Jul 25, 17 12:51 PM
blood-donation is to be encouraged to keep our health service functioning
Jul 25, 17 09:02 AM
Octopus beware the small but deadly blue ring
Jul 25, 17 08:28 AM
blackout this occurs when the electricity suppy goes off
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
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."
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
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.
To date Alzheimer’s doesn’t have a cure but new research suggests that blueberries, a “superfruit,” may help prevent the disease.Home Page - medical - Alzheimers
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