objection: degenerating brains might just be more inviting to pathogens than healthy brains. In that case, the pathogens would be opportunistic, not causal, sneaking across the blood-brain barrier and taking up residence only after Alzheimer’s has developed.

None of the earlier claims that infectious agents spur the development of Alzheimer’s “has held up after rigorous evaluation across multiple laboratories,” said Dr. Lennart Mucke, director of the Gladstone Institute of Neurological Disease. Moreover, he added, previous studies showed only an association, not causation.

But Dudley and his colleagues took a step toward showing causation, and therefore going beyond previous research, by finding that viruses had also slipped their genes into the DNA of cells in the Alzheimer’s brains. The viral genes seem to influence the expression, or activity, of genes associated with Alzheimer’s, including such famous ones as presenilin-1, BACE1, and several that direct the production of amyloid beta precursor proteins.

The viral genes, Dudley said, seem to be activating proteins that in turn activate the Alzheimer’s genes, perhaps “acting as an environmental trigger to some of the genetic risk markers.”

Another hint of causation: “Viruses are overrepresented in the worst cases of Alzheimer’s, and seem to track the severity of disease,” Gandy said.

Herpes viruses are extremely common. HHV-6 is found “in pretty much everybody over 2,” said Robert Moir of Massachusetts General Hospital, co-author of a paper on HHV6 and Alzheimer’s that will appear next month in Neuron. (Like Dudley’s, it took more than a year to be published, including time lost when the journal Cell initially accepted it for review and then rejected it.) But clearly not everyone who carries herpes virus (which often stays dormant for years ) develops Alzheimer’s.

That may be because the viruses don’t usually cross the blood-brain barrier (though there is some evidence they can get in from the nose via the olfactory nerve). But in some people, for unknown reasons, they might.

What this all might mean for Alzheimer’s treatment isn’t clear. The new paper “raises a lot of questions that we should be looking at,” said Heather Snyder of the Alzheimer’s Association, “including [Alzheimer’s-causing] mechanisms involving the immune system.” At minimum, said neuroscientist Miroslaw Mackiewicz of the National Institute on Aging, the study should make scientists consider “drug targets that are above and beyond” those involved in producing amyloid-beta.

There’s also a simple treatment idea, suggested by a little-noticed study published in April. Scientists in Taiwan followed 8,362 people who were diagnosed with herpes infections in 2000, and 25,086 people without the infections. The herpes-infected group was 2.6 times as likely to develop dementia. But in people treated with antiviral drugs, that risk was reduced by 90 percent.



May 19th 2018

Scientists unveiled key factors to support quality of life in dementia


According to a new study by the University of Exeter in collaboration with the Economic and Social Research Council (ESRC) and the National for Health Research (NIHR), good relationships, social engagement, better everyday functioning, good physical and mental health, and high-quality care could lead having a better quality of life for people with dementia.

In order to support people to live as well as possible with dementia, scientists mainly identified key factors that can be targeted. While many investigations focus on prevention and better treatments, but scientists believe that it’s equally vital to understand how we can optimize the quality of life for the 50 million people worldwide who have dementia.

Professor Linda Clare, at the University of Exeter, said, “We now need to develop ways to put these findings into action to make a difference to people’s lives by supporting relationships, social engagement and everyday functioning, addressing poor physical and mental health, and ensuring high-quality care.”

Scientists conducted a systematic review and meta-analysis to examine all available evidence about the factors that are associated with quality of life for people with dementia. They gathered the data from 198 studies which involved more than 37,000 people.

The investigation found that statistic factors, for example, gender, education marital status, income or age were not related to personal satisfaction in individuals with dementia. Nor was the kind of dementia.

Elements that are connected with the low quality of life incorporate poor mental or physical wellbeing, troubles, for example, fomentation or detachment, and neglected needs.

Factors that are connected with better QoL incorporate having great associations with family and companions, being incorporated and engaged with social exercises, having the capacity to oversee regular exercises, and having religious convictions.

Numerous different factors indicated a little yet factually huge relationship with personal satisfaction. This proposes the manner by which individuals assess their personal satisfaction is identified with numerous parts of their lives, every one of which have a humble impact. It is likely that to some degree the viewpoints that are most essential might be diverse for every individual.

Dr Anthony Martyr, a lead author on the study, from the University of Exeter, said: “While in general, it is more of a challenge to maintain a good quality of life as dementia progresses, we found little evidence to show what predicts whether a quality of life will improve or decline over time. The IDEAL programme we are currently leading will follow people living with dementia for several years and will help to answer this question.”

Dr. Doug Brown, Chief Policy and Research Officer at Alzheimer’s Society, said: “Maintaining a healthy social life and doing things you enjoy is important for everyone’s quality of life. As this Alzheimer’s Society funded study highlights, people living with dementia are no exception.”

“Someone develops dementia every three minutes but too many are facing it alone and feel socially isolated a factor that researchers pinpoint contributing to a lower quality of life.”

“People with dementia have a right to continue living a life they love. Alzheimer’s Society’s Dementia Friendly Communities initiative enables individuals, businesses, and communities to involve and empower people affected – but we need all of society to unite to ensure people with dementia feel understood, valued and able to contribute to their community.”

The study supported by the London School of Economics, the universities of Sussex, Bangor, Cardiff, Brunel and New South Wales in Australia, and Kings College London, is published in Psychological Medicine

April 26th 2018

Two million Britons take medicine that may increase the risk of dementia

Medicines taken by up to two million Britons may increase the chance of dementia.

A study highlighted a 30 per cent higher risk from some drugs prescribed for depression, bladder problems and Parkinson's.

The medicines – anticholinergics – have already been linked to falls, confusion and memory problems in the elderly. The latest research found they were more likely to cause dementia – if taken for at least a year.

It suggests anticholinergics may have triggered around 20,000 cases of dementia – out of a national total of 850,000.

The researchers said their results did not prove that some anticholinergics caused the illness.

But they warned that doctors should consider the long-term effects when prescribing them.

The chance of a random individual developing dementia is roughly 10 per cent. But taking anticholinergics was found to increase the risk to 13 per cent.

Published in the British Medical Journal, the study was the largest of its kind to look at the link between the drugs and dementia.

Anticholinergics work by blocking a chemical messenger in the brain called acetylcholine, which can affect moods, movement and the bladder.

One in five people on anti-depressants are prescribed anticholinergics – the most common being amitriptyline. Others include dosulepin and paroxetine. The extra dementia risk was also found for medications prescribed for bladder conditions – such as tolterodine, oxybutynin and solifenacin and Parkinson's drugs, such as procyclidine. The study looked at the medical records of 300,000 patients over 65 – of whom 40,770 had a dementia diagnosis.

Dr George Savva, who led the research at the University of East Anglia's school of health sciences, said: 'We found that people who had been diagnosed with dementia were up to 30 per cent more likely to have been prescribed specific classes of anticholinergic medications.

'And the association with dementia increases with greater exposure to these types of medication.' Doug Brown of the Alzheimer's Society, which sponsored the research, said: 'Guidelines for doctors say that anticholinergic drugs should be avoided for frail older people because of their impact on memory and thinking, but doctors should consider these new findings for all over-65s as long-term use could raise the risk of dementia.'

Dr Noll Campbell, a study co-author, said the results suggested doctors should prioritise alternatives to anticholinergic medications long before symptoms of dementia appear.

Chris Fox, a UEA professor and consultant psychiatrist, said: 'While the associations are moderate, given the high incidence of dementia, they reflect a potentially important risk to patients.

'Doctors and patients should therefore be vigilant about using anticholinergic medications.

'They need to consider the risk of long-term cognitive effects, as well as short-term effects, associated with specific drugs when weighing up risks and benefits.'

Separately, the study gave a clean bill of health to antihistamines. Previous research has suggested anticholinergics, which include hayfever medications, could also increase the risk of dementia.

But the study said there was no higher risk. 

But no reason to panic, say doctors 

Doctors yesterday warned patients against coming off the drugs linked to higher dementia risk.

They said anyone concerned should talk to their GP first. 'Anticholinergics can have many beneficial effects which doctors need to weigh against any potential side effects,' said Dr Carol Routledge of Alzheimer's Research UK.

'Anybody concerned about their current medication should speak to a doctor before stopping a course of treatment.'

Clive Ballard, who is professor of age-related diseases at the University of Exeter, warned that some patients might be taking more than one anticholinergic drug.

The Medicines and Healthcare Products Regulatory Agency said in a statement: 'Patient safety is our highest priority and we continuously monitor the safety of all medicines on the UK market. These findings will be carefully evaluated, as with any study, to determine whether they have any implications for the safe use of anticholinergic medicines.'


