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Thread: Alzheimer's Disease

  1. #21
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    T-minus 2hrs and counting till the big event ... if you do not hear from me for a day or two don't worry, I'll be nursing a hangover
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  2. #22
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    Quote Originally Posted by Dog View Post
    Well it's that time of year again ...

    time to get together and celebrate Dad's life, mourn his passing and try to do something good about it. So once again the family is getting together with friends for some revelries

    Understandable with the geographical nature of members here that most can't actually attend such gallantry. But if you can, you can still be a part of the celebration for the cause ... even if means offering up some kind words.


    https://www.facebook.com/events/1030432687017985/


    http://act.alz.org/site/TR?team_id=3...d=9182&pg=team
    Quote Originally Posted by Dog View Post
    T-minus 2hrs and counting till the big event ... if you do not hear from me for a day or two don't worry, I'll be nursing a hangover
    after nursing a hangover all day and evening I am sorta starting to feel normal ... relatively speaking But just to give folks an update,

    Just over $12,000 raised during the benefit and being handed in to the Alzheimer's Association for the 2016 Walk to End Alzheimer's fundraising for Team O'Grady!!! Holy moly that's a lot of money that will provide services to families dealing with Alzheimer's and fund research to find a cure. We are completely overwhelmed by the unwavering support and continued generosity of our family, friends, local businesses and community! Thank you
    great success.jpg
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  3. #23
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    Researchers testing stem cells to treat Alzheimer's

    http://www.foxnews.com/health/2016/0...ind-trial.html

    In a first-of-its-kind clinical trial, researchers at the University of Miami Miller School of Medicine are using mesenchymal stem cells (MSCs) in an attempt to slow or reverse the symptoms of Alzheimer’s disease. The team is aiming to enroll 30 patients who will be tested and observed for cognitive function, memory, quality of life and brain volume over the course of a year.

    “This is a phase 1 study; we want to prove that it’s safe,” Dr. Bernard Baumel, principal investigator and an assistant professor of neurology at the Miller School of Medicine, told FoxNews.com. “We minimally would like to see that it slows down the progression of the disease.”

    Baumel and his team began investigating MSCs because of their anti-inflammatory properties and because they have shown the ability to develop into many different types of cells. The cells are also thought to promote neurogenesis, which allows the brain to produce new cells in the hippocampus, which is where new memory forms and Alzheimer’s disease begins.

    “[MSCs] are anti-inflammatory and they promote indigenous stem cells in your body to proliferate,” Baumel said. “They stimulate cell growth and have a lot of attributes that are very advantageous for using them in humans.”

    One such attribute is the ability to migrate to areas in the body in which they are needed. Baumel explained that if you were to inject stem cells into the body of someone who had no need for them, they would simply wither away and die. However, for the patients enrolled in the trial, due to the pathology of Alzheimer’s Baumel and his team hope to see the MSCs cross the blood brain barrier and help reduce inflammation, stimulate neural stem cells to proliferate and repair damaged areas. In a best case scenario, Baumel said the team would see MSCs remove the brain inflammation associated with Alzheimer’s altogether.

    The approach has previously been tested in mice with promising results. Researchers pathologically altered the mouse to replicate Alzheimer’s disease, which saw an increase in amyloid plaque build-up and caused them to struggle to move through a maze. Mice treated with MSCs had a marked reduction in plaque and showed improved behavior.

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  4. #24
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    Could Alzheimer’s Stem From Infections? It Makes Sense, Experts Say

    http://www.msn.com/en-us/news/us/cou...d=ansmsnnews11

    Could it be that Alzheimer’s disease stems from the toxic remnants of the brain’s attempt to fight off infection?

    Provocative new research by a team of investigators at Harvard leads to this startling hypothesis, which could explain the origins of plaque, the mysterious hard little balls that pockmark the brains of people with Alzheimer’s.

    It is still early days, but Alzheimer’s experts not associated with the work are captivated by the idea that infections, including ones that are too mild to elicit symptoms, may produce a fierce reaction that leaves debris in the brain, causing Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard group’s data, published Wednesday in the journal Science Translational Medicine, supports it. If it holds up, the hypothesis has major implications for preventing and treating this degenerative brain disease.

