View Full Version : Clock ticking with new plan to fight Alzheimer's Click here to find out more!

05-15-2012, 02:27 AM

tarting Tuesday, embattled families and caregivers can check a new one-stop website — www.alzheimers.gov — for easy-to-understand information about dementia and where to get help in their own communities. The National Institutes of Health is funding some major new studies of possible therapies, including a form of insulin that's squirted into the nose.

Dementia and Alzheimers effect so many of not just the older generation but some as early as in their 40ies. I do hope something good comes from this.

05-15-2012, 07:01 AM
Plus they also had some study on them.....like learning another language. Which somehow tends to lessen, the coming on of Alzheimers.

Last week we had this Older woman just walking around the neighborhood. She said hello to people smiled and kept walking around. Yet one could tell she was looking for something or somebody. My next door neighbor stopped her and began talking to her. Then she waved me over to her. After hearing some of what the lady was saying, my neighbor signaled me she was going to call the police to keep her there talking.

She kept talking about walking down from her house. That she wanted to get back home. But she could not remember her address or phone number. Finally the police showed up and they helped her out. Later we would find out she lived on the other side of town. Totally disoriented and it was a good thing the cops knew who she was. As they had told us she had Alzheimers.

05-24-2016, 11:21 PM
Loss of Y chromosome linked to Alzheimer's in men over 80...
Study links loss of Y chromosome to Alzheimer’s in men
Wed, May 25, 2016 - About one in five men aged over 80 lose the Y chromosome from their blood cells, and this condition has now been linked to an increased risk of Alzheimer’s disease, researchers said on Monday.

The condition known as loss of Y (LOY), is the most common genetic mutation acquired during a man’s lifetime. Previous research has shown LOY can raise the likelihood of cancer and is more frequently found in smokers. Researchers now think the condition might serve as a predictive biomarker for a wider range of health problems. For the study in the American Journal of Human Genetics — led by Lars Forsberg and Jan Dumanski of Uppsala University in Sweden, along with colleagues in Britain, France, the US and Canada — researchers examined LOY cases in more than 3,200 men with an average age of 73.

About 17 percent showed LOY in blood cells. Those who had been already diagnosed with Alzheimer’s had a higher degree of LOY, they found. Also, those who had not yet been diagnosed with dementia, but had LOY were more likely to develop Alzheimer’s in subsequent years. “Having loss of Y is not 100 percent predictive that you will have either cancer or Alzheimer’s,” Forsberg said. Some men with LOY in the study lived with no symptoms well into their 90s. “But in the future, loss of Y in blood cells can become a new biomarker for disease risk and perhaps evaluation can make a difference in detecting and treating problems early,” Forsberg said.

University of California, San Francisco, professor of medicine Chris Lau said that the study sheds little light on why Alzheimer’s risk might be elevated in these men. “Although informative, the study is preliminary in nature and only highlights the fact that the Y chromosome could serve important functions beyond male sex determination and sperm production,” said Lau, who was not involved in the study. “What exactly on the Y chromosome that increases the risk of Alzheimer’s disease is the key issue,” he said.

Since the Y chromosome contains many genes — some unique to men and others shared with women, who do not have a Y chromosome — more research is needed. “It depends on what is lost to determine what is important for Alzheimer’s disease. Without such information, the loss of Y is just an observation,” Lau said.


06-10-2016, 01:35 AM
New blood test for Alzheimer's...
New Blood Test Could Detect Early Stages of Alzheimer’s
une 09, 2016 - University researchers in the United States say they have developed a blood test that appears to be effective in detecting the early stages of Alzheimer’s disease, the most common cause of dementia in elderly people.

Scientists at Rowan University in the eastern state of New Jersey say their blood test can detect mild cognitive impairment, which is generally seen in patients 10 or more years before they develop severe symptoms of Alzheimer's Disease, an affliction that is almost always fatal.

Not everyone with mild cognitive impairment develops Alzheimer's, and the condition known as MCI can be caused by a wide variety of causes, including multiple sclerosis, Parkinson's Disease, vascular problems, depression and traumatic brain injury. The Rowan researchers, writing in a journal of the Alzheimer's Association, say their blood test can distinguish between the various forms of cognitive impairment and identify with nearly 100 percent accuracy those that will most likely progress to advanced Alzheimer'.

One hemisphere of a healthy brain (L) is pictured next to one hemisphere of a brain of a person suffering from Alzheimer disease.