April 23rd 2018

82-year-old dementia patient gets memory back after changing diet

An 82-year-old dementia sufferer who failed to recognise her own son has incredibly got her memory back after changing her diet.

When his mother's condition became so severe she had to be kept in hospital for her own safety, Mark Hatzer thought he had lost another parent.

Sylvia had even phoned the police accusing the nurses who were caring for her of kidnap.

But a diet high in blueberries and walnuts they have devised together has had such a dramatic impact on Sylvia’s condition that their recipes are being shared by the Alzheimer’s Society.

Other foods she began incorporating include broccoli, kale and spinach, sunflower seeds, green tea, oats, sweet potatoes and as a treat ,dark chocolate with a high cocoa content.

Mark, who lives in Prestwich, Greater Manchester, had lost his father to a heart attack in 1987, the Manchester Evening News reported. 

He first noticed his 82-year-old mum’s forgetfulness three years ago.

She would struggle to remember birthdays or arrangements she had made with friends.

After this became increasingly frequent, she was diagnosed with Alzheimer’s in December 2016.

The deterioration was fairly rapid. Alzheimer’s often has the side effect of epilepsy - and after a seizure and fall the following March, Sylvia was taken to North Manchester General Hospital.

Here Mark, 50, ‘reached the lowest point of his life’ when his mum did not recognise him.

Medics asked if Sylvia could be sectioned, as she had accused staff of kidnapping her.

Although this was not necessary in the end, it was two months before it was considered safe for her to be discharged.

One year later and Sylvia, a former telephonist, is still at home and unrecognisable from this low point.

She is held up by charity the Alzheimer’s Society as an example of how the disease can be - if not be completely beaten - arrested significantly.

She can remember birthdays once more, goes to tea dances and can carry out much of her own care needs.

A large part of the transformation is down to a diet and recipes that Mark and Sylvia devised together, containing walnuts, blueberries and other brain-boosting food.

They decided that medication was not in itself enough, so took heed of the fact that rates of dementia are far lower in Mediterranean countries and copied their eating habits.

Mark, whose brother Brent also died in 1977, said: “When my mum was in hospital she thought it was a hotel - but the worst one she had ever been in.

"She didn’t recognise me and phoned the police as she thought she’d been kidnapped.

“Since my dad and brother died we have always been a very close little family unit, just me and my mum, so for her to not know who I was was devastating.

“We were a double act that went everywhere together. I despaired and never felt so alone as I had no other family to turn to.

“Overnight we went from a happy family to one in crisis.

“When she left hospital, instead of prescribed medication we thought we’d perhaps try alternative treatment.

"In certain countries Alzheimer’s is virtually unheard of because of their diet.

“Everyone knows about fish but there is also blueberries, strawberries, Brazil nuts and walnuts - these are apparently shaped like a brain to give us a sign that they are good for the brain.”

But there were other steps mum and son made together.

Cognitive exercises such as jigsaws and cross words, meeting people at social groups and a little pedalling device so Sylvia could exercise in her chair.

Mark, a lawyer, said: “It wasn’t an overnight miracle but after a couple of months she began remembering things like birthdays and was becoming her old self again, more alert, more engaged.

“People think that once you get a diagnosis your life is at an end. You will have good and bad days but it doesn’t have to be the end.

“For an 82-year-old she does very well, she looks 10 years younger and if you met her you would not know she has gone through all this.

“She had to have help with all sorts of things, now she is turning it round. We are living to the older age in this country - but we are not necessarily living healthier.”

Mark and Sylvia’s approach has been assisted and endorsed by the Alzheimer’s Society.

The charity has Mark’s blog about Sylvia’s condition on its website, shares their diet and exercise regime and puts their recipes on flyers.

In addition Mark’s workplace Slater and Gordon has given its support, which has included rolling out new ‘brain-boosting’ menus in the Manchester law firm’s staff canteen.

And the crowning glory is that the mum and son have been invited to the Queen’s Garden Party this summer, in recognition of Sylvia’s efforts to give hope to thousands of others affected by dementia.

Mark said: “For my mum, knowing that she has helped other people, has really helped her.

“I did this for my mum - she has got the condition and she has done all the hard work - but if what we’ve achieved can benefit other people as well then that’s great.

“This country is lagging behind other countries, care homes are bulging with people who have been written off. But as people get older they still have a role to play in society.

“People don’t realise but dementia is the number one killer in this country ahead of heart disease or cancer, but it doesn’t get the same funding, it is a crisis.”

Sue Clarke, from the Alzheimer’s Society, said: “It’s fantastic that Sylvia along with her son Mark have taken action to create a personal plan that works well for her dementia diagnosis.

“There is currently no cure or way of preventing the progression of the condition, but taking regular gentle exercise, eating a healthy diet and doing cognitive exercises can help someone with dementia manage their condition more effectively.

“In the UK, one person develops dementia every three minutes and almost everyone knows someone whose life has been affected. Yet too many people face the condition alone without adequate support.

“Alzheimer’s Society can provide advice on how you can live the well with the condition.”

Dementia Action Week will take place from May 21 to 27, fro more information visit alzheimers.org.uk/DAW. 

April 5th 2018

The magnetic therapy that could recover your memories

Try to recall a conversation without hearing it in your head. It’s difficult, because sound impacts our memory formation. That’s why we forget the milk at the store, and leave without the one thing we came for: we heard the instructions, but we didn’t really listen. 

Maintaining a sound in your mind’s ear—that is, how we imagine it, keep hearing it, and retrieve it after it’s gone—is called auditory working memory.

This cognitive capacity to keep sounds in mind for a short period of time was the focus of a paper published in Neuron by a team at McGill University’s Brain Imaging Centre. The study tested the efficacy of a non-invasive brain therapy called transcranial magnetic stimulation, or TMS. Using a hand-held device placed against the scalp, the researchers positioned the targeted, oscillating pulses (at 5 Hz) into the brain in order to stimulate nerve cells. (The pulses are reportedly not painful.)

The group found some surprising results. TMS seemed to directly improve the working memory of 17 participants in a recall task. Participants were asked to recognize a melody when the order of notes played back was reversed. After TMS treatment, they were able to remember the series of sounds quicker, and more accurately.

“The most exciting aspect is that we found a causal link between brain and behavior,” Philippe Albouy, one of the study’s co-authors, told The Daily Beast. “TMS is easy to control because the stimulation is focused. When you’re targeting a given brain region, you’re sure that you’re hitting that region.”

TMS was recently granted FDA-approval to treat depression, and the treatment is covered by some health insurance plans. The McGill University study focused on theta wave activity in the auditory dorsal stream, a pathway in the brain that helps us process speech. The group also compared the data to the control condition of TMS at 5 Hz with non-rhythmic pulses. The participants’ brain activity was simultaneously tracked with two technologies: a massive, cocoon-like  magnetoencephalography (MEG) scanner, which records the magnetic fields produced by ‘brain waves’; and an electroencephalogram (EEG), a cap-like set of small discs (electrodes) pasted all over the scalp to track the brain’s electrical activity.

“This means that we can use brain activity as a marker for later interventions,” Albouy said. “That’s the interesting part.”

The study’s results suggest broader clinical applications, according to Albouy. TMS, a “relatively painless” tool that doesn’t require anesthesia or hospitalization, has the potential to treat other patients who have deficits in working memory, such as people with Parkinson’s disease or Alzheimer’s disease, or children and adults with ADHD.

“I think you can say that this method could apply to almost everything,” Albouy said. “The only thing is that you have to define a brain marker to a given task. The task can be what you want. It could be attention, visual perception, or memory. Once you have this marker and the region of interest, then you can apply rhythmic stimulation during the task in order to improve performance.”

Though TMS is an emerging, experimental technology, some studies have shown—though at times with mixed results—that the technique has the potential to improve the lives of people with autism and post-traumatic stress disorder (PTSD), and those who struggle with addiction, and chronic pain. A similar study in Science by a team of researchers at the University of Wisconsin-Madison demonstrated that TMS can help us remember: Recent memories can be brought back, and recalled. 

Yet researchers haven’t found a way to help participants sustain their improved working memory. Typically, their performance plummets after leaving the TMS machine behind.

Albouy’s team is working on this problem. He’s currently developing a study with HIV-positive patients who are coping with memory deficits.

“We are trying to see if we can observe any after effects. Then, we will apply it to a clinical population, step by step,” Albouy said. “We’re trying to find some patterns. It’s a promising approach.”

The TMS technique described in the study has the potential to be ready for clinical applications in as soon as a year (next spring), Albouy said. “I’m not sure. I can’t really predict it. We are really in the early stages of this approach, so it’s difficult to predict,” he said.