    The Harvard researchers report a scenario seemingly out of science fiction. A virus, fungus or bacterium gets into the brain, passing through a membrane — the blood-brain barrier — that becomes leaky as people age. The brain’s defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer’s.

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    So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans — and funding — are in place to start those studies, involving a multicenter project that will examine human brains.

    “It’s interesting and provocative,” said Dr. Michael W. Weiner, a radiology professor at the University of California, San Francisco, and a principal investigator of the Alzheimer’s Disease Neuroimaging Initiative, a large national effort to track the progression of the disease and look for biomarkers like blood proteins and brain imaging to signal the disease’s presence.

    Dr. David Holtzman, a professor and the chairman of neurology at the Washington University School of Medicine in St. Louis, was also intrigued. “It is obviously outside the box,” he said. “It really is an innovative and novel study.”

    The work began when Robert D. Moir, of Harvard Medical School and Massachusetts General Hospital, had an idea about the function of amyloid proteins, normal brain proteins whose role had long been a mystery.

    The proteins were traditionally thought to be garbage that accumulates in the brain with age. But Dr. Moir noticed that they looked a lot like proteins of the innate immune system, a primitive system that is the body’s first line of defense against infections.

    Elsewhere in the body, such proteins trap microbes — viruses, fungi, yeast and bacteria. Then white blood cells come by and clear up the mess. Perhaps amyloid was part of this system, Dr. Moir thought.

    He began collaborating with Rudolph E. Tanzi, also at Harvard Medical School and Massachusetts General Hospital, in a study funded by the National Institutes of Health and the Cure Alzheimer’s Fund. The idea was to see if amyloid trapped microbes in living animals and if mice without amyloid proteins were quickly ravaged by infections that amyloid could have stopped.

    The answers, they reported, were yes and yes.

    In one study, the group injected Salmonella bacteria into the brains of young mice that did not have plaques.

    “Overnight, the bacteria seeded plaques,” Dr. Tanzi said. “The hippocampus was full of plaques, and each plaque had a single bacterium at its center.”

    In contrast, mice that did not make beta amyloid succumbed more quickly to the bacterial infection, and did not make plaques.

    For years, researchers had been fixated on the idea of plaques as a sort of trash that gathered in the brain. Few had asked if there might be some other explanation.

    As Dr. Samuel E. Gandy, a professor of neurology and psychiatry at the Icahn School of Medicine at Mount Sinai Hospital in New York, explained, there was a long and persuasive body of research laying out the Alzheimer’s pathway: Plaques form and set off the formation of tangled threadlike tau proteins. Then, as tangles of tau kill nerve cells, the brain becomes inflamed, resulting in the killing of many more nerve cells.

    There were a few puzzling clues that something else might be going on, but they did not make much sense.

    For example, Dr. Weiner said, some investigators reported that people who had developed Alzheimer’s had higher levels of antibodies to herpes, an indicator of a previous infection, than people who did not have the disease.

    “The suggestion that herpes was causative seemed a bit far-fetched,” he said.

    The new paper, Dr. Gandy and Dr. Weiner said, provides a plausible explanation.

    Dr. Berislav Zlokovic, the director of the Zilkha Neurogenetic Institute at the University of Southern California, said his studies of the blood-brain barrier also fit well with the new hypothesis. When he discovered that the barrier started to break down with aging, he noticed that the leakiest part was the membrane that protects the hippocampus, the site of learning and memory. That is also where Alzheimer’s plaques form.

    Dr. Tanzi and Dr. Moir’s hypothesis, he said, “is very hypothetical at this point, but it does make sense.”

    Of course, there must be more to Alzheimer’s than the brain’s innate immune system. What about people who have a mutated gene that guarantees they will develop the disease at an early age?

    For them, Dr. Tanzi says, the problem is that they vastly overproduce beta amyloid. There is so much that it clumps on its own, without the presence of microbes.