The small-scale study conducted at Rowan, in Glassboro, New Jersey, tested the blood of 236 subjects, 50 of whom had MCI. “Our results show that it is possible to use a small number of blood-borne autoantibodies to accurately diagnose early-stage Alzheimer’s,” said Cassandra DeMarshall, the study's lead author and a doctoral candidate at the public university. “These findings could eventually lead to the development of a simple, inexpensive and relatively noninvasive way to diagnose this devastating disease in its earliest stages.”

The original proof-of-concept study would need to be repeated on a larger scale, experts said, but if the original findings are confirmed, patients suffering from mild cognitive impairment could seek appropriate early treatment, including lifestyle changes. This could also ease the significant financial and psychological cost for family members responsible for caring for elderly Alzheimer's patients. DeMarshall said about 60 percent of the patients her team studied had MCI caused by an early stage of Alzheimer's Disease, so "to provide proper care, physicians need to know which cases of MCI are due to early Alzheimer’s and which are not.”

Dr. Robert Nagele, the research team leader, said the results now being reported were particularly important because pre-Alzheimer's changes in the brain begin "at least a decade before the emergence of telltale symptoms.” “To the best of our knowledge," Naegele said, "this is the first blood test using autoantibody biomarkers that can accurately detect Alzheimer’s at an early point in the course of the disease when treatments are more likely to be beneficial – that is, before too much brain devastation has occurred” Nagele is director of the Biomarker Discovery Center at Rowan’s New Jersey Institute for Successful Aging, and the co-founder and chief scientific officer of Durin Technologies Inc. His team's research is to be published in a forthcoming issue of Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring.

New Blood Test Could Detect Early Stages of Alzheimer?s (http://www.voanews.com/content/mht-new-blood-test-could-detect-early-stage-alzheimers/3369318.html)

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Study: Fitness in Middle Age Cuts Risk of Stroke After 65
June 09, 2016 - Doctors urged to count lack of exercise between ages of 45 and 50 as a risk factor for stroke

The more fit a person is in middle age, the less likely he or she will have a crippling stroke after age 65. That is the result of a new study by the University of Texas Southwestern Medical Center.

A stroke patient undergoes an electrocardiogram while recovering at Juntendo University Hospital in Tokyo.

Doctors studied 20,000 men and women between the ages of 45 and 50, and concluded that those who were most fit from moderate to vigorous exercise had a 37 percent lower risk of a stroke than those who were the least fit.

They say the reduced risk of a future stroke was present even when the subjects had other risk factors, including high blood pressure and type-2 diabetes. The study urges doctors not to ignore low levels of exercise and fitness as risk factors for a stroke. The study was published in the latest issue of the medical journal called Stroke.


07-14-2016, 12:06 AM
Uncle Ferd says Granny been gettin' dat wild-eyed goofy look about her lately...
Eye Test Could Detect Early Stages of Alzheimer’s
July 12, 2016 - A simple eye test may eventually be used detect the early stages of Alzheimer’s disease, according to a new study on laboratory mice.

Writing in the journal Investigative Ophthalmology & Visual Sciences, researchers from the University of Minnesota say the discovery could pave the way for a noninvasive test for humans. "Using currently available detection methods, you have to wait until the plaque is formed to identify Alzheimer’s disease," said Robert Vince, Ph.D., director of the Center for Drug Design at the University of Minnesota. "This technology is a noninvasive way to identify Alzheimer’s disease before plaque is formed."

Alzheimer's disease patient Isidora Tomaz, 82, rests in her house in Lisbon, Portugal

Researchers say they used a kind of camera to detect differences in the way light is reflected off the retinas of mice as they age and accumulate “building blocks” of amyloid plaque, which has long been associated with the degenerative disease.

The test now moves to humans to determine how the retinas of healthy people compare to those with Alzheimer’s. More than 5 million Americans suffer from Alzheimer's Disease, the most damaging form of dementia, and it is the sixth leading cause of death in the United States.

Eye Test Could Detect Early Stages of Alzheimer?s (http://www.voanews.com/content/mht-eye-test-could-detect-early-stages-of-alzheimers/3415299.html)

09-01-2016, 09:48 PM
Big Alzheimer's breakthrough...
Alzheimer's disease breakthrough as new drug clears toxic proteins from patients' brains
Friday 2nd September, 2016 - An antibody that can almost completely clear the visible signs of Alzheimer’s disease from the brain has been discovered in a breakthrough that left one scientist “trying not to get too excited”.