Another future path for research is how sound impacts long-term, rather than working, memory. Evocative or emotionally-charged sounds can change what we can remember—and what we forget. Sound can take over what we think and how we feel. It’s how a song takes you back. It’s how accents move through families and time zones. It’s anticipating the pause before someone tries to pronounce your last name. (The author's last name, for example, “Beebe,” is pronounced bee-bee, like two insects buzzing.) It’s the lilt in the voice of the person you love, the music of how they talk or laugh or scream or sing.

March 28th 2018

Alzheimer’s memories could be switched back on with implant

Alzheimer’s sufferers could once again remember the faces of loved ones, or find their way back home, after scientists developed a way to boost memories.

In a groundbreaking pilot study, US researchers recorded memories as they were being formed and then later played them back into the brains of 10 patients.

They found that it increased memory performance by up to 37 per cent.

The study was funded by US Department of Defense's military research department, (Darpa), and focused on improving episodic memory, which is the most common type of memory loss in people with Alzheimer's disease, stroke and head injury.

Episodic memory is information that is new and useful for a short period of time, such as where you parked your car or left your keys.

“This is the first time scientists have been able to identify a patient's own brain cell code or pattern for memory and, in essence, write in that code to make existing memory work better, an important first step in potentially restoring memory loss,” said Dr Robert Hampson, professor of physiology/pharmacology and neurology at Wake Forest Baptist.

 “In the future, we hope to be able to help people hold onto specific memories, such as where they live or what their grandkids look like, when their overall memory begins to fail.”

"We envision this system being made into an implant to provide continuous support to a person’s ability to encode and store new memories.

"A patient would visit with a clinician periodically to ensure the system is working properly, but the closed-loop system is being designed to continuously read, analyze, and support the patient’s innate memory function." 

Around 850,000 people are suffering from dementia in Britain, and around two thirds have Alzheimer’s disease, in which sticky amyloid plaques build up in the brain, preventing brain cells from communicating, and wiping out memory.

For the new study, researchers enrolled 10 epilepsy patients who were already participating in an separate experiment mapping their brains, and so already had electrodes implanted in their heads.

The participants were asked to study a simple image - such as a coloured block - while their brain activity was recorded. Scientists then blanked the screen and asked them to choose the correct image from five options.

They found that when they asked people to remember, while playing back the recorded memory into the hippocampus region of their brains, their performance improved by 37 per cent. The hippocampus is responsible for forming memories, and spatial recognition and is one of the first areas to be damaged in Alzheimer’s disease.

In a second test, participants were shown a highly distinctive photographic image, followed by a short delay, and asked to identify the photo out of four or five others on the screen 75 minutes later. They found that playing back the recorded memories boosted recall by 35 per cent.

“We showed that we could tap into a patient's own memory content, reinforce it and feed it back to the patient,” added Dr Hampson.

"Even when a person's memory is impaired, it is possible to identify the neural firing patterns that indicate correct memory formation and separate them from the patterns that are incorrect.

“We can then feed in the correct patterns to assist the patient's brain in accurately forming new memories, not as a replacement for innate memory function, but as a boost to it.”

Commenting on the research, British experts said the study provided important ‘stepping stones’ into understanding how memories form, which could one day lead to new treatments for Alzheimer’s disease.

Dr James Pickett, Head of Research at Alzheimer’s Society, says: “Future tests using this method in people with Alzheimer’s could represent a vitally needed new form of treatment for dementia.

“With no new drug for dementia in the past 15 years, and one person developing the condition every three minutes, it’s more urgent than ever to find new ways to treat the condition.

“These kind of ‘first-in-human’ studies are important stepping stones to understanding how we make memories.”

Dr David Reynold’s, Chief Scientific Officer at Alzheimer’s Research UK, added: “People with Alzheimer’s disease often have difficulty recalling recent events, even while still being able to remember things that happened decades earlier.

"Techniques that boost a person’s ability to lay down new memories could potentially help tackle one of the most common symptoms affecting people with dementia.

“Complex technologies like this take years of research to hone, but improving life changing symptoms like memory loss is an urgent goal for dementia research. To accelerate progress towards new treatments we must see continued investment in research.”

The research was published in the Journal of Neural Engineering.

March 20th 2018

Stem cell transplant trial has 'miraculous' effects on multiple sclerosis sufferers

Doctors are hailing a new stem cell treatment for the degenerative disease multiple sclerosis, after trials showed it to reboot patients' immune systems, halting the disease.

Patients said the results were ‘a miracle’ and had seen them return to normal life after the disease left them in a wheelchair or unable to read.

Around 100,000 people in the UK have multiple sclerosis, a condition where the immune system attacks the nerves of the brain and spinal cord causing problems with vision, movement, and balance.

Early results from a clinical trial run from four international centres show that wiping out the patients’ immune systems with chemotherapy, and restoring them with the new stem cell treatment, appears to halt the disease and improve symptoms.

“We are thrilled with the results – they are a game-changer for patients with drug-resistant and disabling multiple sclerosis,” Professor John Snowden, director of blood and bone marrow transplantation at Sheffield’s Royal Hallamshire Hospital which led the UK part of the trial, told the BBC.

Independent experts also welcomed the trial, and called on the NHS to ensure everyone who could benefit from stem cell transplantation can access it.

The treatment, called haematopoietic stem cell transplantation (HSCT), was trialled in a group of 100 patients with relapsing remitting multiple sclerosis – the most common form of the disease.

This type of MS usually strikes in a patient’s 20s or 30s, with new symptoms appearing (relapsing) followed by a period of remission where symptoms may improve or remain stable for months, or longer.

Some patients do not respond to drug treatments intended to slow the disease and these relapses become more common.

In the trial, 110 patients who had two periods of relapse in the past year were registered at hospitals in Sheffield and Chicago, as well as Sao Paolo in Brazil and Uppsala in Sweden.

All patients underwent chemotherapy to wipe out their defective immune cells, then half were given a boost of stem cells taken from their blood and bone marrow while the rest underwent conventional drug therapies.

In the trial’s first year only one patient in the stem cell group experienced a relapse in their symptoms, compared to 39 in the drug group.

The patients were followed up with after three years, on average, the stem cell transplant only failed in three of the 52 original patients (six per cent) compared with a failure rate of 60 per cent in the drug group.

Those patients who continued to deteriorate were allowed to switch to the stem cell treatments. Around 30 did, and their condition also improved.

Two years ago Louise Willetts’ MS had become extremely severe. She was in a wheelchair and struggling to read, and had given up on her family and career ambitions.

“It does feel like a miracle. I almost have to pinch myself and think ‘Is this real l? Is it really gone, is it ever going to come back?'” she told the BBC in an interview.

Since she became one of the trial participants at Royal Hallamshire Hospital, Louise is symptom-free and there is no sign of the disease attacking her brain.

“It feels like my diagnosis was just a bad dream because I have just gone back to how I was before I got diagnosed,” she said.

The results were presented at the Annual Meeting of the European Society for Blood and Bone Marrow Transplantation on Sunday, but they have yet to be published in a peer-reviewed journal.

However, scientists said the reported results were more impressive than anything seen in previous trials.

Professor Basil Sharrack who was also part of the Sheffield team, said: “Almost all patients receiving HSCT showed no signs of their disease being active a year on from having the treatment.

“More importantly, their level of disability improved significantly.”

Dr Susan Kohlhaas, director of research at the Multiple Sclerosis Society, said the next step was to compare this stem cell transplant with less drastic treatments and to make it available to as many people who could benefit as possible.

“The trial results are important and show this area needs further research.

“While HSCT appears to be effective for some people with MS, it remains a high-risk treatment that won’t be right for everyone.

“HSCT will soon be recognised as an established treatment in England. And when that happens our priority will be making sure those who could benefit can actually get it.

“We’ve seen life-changing results for some people and having that opportunity can’t depend on your postcode.” 

March 4th 2018

No firm proof that a healthy diet protects against dementia, scientists conclude

There is no firm evidence to conclude that a healthy diet protects against dementia, government advisers say.

The Scientific Advisory Committee on Nutrition (SACN) said there is no proof that any specific nutrient or food supplement can ward off the brain-wasting disease.

The review considered dozens of trials examining the role of different types of diets and supplements.

It said several studies found those eating the Mediterranean diet - a regime rich in fish, vegetables, fruit and legumes - were less likely to develop dementia

But the review concluded that such evidence was “observational” - meaning it could not demonstrate that the healthy eating habits were the reason for the lower rates of disease.

Those choosing such a diet may have had other habits - such as higher exercise levels - which are also linked to a lower rate of dementia.

Previous research has suggested omega-3 fish oils and vitamin B may ward off the brain-wasting disease. But the review said: “There is no evidence that specific nutrients or food supplements affect the risk of cognitive impairment or dementia”.

The committee advises the Department of Health and Public Health England (PHE) on health matters.