    Not everyone who has had a brain infection develops Alzheimer’s, though. Why would some be more vulnerable than others? According to the new theory, it probably has to do with the brain’s ability to clear out the balls of beta amyloid after they have killed microbes, Dr. Tanzi said. For example, it is known that people with a gene called ApoE2 have brains that are good at sweeping out plaque, and have a low risk of Alzheimer’s in old age. Those with a different version, ApoE4, are inefficient in removing plaque and have a high risk of Alzheimer’s.

    Recent data suggests that the incidence of dementia is decreasing. It could be because of better control of blood pressure and cholesterol levels, staving off ministrokes that can cause dementia. But could a decline in infections also be part of the picture?

    “That’s a possibility,” Dr. Weiner said.

    At this point, the Harvard researchers have what many say is an intriguing hypothesis, but they readily acknowledge that much work lies ahead.

    The Cure Alzheimer’s Fund is starting a large collaborative project that will use gene sequencing technology to carefully look for microbes in brains from people who had Alzheimer’s and those who did not. Researchers will also look for microbes in plaques found in human brains.

    That, though, “is a big, big second step,” Dr. Tanzi said. “First, we need to ask whether there are microbes that may sneak into the brain as we age and trigger amyloid deposition.”

    “Then,” he said, “we can aim at stopping them.”
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  5. #25
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    Researchers Believe Vaccine Breakthrough Could Reverse Dementia

    http://www.ibtimes.com/alzheimers-cu...mentia-2391280

    A group of researchers believe they're closing in on a vaccine that would prevent Alzheimer's and dementia and perhaps even reverse the disease in the early stages, according to the Australian Broadcasting Corporation.

    The work by researchers at the Institute of Molecular Medicine, the University of California and Australia's Flinders University could bring a vaccine with the next five years and is a "breakthrough discovery," wrote The Australian newspaper.

    There are some 7.5 million new cases of Alzheimer's — a degenerative disease that causes serious problems with memory, thinking ability and behavior — diagnosed around the world. About 5 million people in the U.S. suffer from the disease and one-in-three senior citizens suffer some form of dementia, according to the Alzheimer's Association.

    The researchers have said the potential vaccine would work by fixing issues with proteins that stop functioning properly in the brain and cause the disease. "[The proteins are] a bit like the car in your driveway," Flinders University medicine professor Nikolai Petrovsky told the Australian Broadcasting Corporation. "You need to remove them from the brain otherwise if you left broken down cars in your driveway eventually you couldn't get out. Essentially that's what happens in people who get Alzheimer's or dementia is they have lots of these broken down proteins in the brain."

    Petrovsky described what is surely a complicated process is relatively simple terms, saying, "essentially what we have designed is a vaccine that makes the immune system produce antibodies and those antibodies act like tow trucks so they come to your driveway, they latch on to the breakdown protein or car and they pull it out of the driveway."

    Petrovsky told The Australian that the main component left to figure out is if the vaccine can be made powerful enough to work as a preventative measure. "You could actually give it to everyone, say when they turn 50, a bit like we give all high-risk groups a flu shot, and thereby stop it in its tracks. You can immunize for it before it even starts," he told the newspaper.

    Clinical trials on humans are expected to begin within the next few years, Petrovsky said.
    Last edited by Dog; 07-14-2016 at 05:31 PM.
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  6. #26
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    new imaging technology could point to cause of Alzheimer's

    http://www.foxnews.com/health/2016/0...lzheimers.html

    Despite the prevalence of Alzheimer’s disease, relatively little is known about its causes. Now, scientists at Rockefeller University in New York City and funding from the Fisher Center for Alzheimer’s Research Foundation have developed a potentially groundbreaking way to create 3-D images of the protein that may lead to the debilitating disease.

    Over five million Americans suffer from Alzheimer’s, according to the National Institutes of Health (NIH). The form of dementia robs people of their memory, their ability to think and eventually their brain function. Scientists say the buildup of beta amyloid, a protein, is related but it’s not yet known why this plaque develops in the first place.

    Gathering images of beta amyloid is difficult, requiring thin slices of brain matter to be observed under a microscope. This 2-D imaging has many limitations, especially with regards to the complexity of the brain. The Rockefeller/Fisher Center team is working to make it possible to create 3-D images.