Researchers scanned the brains of people with the degenerative condition as they were given doses of the drug, which is based on an immune cell taken from the blood of elderly people aged up to 100 who showed no signs of the disease. After a year, virtually all the toxic “amyloid plaques” that build up in Alzheimer’s patients appeared to have gone from the brains of those given the highest doses of the antibody. The scientists, who described their results in a paper in the journal Nature, also said the patients showed signs that the rate of their cognitive decline had slowed. The findings of the trial suggest the plaques are at least part of the cause of the disease – not simply a byproduct. And, if the results are confirmed in larger clinical trials already under way around the world, one expert said it could be a “game-changer” for efforts to prevent Alzheimer’s.

One of the researchers, Professor Roger Nitsch, of Zurich University, described what they found when they scanned the brains of patients given either a placebo or three different doses of the antibody, called aducanumab. “One year later, the images of the placebo group are basically unchanged. In the three doses groups, a very clear reduction in amyloid plaques is shown – the higher the dose, the larger the degree of reduction,” he said. “In the 10mg dose group, after one year you can see no red on the image, meaning the amyloid has almost completely disappeared. “Compared to other studies published in the past, the effect size of this drug is unprecedented.”

The brains of Alzheimer's patients, showing how different doses of the drug reduced the number of amyloid plaques, in red, over a year

Commenting on the research in a separate Nature article, Professor Eric Reiman, of Arizona University, wrote: “If these preliminary cognitive findings are confirmed in larger and more-definitive clinical trials, which are now under way, it would provide a shot in the arm in the fight against Alzheimer’s disease. “But although the authors’ additional cognitive findings are encouraging, they are not definitive. It would be prudent to withhold judgement about aducanumab’s cognitive benefit until results from the larger trials are in.” But he added: “Confirmation that an anti-amyloid plaque treatment slows cognitive decline would be a game-changer for how we understand, treat and prevent Alzheimer’s disease. “Now is the time to find out.” The study, led by scientists at pharmaceutical companies Biogen and Neurimmune, sparked major interest from experts in the field.

Dr Tara Spires-Jones, interim director of Edinburgh University’s Centre for Cognitive and Neural Systems, said the research showed the antibody “robustly reduced amyloid pathology in a small group of people in very early stages of the disease”. “I am cautiously optimistic about this treatment, but trying not to get too excited because many drugs make it through this early stage of testing then go on to fail in larger trials,” she said. And Dr James Pickett, head of research at the Alzheimer’s Society, said: “These results are the most detailed and promising that we’ve seen for a drug that aims to modify the underlying causes of Alzheimer’s disease. “The study showed that the drug was first able to remove clumps of amyloid – a toxic protein associated with Alzheimer’s – from the brain of mice and also, excitingly, in people. “What is most compelling is that more amyloid was cleared when people took higher doses of the drug. “No existing treatments for Alzheimer’s 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.”

MORE (http://www.belfasttelegraph.co.uk/news/health/alzheimers-disease-breakthrough-as-new-drug-clears-toxic-proteins-from-patients-brains-35013793.html)

07-30-2017, 12:55 AM
Uncle Ferd says dey oughta test it on Granny...
Breakthrough Drug Restores Brain Function in Alzheimer’s Animal Model – Large-Scale Clinical Trial Now Planned
July 28, 2017 - Scientists from the Technical University of Munich have published a new paper showing that using a BACE inhibitor drug reduces the amount of amyloid beta in the brains of mice and restores the normal function of nerve cells and significantly improves memory.

Amyloid beta is a protein believed to be a major cause of Alzheimer’s disease and significant research around the world has focused on finding ways to remove or reduce the accumulation of amyloid beta in the brain. No drug on the market today can effectively treat Alzheimer’s disease and with 50 million already suffering from Alzheimer’s globally and tens of millions more projected to be diagnosed with the disease as the global population ages in the coming decades, it’s becoming a serious concern for governments and policy makers.

This new study led by Dr. Aylin Keskin, tested a substance that inhibits beta secretase in a mouse model of Alzheimer’s disease. The mice used in the study accumulate large amounts of amyloid beta, which then become amyloid beta plaques in the brain and lead to cognitive decline. The mice were feed the beta secretase inhibitor for up to eight weeks, after which the scientists examined the brains of the mice using an imaging technique known as two-photon microscopy to see the details of individual nerve cells.

https://i2.wp.com/www.singularityarchive.com/wp-content/uploads/2017/07/csm_Busche_Fluoreszenz_3831dcaf50.gif?resize=386%2 C386&ssl=1
Amyloid-β plaques (blue) and nerve cells (green) in the brain of an Alzheimer mouse model.