Dr Alison Tedstone, PHE chief nutritionist, said: “This report broadly supports existing advice to eat a healthy diet, as depicted in the Eatwell Guide.

“However, while the report indicates there isn’t currently enough overall evidence to support a relationship between diet and the prevention of dementia, a healthy balanced diet is vital in achieving a healthy weight and avoiding obesity-related health problems - including type 2 diabetes, heart disease and some cancers.”

Britain’s obesity rates are the worst in western Europe, with rates rising even faster than those in the US.

The SACN report concluded that that adherence to a Mediterranean dietary pattern is associated with a reduced risk of mild cognitive impairment and dementia, including Alzheimer's disease.

But the authors stressed that most evidence behind this finding comes from observational studies - which means that no firm conclusions can be drawn about cause and effect - and they called for more evidence to establish the link.

And there is not enough evidence to confirm a link between taking individual nutrients - including B vitamins, vitamins C and E and omega-3 fatty acids - and risk of dementia.

Dr Matthew Norton, director of policy and impact at Alzheimer's Research UK, said: "The brain, just like other parts of the body, can be affected by the way we live our lives. While a balanced diet is one way to maintain a healthy brain, the best current evidence suggests supplements or nutrients offer no additional preventative value.

"Wider evidence points to a number of other lifestyle factors that can also play a role. Not smoking, staying mentally and physically active, only drinking in moderation and keeping blood pressure and cholesterol in check are all ways to keep the brain healthy into later life."

Feb 2nd 2018

'The holy grail': Simple BLOOD TEST could detect Alzheimer's disease before symptoms appear

Results showed that the test was accurate 90 per cent of the time.

In what is being described as the ‘holy grail of Alzheimer’s research’, scientists have developed a blood test that can detect the build-up of toxic proteins linked to dementia . 

Researchers from the National Centre for Geriatrics and Gerontology in Japan developed the test, which detects amyloid-beta levels in the blood, indicative of levels in the brain.

The team hopes the test could one day be used to treat patients with dementia before symptoms occur.

In the study, the researchers tested the method on 373 people, including healthy people, those with memory loss and people diagnosed with Alzheimer’s disease.

While there are currently brain scans available that can detect amyloid-beta levels, these are expensive and impractical.

The researchers hope their blood test could offer a cheaper and easier alternative in the near future - although they highlight that further trials are needed.

Dr Doug Brown, Chief Policy and Research Officer at Alzheimer’s Society, said: “A blood test is much quicker and cheaper than a brain scan or spinal tap, so this could be a useful tool for researchers to identify people at risk of Alzheimer’s for further investigation.”

Professor Paul Morgan, an immunology expert from Cardiff University , described the findings as the ‘holy grail’ of Alzheimer’s research.

He said: “The availability of such markers would facilitate early diagnosis, allow early intervention and perhaps provide a means of demonstrating response to intervention.”

Jan 31st 2018

Mind diet: Medical researchers reveal new eating plan to combat cognitive decline

A new diet created by scientists may help slow cognitive decline in stroke survivors. 

Called the MIND diet (short for Mediterranean-DASH Diet Intervention for Neurodegenerative Delay), the eating plan is a mix of the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) diets.

Both diets have been found to reduce the risk of cardiovascular conditions such as hypertension, heart attack and stroke.

Key foods to eat on the MIND diet are vegetables, berries and fish, and foods to avoid are sugar and pastries.

The preliminary findings from researchers at Rush University Medical Centre were presented at the American Stroke Association's International Stroke Conference 2018 in Los Angeles and are particularly significant because stroke survivors are twice as likely to develop dementia compared to the general population.

“The foods that promote brain health, including vegetables, berries, fish and olive oil, are included in the MIND diet,” said Dr. Laurel J. Cherian, a vascular neurologist and assistant professor in Rush’s Department of Neurological Sciences. “We found that it has the potential to help slow cognitive decline in stroke survivors.”

Study co-author Martha Clare Morris, ScD, a Rush nutritional epidemiologist, and her colleagues developed the MIND diet based on information from years of research about what foods and nutrients have good and bad effects on the functioning of the brain.

The researchers found that following the diet could reduce the risk of Alzheimer’s in the elderly and even those who didn’t adhere to the diet strictly had a reduced risk of AD and cognitive decline.

There are 15 dietary components of the MIND diet - 10 “brain healthy food groups” and five unhealthy groups.

The foods in the unhealthy list are red meat, butter, cheese, pastries and sweets, and fried or fast food.

Butter is limited to less than 1.5 teaspoons a day, you should have less than five servings a week of sweet treats and pastries, and less than one portion a week of whole fat cheese and fried or fast food.

What foods should you eat?

To adhere to the MIND diet you need to make sure you eat at least three servings of whole grains a day, as well as two portions of vegetables, one of which must be a leafy green.

A glass of wine a day is also encouraged, you should snack most days on nuts, have beans roughly every other day, eat poultry and berries at least twice a week and have fish once a week.

“I was really intrigued by the results of a previous MIND study, which showed that the people who were most highly adherent to the MIND diet cognitively functioned as if they were 7.5 years younger than the least adherent group,” Cherian said.

“It made me wonder if those findings would hold true for stroke survivors, who are twice as likely to develop dementia compared to the general population.”

From 2004 to 2017, Cherian and colleagues studied 106 participants of the Rush Memory and Ageing Project who had a history of stroke for cognitive decline, including decline in one’s ability to think, reason and remember.

They assessed people in the study every year until their deaths or the study’s conclusion, for an average of 5.9 years, and monitored patients' eating habits using food journals.

Participants were put into groups based on whether they were highly adherent to the MIND diet, moderately adherent or least adherent. Other factors known to affect cognitive performance were also taken into consideration, such as age, gender, education level, participation in cognitively stimulating activities, physical activity, smoking and genetics.

The study participants whose diets scored highest on the MIND diet score had substantially slower rate of cognitive decline than those who scored lowest.

Jan 29th 2018

SEX can make you look seven years younger - but that's not the only benefit

Partner “not in the mood” again? Then it might be worth sharing the following to change their mind!

According to the latest studies, regular sex – that’s one to two lovemaking sessions per week – can provide some incredible boosts to your health and wellbeing.

1. Look younger

Dr David Weeks, clinical neuropsychologist revealed to a psychology conference that his extensive research had found older men and women with an active love life looked five to seven years younger than their actual age.

But you don’t have to be at it every night to enjoy youth-enhancing effects! In fact, during his 10-year study, Weeks found quality was as important as quantity, with the anti-ageing benefits stronger if the sex was classed as “loving”.

2. Boost your fertility

This will sound like music to most men’s ears – studies have found that the more often you make love, the better quality your sperm will be.

Semen health was found to be best when sex had last occurred less than two days before the sperm was tested and was greatly decreased after 10 days of abstinence.

ALSO READ: Why women should stop faking orgasms

If you’re trying for a baby, keep sperm fresh and in tip-top shape by having sex at least twice a week, and not only around the time of the woman’s ovulation.

Frequent sex has also been found to help balance a woman’s hormones and regulate her periods, which can further boost chances of conceiving.

3. Fight colds and flu

Having sex once or twice a week has been found to raise your body’s levels of an antibody called immunoglobulin A, or IgA, which can protect you from colds and flu. One study found people who have sex more than once a week have 30% higher levels of IgA than those who abstain.

4. Disease-proof your body

Having high levels of the natural steroid DHEA, known as “the anti-ageing hormone”, is believed to be key to keeping your body fitter for longer. During sex, DHEA is secreted throughout the body, and after an orgasm, the level in the bloodstream soars to five times its normal amount.

5. Lengthen your life

ALSO READ: Guide to dating a younger man

A study carried out found people who climaxed at least three times a week had a 50% lower chance of dying for any medical reason than those who only climaxed once a month.

6. Shift your middle-age spread and keep fit

Thirty minutes of vigorous sex burns up to 100 calories, which is the same as a small glass of wine.

And if you have moderately active sex twice a week, you’ll burn an extra 5,000 calories a year!

Varying your positions is also a great, fun way to tone different muscle groups and keep limbs lean and flexible.

7. Ease those nasty period cramps

Many women say period pain diminishes if they do the deed during a cramp attack.

One theory why is that muscle contractions that occur when you reach peak levels of excitement relieve tension in the muscles of your uterus – the ones that cause menstrual cramps – therefore easing the pain.

8. Helps lower your risk of incontinence

Good sex is a great workout for a woman’s pelvic floor muscles – the muscles that control orgasms and also stem the flow of urine, reducing leakage and incontinence.

Pregnancy and the menopause can weaken these muscles significantly, but the stronger they are, the lower your risk of developing stress incontinence and prolapse later.

And let’s face it, sex is far more enjoyable than the chore of doing pelvic floor exercises on your own!

9. Prevent a heart attack

Lots of studies have found that regular sex can ward off heart attacks, not bring them on as it was once feared.

One study at Queen’s University Belfast found that having sex three times a week could halve your risk of having a heart attack or stroke.

Another study in Israel found that women who had two orgasms a week were up to 30% less likely to have heart disease than those who did not enjoy sex or didn’t have an orgasm.

10. Increase your attractiveness to others

High sexual activity makes the body release more pheromones, chemicals that enhance your appeal to the opposite sex.

This is why the more sex you have with your partner, the stronger your desire will be to have sex with them again.

11. Smooth out your wrinkles

The hormone oestrogen is pumped out during sex, which can in turn have a plumping effect on the skin, helping to smooth out those fine lines. This is especially useful following the menopause, when a woman’s skin can become drier and more wrinkled, as oestrogen levels naturally drop.

One American study found that menopausal women who had sex every week had oestrogen levels that


12. Give yourself an all-over healthy glow

According to research carried out at the Royal Edinburgh Hospital, sex promotes skin renewal because it is an aerobic form of exercise.

The scientist behind this study found that vigorous sex pumps higher levels of oxygen around the body, increasing the flow of blood and nutrients to the skin, and pushes newer, fresher skin cells to the surface, making skin look healthier.

13. Improve your self-esteem

One of the most important benefits, noted in a recent survey undertaken by the University of Texas, US, was that participants who had sex regularly felt more confident about their bodies.

14. Lower your blood pressure

A Scottish study found men and women who had plenty of sex coped well with stress and had lower blood pressure than those who abstained. Researchers at Brigham Young University in the US also linked frequent intercourse to lower blood pressure.

15. Banish depression

Like any exercise that raises your heart rate, sex causes your brain to release feel-good chemicals that boost your levels of serotonin – the happy hormone – to lift your mood. Serotonin is the body’s key antidepressant chemical and one of the major reasons people smile and feel happy and relaxed after sex.

Sexually active women in long-term relationships are also less likely to feel depressed than women who go without sex, according to a study of nearly 300 women by psychologist Gordon Gallup in the American Archives Of Sexual Behavior.

16. Cure that headache (yes, really!)

“Having a headache” might be an age-old excuse not to have sex, but the scientific evidence says that, to the contrary, sex can help shift pain! This is because making love causes a surge in the “love” hormone oxytocin, plus other feel-good endorphins, which can ease pain.

Women have reported that their pain from both headaches and arthritis improved post-coitus.

17. Slash stress

Research has also shown that touching and cuddling during and after sex reduces the body’s levels of cortisol – the hormone that is secreted when you’re stressed.

18. Kick your insomnia into touch

The oxytocin released when you orgasm has another benefit – it can help you drop off, research claims.

Both men and women release this feel-good hormone just before orgasm, and as it courses through your system, it promotes relaxation and sleepiness. So there is actually a genuine excuse for him to fall asleep so quickly after sex...

19. Strengthen your bones

As regular sex can boost oestrogen levels in post-menopausal women, it can offer some protection against the bone-thinning condition osteoporosis that is triggered by a lack of oestrogen.

And men can benefit too, as testosterone levels have been found to increase during and after sex, which can provide some protection against male osteoporosis.

20. Cut your risk of prostate cancer

Researchers at Nottingham University have found that men who enjoy a regular sex life in their 50s are at lower risk of developing prostate cancer.

This is because sex clears the prostate of toxins that could otherwise linger and trigger cancerous changes.

21. Feel better all day

If you decide to go for a spot of morning passion to start your day, the boost to your mood it provides can continue right through until night-time, according to research.

The American scientist Dr Debby Herbenick found that adults who made love first thing in the morning were not only more upbeat for the rest of the day, but they also benefited from a stronger immune system than those people who simply opted for a cup of tea and some toast before heading out of the door.

In other words – why wait until tonight?

Jan 27th 2018

Eating turmeric once a day could improve memory and happiness

An ingredient that is used to give curry its bright colour could also improve your memory and mood, new research suggests.

Found in turmeric, curcumin is hailed as an anti-inflammatory with antioxidant properties, and it has also been suggested as a possible reason that senior citizens in India - where curcumin is somewhat of a staple - have lower rates of Alzheimer's disease and better cognitive performance.

Published in the American Journal of Geriatric Psychiatry, the research conducted by the University of California Los Angeles set out to examine the effects of the ingredient on people with mild, age-related memory loss. 

“Exactly how curcumin exerts its effects is not certain, but it may be due to its ability to reduce brain inflammation, which has been linked to both Alzheimer's disease and major depression,” said Dr. Gary Small, director of geriatric psychiatry at UCLA's Longevity Center and study author.

The 40 participants were aged between 50 and 90-years-old and all presented with mild memory complaints.

Half of them were assigned 90 milligrams of curcumin twice daily for 18 months, while the rest were given a placebo.

After monitoring curcumin levels in their blood and undergoing cognitive assessments and PET scans, the study found that those who took curcumin saw significant improvement in both memory and mood.

In memory tests, the people taking curcumin improved by 28 percent over the 18 months and also showed mild improvement in their overall disposition. 

Now, the researchers plan to conduct a follow-up study with a larger number of participants.

They also hope to explore whether its effects vary according to people’s age or their genetic risk for Alzheimer’s, and it’s potential to help with mild depression.

“These results suggest that taking this relatively safe form of curcumin could provide meaningful cognitive benefits over the years,” Small concluded

Jan 1st 2018

A diabetes drug may be used to treat Alzheimer’s disease

A diabetes drug may one day be used to treat Alzheimer’s disease after “significantly” reversing memory loss in mice, scientists believe.

Employed to treat type 2 diabetes, it helped cut the volume of amyloid plaques lined to the degenerative brain disorder, University of Lancashire researchers found.

It also raised levels of a chemical which helps brain cells function.

Prof Christian Holscher, who led the team, said: “Multiple receptor drugs have shown neuro-protective effects.

"Here a triple receptor shows promise as a potential treatment for Alzheimer’s.

“These very promising outcomes demonstrate the efficacy of these novel multiple receptor drugs that originally were developed to treat type 2 diabetes but have shown consistent neuro-protective effects in several studies.

"Clinical studies with an older version of this drug type already showed very promising results in people with Alzheimer's disease or with mood disorders.

He said more tests are needed.

Dr Doug Brown, of The Alzheimer’s Society, said: "With no new treatments in nearly 15 years, we need to find new ways of tackling Alzheimer's.

"It's imperative that we explore whether drugs developed to treat other conditions can benefit people with Alzheimer's and other forms of dementia.

"This approach to research could make it much quicker to get promising new drugs to the people who need them.

"Although the benefits of these 'triple agonist' drugs have so far only been found in mice, other studies with existing diabetes drugs such as liraglutide have shown real promise for people with Alzheimer's, so further development of this work is crucial."

In the UK around 850,000 have dementia, mostly Alzheimer’s.

Type 2 diabetes is known to be a risk factor for Alzheimer's.

The tests used genetically modified mice who had been given genes linked to an inheritable form of the brain disease.

Dec 23rd 2017

Forgetting a loved one's Christmas present could be an early sign of dementia, health officials have warned. Families are being urged to look out for signs of Alzheimer’s disease when they see elderly relatives over the festive season.

Prof Alastair Burns, the NHS national clinical director for dementia,said forgetting a present, a loved one’s name or getting confused while cooking Christmas dinner could be a warning of the early signs of dementia.

Charities said their helplines receive a surge in calls in January, after families became aware that that older relatives were struggling.

“Something as simple as forgetting to put the oven on for the Christmas turkey may be a warning that a loved one is experiencing the early stages of dementia,” officials said.

Prof Burns said: “Dementia is something that happens slowly so it may slip by unnoticed in people we see regularly. That’s why the Christmas visit to wider family and friends is an opportunity to spot the early warning signs.Confusion in a new environment - such as a hotel or unfamiliar home of a relative could also signal problems they warned. So could forgetting a present for a niece or nephew, or repeatedly forgetting the names of loved ones, they said.

“The important thing is to look for changes in normal behaviour,” he said.

“While it may be tempting to put forgetfulness down to one too many Christmas brandies, it could be a sign of something more serious so I would urge everyone to take a bit of extra time to consider if someone they know may need help.”

Dec 19th 2017

There’s no proven method for preventing dementia in later life, a review of multiple studies has found.

Researchers wanted to determine whether physical activity, prescription medications, brain training or over-the-counter vitamins and supplements could help prevent dementia.

The vast majority of research showed that none of the interventions worked.