The brains of the mice in the study showed amyloid beta and brain functions actually normalized. The brains showed less hyperactive nerve cells, and the slow-wave brain patterns looked like patterns found in healthy mice. A major discovery from the study was that the memory of the mice significantly improved and they were able to remember and location of a hidden platform in a water-filled maze as fast as healthy mice. “What really impressed and amazed us was the reversibility of the symptoms. Before the treatment, the mice had a marked clinical picture with amyloid beta plaques in their brain. Nevertheless, the substance was able to restore important brain functions and abilities,” said Dr. Keskin.

Clinical trials in humans

The results from the study will soon be trialed in human Alzheimer’s patients with a large-scale clinical trial currently being planned with around 1000 participants that will test a modified form of the BACE inhibitor drug. Co-author of the study, Dr. Marc Aurel Busche said “Needless to say, we very much hope that the promising discoveries in the animal model will translate to humans.”


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Gene Editing Has Successfully Treated Muscular Dystrophy in Dogs – Human Trials Next
July 26, 2017 - In new research published on Monday, an international team of researchers report that they have been able to reverse the symptoms of Duchenne muscular dystrophy in dogs using a single injection of a novel gene therapy.

The symptoms of the disease did not return in the dogs for the two year duration of the study. Duchenne muscular dystrophy is a severe from of muscle wasting disease that affects one in 5000 males at birth and the average expectancy of patients is 26 years. The disease is genetic and caused by mutations that disrupt the production of dystrophin, which is required for muscles to function properly. The team comprised of researchers from Genethon, the AFM-Telethon laboratory, Inserm (UMR) and the Royal Holloway University of London said in a statement that these results are “paving the way for human clinical trials.”

The researchers created a novel gene transfer therapy that restores the dystrophin expression. They injected the dogs with with the gene microdystrophin, a compressed version of the dystrophin gene. Researchers had previously been unable to successfully use the dystrophin gene in gene therapy due to its relatively large size of 2.3 million base pairs. After a single injection the dogs in the study demonstrated “significant restoration of muscle function with a stabilisation of clinical symptoms for more than two years after injection,” said the team.

This is “really a very exciting study indeed”, said Geneticist Darren Griffin of the University of Kent. “The disease has long been a target for gene therapy and it is only to be hoped that sufficient funds can be awarded for this research to reach its natural conclusion and go into full clinical trials,” he said, quoted by the AFP. Muscle weakness caused by Duchenne muscular dystrophy usually appears around the age of four in boys and advances rapidly leaving most unable to walk by the age of 12. Few patients of Duchenne muscular dystrophy survive into their 40s.



Scientists Regenerate Retinal Cells and Restore Vision in the Eyes of Adult Mice Using Gene Activation
July 28, 2017 - A group of scientists from the University of Washington have shown in new research published in Nature that they can regenerate the retina cells in the eyes of adult mice.

The research may one day make it possible to regenerate the retina cells in eyes of patients with age-related macular degeneration, glaucoma and other pathologies of the eye. The cells of our retinas lack the stem cells that some tissues have that allow them to divide and regenerate. Because of this, damage to the retina is often untreatable with today’s medicine and leads to permanent vision loss.

The scientists created a mouse that had a version of a gene known as Ascl1, the gene enables cells called Müller glia to regenerate damaged retinas. The Ascl1 gene was activated with an injection of the drug tamoxifen. Previous research by the scientists had shown that the Ascl1 gene would only lead to regeneration of the retina if activated within two weeks of the mice birth. The new paper published on Wednesday, demonstrates that that, by using a drug that blocks epigenetic regulation called a histone deacetylase inhibitor, it enables the activation of the Ascl1 gene in the eyes of adult mice.

The Müller glia cells are then able differentiate into functioning interneurons. The paper shows that these interneurons then propagate into the mice retina, forming connections with other retinal cells, and react normally to signals from the light-detecting retinal cells. The lead researcher of the team, Prof. Tom Reh said in an interview with the University of Washington Health Science NewsBeat they hope to discover if other factors exist that can be activated to allow the Müller glia cells to regenerate into all the different cell types of the retina.