The number of people with dementia is expected to increase dramatically as the population ages, which is why researchers from the Minnesota Evidence-based Practice Centre (EPC) wanted to analyse possible interventions for the disease.

Findings from four systematic evidence reviews, published in the journal Annals of Internal Medicine, concluded that nothing seemed to be able to prevent dementia in patients who did not have it at the time.


For the first review, researchers looked at data from 16 trials comparing physical activity with inactivity.

They found insufficient evidence to be able to draw conclusions about the effectiveness of aerobic training, resistance training, or tai chi for improving cognition.

That said, they did find ‘low-strength’ evidence that combining different types of interventions at the same time - such as physical activity, diet and cognitive training - improved overall cognitive test performance.

Prescription drugs

The researchers also reviewed data from 51 trials comparing the effect of prescription medication on cognitive outcomes.

The evidence did not support the use of any of the studied pharmacologic treatments (dementia medications, antihypertensives, diabetes medications, NSAIDs or aspirin, hormones, and lipid-lowering agents) for cognitive protection.

Related: 5 Surprising Causes Of Alzheimer's Disease (provided by Prevention)


A review of 11 trials of adults with either normal cognition or mild cognitive impairment at the time of enrollment found insufficient evidence that brain training exercises could prevent dementia.

Vitamins and supplements

Researchers reviewed 38 trials comparing over-the-counter (OTC) supplements, including omega-3 fatty acids, soy, ginkgo biloba, B vitamins, vitamin D plus calcium, vitamin C, beta carotene and multi-ingredient supplements.

They compared these with either a placebo supplement or other interventions for preventing or delaying cognitive decline, and found insufficient evidence to suggest that any of the supplements worked.


The researchers said the reasons why these interventions fail is not entirely clear. It is possible that they simply do not work to improve cognition, or it could be that the studies started the interventions too late in life or didn’t use them for long enough.

They noted that while there was no evidence about whether an intervention to practice a healthy lifestyle earlier in life protects against cognitive decline or dementia, it is unlikely to worsen cognition and may have other health benefits.

Commenting on the study, James Pickett, Head of Research at Alzheimer’s Society, told HuffPost UK: “There is no sure way to prevent dementia and, as these studies show, we have not yet found a successful way to reduce cases of the condition. However, studies looking at natural lifestyle differences like exercise, diet and smoking show that these factors do play a role in determining a person’s dementia risk.

“We need much more focus on research into reducing the risk of dementia if we are to develop intervention and prevention programmes that work.”

Related: ‘Super Mario 64’ Can Help Againtst Alzheimer’s? (provided by Wochit News)

Dec 12th 2017

Hearing loss could be an early sign of dementia

New research has shown an association between

Dementia can have a devastating effect on sufferers and their families, but scientists are still trying to understand exactly why and how it develops, and as yet there is no cure.

One of the latest discoveries is that hearing loss could be an early sign of the disease, with researchers at Trinity College Dublin finding an association between age-related hearing loss (ARHL) and the development of dementia.

The study

In a review of over 20,000 participants, ARHL was linked to decline in a number of areas of cognitive functioning, including episodic memory and a slower processing speed. Previous studies have shown that hearing loss precedes the onset of dementia by five to 10 years.

As a result of the study, experts say that a hearing aid could help prevent dementia by improving verbal communication and keeping the brain healthy. David Loughrey, a PhD candidate who worked on the research, told the Daily Mail:

"Hearing loss is easily diagnosed and can be treated. Although associations were small, treatment may cumulatively benefit cognition.  

Dr Carol Routledge, director of research at Alzheimer's Research UK said there may be a link between hearing loss and dementia, but the lack of mental stimulation experienced by those who are hard of hearing may also play a role. She said:

"This small but statistically robust association between hearing loss and a decline in memory skills adds to mounting evidence of a link, but the study does not conclusively show that hearing loss is driving memory problems... Hearing loss is associated with dementia risk factors like heart disease, which could also be an underlying reason for the link observed in this study."

She added;

"Some research suggests that being socially engaged and mentally active could help to boost cognitive reserve – a kind of mental resilience that may delay the effects of a disease like Alzheimer's... As things that we hear can provide mental stimulation and a means of social interaction, a loss of hearing could influence cognitive reserve, leaving people more vulnerable to memory and thinking decline."

Nov 22nd 2017

DEMENTIA development could be aided by virus, toxins and heat on cells, according to scientists. Discovery hailed as "new chapter" in Alzheimer’s research.

Dementia - and its most common form, Alzheimer’s disease - are on the rise, with over a million sufferers predicted in the UK by 2025.

Scientists now know that the neurodegenerative disease is caused by gradual death of brain cells. 

While a cure is still to be found, it is thought clearing dementia-causing plaques and tangles from the brain could be the answer - and our exposure to viruses and toxins may have something to do with it.

A new study by Boston University in the United States has found that reducing levels of ‘stress granules’ may help fight the disease, and the discovery has been hailed as a “new chapter” in Alzheimer’s research.

These ‘stress granules’ are blobs of molecules called RNA that are caused when our cells are exposed to viruses, toxins and heat.

While stress may seem to have a more obvious effect that triggers muscles to tense, heart rate to speed up and blushing, cells can become ‘stressed’ too and this could affect long-term health.

Researchers found that lowering levels of ‘stress granules’ in mice altered the type and amount of clumping in the brain of tau - a protein that causes Alzheimer’s when it becomes defective and tangles around the nerve cells.

By reducing ‘stress granules’, they were able to increase life span and boost memory in mice.

Scientists believe the new findings could provide a better understanding of Alzheimer’s, and possibly lead to a future cure.

“This is a pretty big new chapter in the study of Alzheimer’s disease,” said Professor Benjamin Wolozin, senior study author from Boston University.

“Amyloid is still toxic. Tau is still toxic. Those are still important targets. 

“But there’s this whole other pathway that you can really go in and start drugging.”

The researchers explained that when a cell is met with stress, it stops doing all unnecessary activities so it can focus on dealing with the stress.

To do this, the cell gathers RNA - which does all the non-essential work of a cell - into ‘stress granules’ for safe-keeping, and it will then revisit them once the stress has passed.

However, sometimes they’re forgotten about and in people who have Alzheimer’s the ‘stress granules’ have been left untouched and can be found in the tau tangles of patients.

Researchers are hopeful what has been shown in mice will translate to humans.


Aug 25th 2017

Those who suffer from long-term gum disease are 70% more likely to develop dementia, researchers have found.

According to The Times, scientists believe that inflammation caused by years of mouth problems could eventually damage the brain.

Although researchers could not prove that gum disease is a direct cause of Alzheimer's, they did say that thorough tooth-brushing could be advised to ward off dementia if the link was confirmed by further research.

The study, conducted in Taiwan, looked at 28,000 people, comparing those who had a recent diagnosis of chronic periodontitis with those who didn't over a 10-year period.

There was a marked increase in the occurrence of Alzheimer's in those who had long term gum disease; these individuals were 70% more likely to develop the condition.

James Pickett, head of research at the Alzheimer's Society, told The Times:

"Although at first if does not seem obvious that gum disease could be linked to brain health, it is plausible that an immune reaction triggered by the gum disease could make its way to the brain and contribute to the development of dementia."

However, he told people with long term gum disease not to panic, adding that while a 70% increase "sounds like a big risk, only about one in 100 people with gum disease went on to develop dementia, showing that this figure is not necessarily a cause for alarm".

Aug 19th 2017

Restoring memory loss.

Experts say that the number of people living with Alzheimer’s disease is growing—and fast. While more than five million Americans live with this form of dementia today, that number could more than triple by the year 2050. But here’s some good news: Thanks to the most revolutionary research yet, doctors could soon restore memory loss in Alzheimer’s patients for good.

MIT researchers have successfully reversed memory loss in mice, according to a study published in the journal Cell Reports. They did so by blocking the enzyme HDAC2, which interferes with the genes associated with memory.

Memory loss in Alzheimer’s patients takes place when HCAC2 creates a blockade that shuts down the brain’s memory genes, causing forgetfulness and making memory formation more difficult. Since past research has failed to block the enzyme without toxic side effects, these results are groundbreaking.

'This is exciting because for the first time we have found a specific mechanism by which HDAC2 regulates synaptic gene expression,' lead author Li-Huei Tsai said. “If we can remove the blockade by inhibiting HDAC2 activity or reducing HDAC2 levels, then we can restore expression of all these genes necessary for learning and memory.'

Other researchers find Tsai’s research encouraging, as well. “As Alzheimer’s is now the biggest killer for women and the third for men, it is important that we think about putting as much emphasis on prevention as we do on treatment,” Dr Marilyn Glenville, one of the UK’s leading nutritionists and author of Natural Solutions for Dementia and Alzheimer’s, told The Independent. Maintaining these daily habits can keep your brain sharp and prevent Alzheimer’s disease.

Although the procedure has only been tested on mice so far, Tsai hopes that it will one day successfully restore long-term memory in humans, too. In the meantime, losing a loved one to Alzheimer’s is tough for both parties—and many don’t recognize the earliest symptoms. 

Aug 18 2017

People who can't distinguish between the smell of bubble gum and petrol could be at risk of developing dementia, according to new research.

By the time people start exhibiting the symptoms of Alzheimer's (such as memory loss), it's almost too late – the damage to your brain may have already been happening for decades. That's why so many scientists are trying to find ways to detect the disease at its earliest stage.

But now researchers at the Centre for Studies on Prevention of Alzheimer's Disease at the Douglas Mental Health Research Centre of McGill University believe your sense of small may be a useful marker for early signs of the disease.

The scientists asked 300 people with an average age of 63 who all had a parent with Alzheimer's disease to take multiple choice scratch-and-sniff tests to identify smells such as bubble gum, petrol or lemon. A third of these volunteers had regular lumbar punctures to measure for Alzheimer's related proteins in their spinal fluid.

Those who found it hardest to identify the smells were those who had more biological markers for dementia.

Marie-Elyse Lafaille-Magnan, a doctoral student at the centre said: "This is the first time anyone has been able to show clearly that the loss of the ability to identify smells is correlated with biological markers indicating the advance of the disease. For more than 30 years scientists have been exploring the connection between memory loss and the difficulty patients may have in identifying different odours."

Dr Carol Routledge, director of research at Alzheimer's Research UK cautioned that much larger research studies would be needed to determine how recognising smells is affected by brain changes in dementia and to see if a smell test could be developed for identifying those at risk of developing the condition.

She said: "While an odour detection test may one day support diagnostic approaches like brain scanning and pen and paper tests, this test is not yet able to reliably predict who will go on to experience memory and thinking decline or develop the symptoms of dementia."

March 31st 2017

New hope for Alzheimer sufferers

Makers of an Alzheimer’s drug are hoping it will become the first new treatment for the disease available to sufferers for over a decade if trials conclude successfully later this year.

The drug, called intepirdine, works by increasing the release of a chemical in the brain that plays an important role in memory function.

Its developers say unlike more experimental treatments, which have caused excitement in early stages but then failed in clinical trials, the drug works in tandem with existing medication to help people with dementia live more independently for longer.

“Studies based on theory can be successful, but several hundred of them have failed,” said Lawrence Friedhoff, chief development officer at Axovant, the company producing the drug.

“Our trial is replicating a study that already shows statistically significant benefit in humans, so it has a much higher chance of being successful.”

Alzheimer’s is the most common cause of dementia, a degenerative brain condition that affects more than 850,000 people in the UK, most of whom are over 65.

The last Alzheimer's drug to be approved was donepezil in 2002.​

While the intepirdine trial is not guaranteed to succeed, this drug is the only plausible new treatment being submitted for approval in the next few years, following a string of failures.

Among current drugs prescribed for the symptoms of the disease are medicines that prevent the breakdown in the brain of acetylcholine, which carries messages from one cell to another.

This new treatment could help slow memory loss in Alzheimer’s patients by increasing levels of acetylcholine in the brain, Dr Friedhoff told The Independent.

“Patients with Alzheimer's disease have less acetylcholine in their brains and less release of it than other people. And we know that can be part of what causes memory problems,” he said.

“The old drugs prevent the breakdown [of acetylchlone], the new drug promotes its release, and together they work better than either alone.”

Many other new Alzheimer’s drugs that have been trialled in recent years focussed on tackling the production of toxic amyloid proteins, which are associated with the formation of a nerve-cell destroying plaque in the brain.

But a number of high-profile trials, including one by pharmaceutical giant Merck that took place last year, ended in disappointment when the drugs in question were not found to be effective in a clinical setting.

“As far as I can tell, the only drug with reasonable chance of being approved in the next couple of years is ours,” said Dr Friedhoff. “The others have generally been based on this amyloid hypothesis and have either failed or are not going to read out for a couple of years from now.

“Most of the other trials have been based on the assumption that amyloid is important in causing Alzheimer's disease, as opposed to something that happens alongside it. 

“That assumption, I think, is probably wrong, which would explain why so many of these other drugs have failed," he said, adding: “Although I thought it was an interesting idea 15 years ago, I lost faith in it a long time ago as an approach to treating Alzheimer's.”

Tara Spires-Jones, interim director of Edinburgh University's Centre for Cognitive and Neural Systems, said the early data on the treatment looked “promising”.

She said if the drug were approved, while Alzheimer's patients would benefit, it would not stop or slow the progression of the disease, as amyloid-based treatments aimed to.

“It may provide more symptomatic benefit, but like the drugs that currently exist, it will not change the course of the disease. But it is great that people have another option, and maybe it will work better than the ones that are currently available,” she said.

Around 1,150 patients with mild to moderate Alzheimer’s are taking part in the current international trial, which has been offered at clinics around the UK including one in Plymouth.

If the trial is successful when it is completed this autumn, the drug will be submitted for approval in the US, which could take place as soon as this time next year, and then in Europe.

Two different compounds that work in a similar way to intepirdine have reached the end of testing in the last two months, but have been unsuccessful.

One of them, produced by a European drug company called Lundbeck, "attached itself to the same molecule, but the structure was quite different”, said Dr Friedhoff.

Trials of this drug hit problems because of raised liver toxicity – but if intepirdine can overcome any similar stumbling blocks, the path will be left clear for its approval.

James Pickett, head of research at the Alzheimer's Society, said the failure of the other two compounds should generate an "element of caution" around Dr Friedhoff's claims, but said its success was possible.

"It's completely plausible that there are subtleties between them, and difference in the way these things get into the brain," he told The Independent.

March 9th 2017

Memory loss and cognitive decline are commonly thought to be the earliest signs of the neurodegenerative disorder Alzheimer's, but a new study has found declines in glucose levels in the brain come even sooner — before the first symptoms appear. Even better? The same team also believes they have figured out a way to stop these levels from falling in the first place, a finding that could potentially prevent Alzheimer's.

Although doctors have long noted the association between declining glucose levels in the brain and the onset of Alzheimer’s disease, for the first time ever, a study now published online in the journal Translational Psychiatry has proved that these declining energy levels are a direct trigger for the cognitive impairments traditionally associated with the disease. According to a recent statement on the study, this may explain why diabetes, a condition in which glucose cannot enter the cells, is a known risk factor for dementia. According to the study, a protein known as p38 may be able to prevent this deprivation from occurring.

"The findings are very exciting," explained lead researcher Dr. Domenico Praticò in a statement. "There is now a lot of evidence to suggest that p38 is involved in the development of Alzheimer's disease."

For the study, the team purposely deprived the brains of mice of glucose in order to observe the result. As expected, these mice exhibited signs of decline to suggest that neural communication pathways in their brains had broken down. What’s more, the glucose-deprived mice performed significantly worse than control mice in maze memory tests. These mice also displayed high levels of phosphorylated tau and dramatically increased amounts of cell death in the brains, two other well known indications of Alzheimer's onset.

The study also identified p38 as a possible candidate for the development of a drug to prevent the onset of cognitive decline caused by low glucose levels. According to the research, this protein is naturally made in the body as a response to glucose deprivation. Future research will further investigate p38's role in memory impairments. 

Preventing Alzheimer's disease is a major goal for scientists around the world, and this year there have been several breakthroughs in this effort. For example, this July a team from Flinders University in Adelaide Australia in partnership with a research team at the Institute of Molecular Medicine, and University of California, Irvine released their efforts on creating a drug that could prevent brain protein buildup, the main hallmark of the disease. According to the research, these findings could lead to a vaccine against Alzheimer’s in as little as five years.

Along the same vein, researchers from Baylor College of Medicine, Texas Children's Hospital and Johns Hopkins University School of Medicine are hoping to create a pill that when taken could prevent the accumulation of toxic molecules in the brain that eventually go on to form these brain plaques.

Source: Practico D, Lauretti E, Li J, Di Meco A. Glucose deficit triggers tau pathology and synaptic dysfunction in a tauopathy mouse model. Translational Psychiatry. 2017

Sep 1st

New Alzheimers drug trial clears toxic brain proteins and slows memory lossThis is incredible.BEC CREW1 SEP 2016 

A new drug trial for Alzheimers patients has just been completed, and researchers are calling the results the most promising yet in the fight against the disease.The drug targets amyloid deposits - toxic proteins linked to the onset of Alzheimers - and after just 12 months, patients on the highest dose had no detectable signs of these deposits. Not only that, but for the 20 early-stage Alzheimers patients who took the highest dose of the drug for more than six months, there were indications that their cognitive decline and memory loss had been slowed down. "This is the best news we’ve had in my 25 years of doing Alzheimers research, and it brings hope to patients and families affected by the disease," one of the researchers, neurologist Stephen Salloway from Butler Hospital in Providence, Rhode Island, told Nature."Compared to other studies published in the past, the effect size of this drug is unprecedented," another of the team, Roger Nitsch from Zurich University, Switzerland, told The Independent.Before we go into the details, let’s be clear that this is just one trial with a small number of participants, and "cautiously optimistic" is the name of the game here. Nothing is confirmed until the results are replicated in a much longer trial with a larger and more diverse sample set, so while we can be excited about the incredible potential of this drug, we need to wait for follow-up trials.So with that in mind, here’s what happened. The team recruited 165 participants who had been diagnosed with the early stages of Alzheimers disease to test the efficacy of a drug based on an antibodycalled aducanumab.Aducanumab has been shown to naturally occur in people who age without experiencing significant cognitive decline, so the researchers decided to see what would happen if they injected high doses of the antibody into people with early-stage Alzheimers.It’s not clear how this antibody works, but the team announced at a recent conference that it appears to target amyloid deposits in the brain, but not in the bloodstream."The hypothesis suggests antibodies that attack amyloid in the bloodstream get sidetracked and never make it into the brain," Karen Weintraub explains over at Scientific American. "By focusing on brain amyloid, aducanumab seems to be able to cross into the brain to reach its target."The 165 participants were split into different groups, and some received the aducanumab drug in different doses, and one group of 40 received a placebo.Of the 103 patients who were given the drug once a month for up to 54 weeks, they all experienced a reduction in the amount of amyloid deposits in their brains. And the researchers found that the higher the dose, the more deposits were cleared from the brain.In the group of 21 patients who received the highest dose, no detectable signs of amyloid deposits remained in their brains after a year. The red represents amyloid-beta plaques. Credit: Ayres, Michael/Sevigny et al/NatureSimilar results were reported in a pre-trial mouse study, which saw mouse brains cleared of amyloid deposits after aducanumab treatment."This drug had a more profound effect in reversing amyloid-plaque burden than we have seen to date," Alzheimer’s researcher Eric Reiman from the Banner Alzheimers Institute in Phoenix, Arizona, who is not involved in the study, told Erika Check Hayden at Nature."That is a very striking and encouraging finding and a major advance."No one’s entirely sure what causes Alzheimers disease, but it’s thought to result from a buildup of two types of lesions in the brain: amyloid deposits - or 'plaques' - and neurofibrillary tangles. Amyloid deposits sit between the neurons as dense clusters of beta-amyloid molecules - a sticky type of protein that easily clumps together - and neurofibrillary tangles are caused by defective tau proteins that clump up into a thick, insoluble mass inside the neurons. This causes disruptions to the transportation of essential nutrients around the brain, which is thought to bring on the cognitive decline and memory loss associated with Alzheimers disease.Over the years, the roles of amyloid deposits and neurofibrillary tangles in the onset of Alzheimer’s have been debated, because it’s not yet clear if one causes the other, or if one has a greater overall effect. But this new trial suggests that if you can get rid of the amyloid deposits, you have a chance at stalling the progression of the disease. The researchers report that they saw slower cognitive declines in 91 patients treated with the drug."Aducanumab also showed positive effects on clinical symptoms," Nitsch explained in a press statement. "While patients in the placebo group exhibited significant cognitive decline, cognitive ability remained distinctly more stable in patients receiving the antibody."The results are definitely exciting, but it’s time to replicate them in a larger group of patients. The team is now recruiting another 2,700 patients from 20 different countries to participate in a new 18-month trial, the results of which are expected in 2020."These results are the most detailed and promising that we’ve seen for a drug that aims to modify the underlying causes of Alzheimers disease,” James Pickett, head of research at the Alzheimers Society, who was not involved in the study,told Ian Johnston at The Independent. "No existing treatments for Alzheimers directly interfere with the disease process – and so a drug that actually slows the progress of the disease by clearing amyloid would be a significant step."

Aug 13th

A cheap blood test which can identify people who are at high risk of developing Alzheimer’s disease in just three hours, has been developed by scientists.

People carrying the APOE4 genetic mutation are up to 12 times more likely to develop dementia in later life, making them ideal candidates for early intervention to prevent the disease.

However current DNA testing is expensive and can take days for results to come back.

The new £25 test, developed by London-based biotech company Randox Laboaratories uses a biochip – a type of ‘lab on a chip’ – to quickly analyse genetic material in the blood and look for mutant genes.

Tests have shown that it is 100 per cent accurate, meaning there is no chance of a false positive, or the chip missing a high-risk patient. 

The biochip is likely to be used for research purposes in the first instance but could later become part of widespread screening for Alzheimer’s disease. The company said several major healthcare providers had already expressed interest.

I recently read a report about stroke victims responding very well to having stem cells injected into their brains.

I wonder if this would work for Alzheimers sufferers

Avoiding Alzeheimers

As we get older we have to struggle to avoid this dreaded disease, and the only way we can do that is to keep our brains as active as possible for as long as we can, we can do this by challenging your thinking, playing games even if you are not physically active you can play games on paper or by using a board game, it all helps to keep our brains working.

Neurodegenerative disorders like Parkinson's and Alzheimer's are extremely widespread, affecting millions of people across the planet, but treatments are limited, and there's currently no cure available. New work is showing promise in the development of a new treatment, with scientists identifying a compound that can reverse symptoms of the diseases. The method hasn't been tested on human patients just yet, but it's been found to be effective in genetically modified fruit flies.

Combating neurodegenerative disorders represents one of the biggest challenges in modern medicine. Our understanding of conditions like Alzheimer's is improving rapidly, but actually finding effective treatments, and even cures, is proving extremely difficult.

The new study is a collaborative effort between the University of Maryland and the University of Leicester in the United Kingdom. It focuses on metabolites related to an amino acid called tryptophan, which breaks down into numerous compounds when it degrades in the body, which in turn have effects on the nervous system.

Two of these compounds are polar opposites, with 3-hydroxykynurenine (3-HK) having toxic properties and kynurenic acid (KYNA) helping to prevent nerve cell degeneration. The team believes that the amount of the two compounds present in the brain could play a big role in Alzheimer's, Parkinson's and Huntington's disease.

To test that theory, they worked with fruits flies genetically altered to model Alzheimer's and Parkinson's diseases, giving them a chemical that inhibits an enzyme known as trytophan-2,3-dioxygenase (TDO). The enzyme controls the relationship between 3-HK and KYNA, with its inhibition shifting metabolism towards the latter. The effect on the flies was significant, improving their movement and lengthening their lifespans.

"A key finding of our study is that we can improve 'symptoms' in fruit fly models of Alzheimer's and Parkinson's disease by feeding them a drug-like chemical," said study co-author Carlo Breda of the University of Leicester. "Our experiments have identified TDO as a very promising new drug target."

Looking forward, the researchers hope to test the treatment on human patients to see if it does indeed represent a new means of combating neurodegenerative disorders.

New research indicates that an early symptom of Alzheimer’s disease can take the form of a commonly overlooked issue, one that can appear nearly 20 years before the disease can be officially diagnosed.

This is getting lost easily and having difficulty navigating.

The study — since published in the Journal of Alzheimer’s disease — split participants into three groups: people with preclinical Alzheimer’s disease that showed changes in their brain, people with Alzheimer’s-associated brain and spinal fluid changes, and people with early-stage Alzheimer’s.

These participants were measured against a control group of 42 healthy people.

Participants were tested on their ability to navigate a virtual maze after being given either 20 minutes to learn a preselected route, or, after they explored the maze with a joystick.

They then had to recreate their set route or find their way to landmarks within the maze.

The study found that the group with preclinical Alzheimer’s disease had little trouble remembering a set route, however they struggled to create a mental map of the maze.

These findings are consistent with other research on early stage Alzheimer’s patients.

A likely explanation for these findings is that Alzheimer’s first surfaces in the hippocampus (pictured below); an area of the brain that’s responsible for memory forming and for spatial navigation.


Denise Head, a senior author of the study, said in a statement: “These findings suggest that navigational tasks designed to assess a cognitive mapping strategy could represent a powerful new tool for detecting the very earliest Alzheimer’s disease-related changes in cognition.”

She added that spatial navigation tasks of this form were more sensitive at detecting preclinical Alzheimer’s than the standard episodic memory test.

“Future research should examine whether cognitive mapping deficits in individuals in preclinical Alzheimer’s are associated with an increased risk of developing symptomatic Alzheimer’s,” the research team noted.

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we advise the World