    Previously, researchers would scan micro-slides of brain matter and layer them to construct a 3-D view, but this was “very, very time consuming and you also include a lot of artifacts when you try to reconstruct a 3-D tissue.” Dr. Marc Flajolet, a research assistant professor at Rockefeller University, told FoxNews.com.

    Dr. Paul Greengard is a Nobel Laureate and director of the Fisher Center. He has dedicated his life to Alzheimer’s research. He, along with Flajolet, wanted to move imaging forward to get a better understanding of the disease.

    “When new technologies were coming around we decided it was a good time to try,” Flajolet told FoxNews.com. Under the guidance of Greengard, Flajolet worked closely with Dr. Thomas Liebmann, a post-doctoral fellow in the Greengard lab, to develop a new type of 3-D imaging called iDisco. The technique combines multiple technologies and microscopic techniques to see an entire brain sample in 3-D.

    iDisco works by washing the mouse brain or sections of human brain through complex solvents to make the lipids, or fat, in brain matter transparent. Then the team uses state-of-the-art microscopes to scan what’s visible— the beta amyloid plaque.

    “The microscope that is used in this case is called the Light Sheet Microscope,” Dr. Marc Tessier-Lavigne, president of Rockefeller University, told FoxNews.com. “That sends a sheet of light through the brain, scanning each plane in the brain in successive turns collecting all the information and using that data to reconstruct a three-dimensional brain.”

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  7. #27
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    2016 Walk to End Alzheimer's - Rockland County, NY

    http://act.alz.org/site/TR/Walk2016/...=9182&pg=entry


    9b41ad2f_walktoendalzheimers2015.jpg


    another year and another great effort in raising awareness and funding for the fight
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  8. #28
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    This could be huge!

    http://www.sciencealert.com/new-alzh...emory-function

    New Alzheimer’s treatment fully restores memory function

    Australian researchers have come up with a non-invasive ultrasound technology that clears the brain of neurotoxic amyloid plaques - structures that are responsible for memory loss and a decline in cognitive function in Alzheimer’s patients.

    If a person has Alzheimer’s disease, it’s usually the result of a build-up of two types of lesions - amyloid plaques, and neurofibrillary tangles. Amyloid plaques sit between the neurons and end up as dense clusters of beta-amyloid molecules, a sticky type of protein that clumps together and forms plaques.

    Neurofibrillary tangles are found inside the neurons of the brain, and they’re caused by defective tau proteins that clump up into a thick, insoluble mass. This causes tiny filaments called microtubules to get all twisted, which disrupts the transportation of essential materials such as nutrients and organelles along them, just like when you twist up the vacuum cleaner tube.

    As we don’t have any kind of vaccine or preventative measure for Alzheimer’s - a disease that affects 343,000 people in Australia, and 50 million worldwide - it’s been a race to figure out how best to treat it, starting with how to clear the build-up of defective beta-amyloid and tau proteins from a patient’s brain. Now a team from the Queensland Brain Institute (QBI) at the University of Queensland have come up with a pretty promising solution for removing the former.

    Publishing in Science Translational Medicine, the team describes the technique as using a particular type of ultrasound called a focused therapeutic ultrasound, which non-invasively beams sound waves into the brain tissue. By oscillating super-fast, these sound waves are able to gently open up the blood-brain barrier, which is a layer that protects the brain against bacteria, and stimulate the brain’s microglial cells to activate. Microglila cells are basically waste-removal cells, so they’re able to clear out the toxic beta-amyloid clumps that are responsible for the worst symptoms of Alzheimer’s.

    The team reports fully restoring the memory function of 75 percent of the mice they tested it on, with zero damage to the surrounding brain tissue. They found that the treated mice displayed improved performance in three memory tasks - a maze, a test to get them to recognise new objects, and one to get them to remember the places they should avoid.

    "We’re extremely excited by this innovation of treating Alzheimer’s without using drug therapeutics," one of the team, Jürgen Götz, said in a press release. "The word ‘breakthrough’ is often misused, but in this case I think this really does fundamentally change our understanding of how to treat this disease, and I foresee a great future for this approach."

    The team says they’re planning on starting trials with higher animal models, such as sheep, and hope to get their human trials underway in 2017.
    Last edited by Dog; 10-25-2016 at 11:16 PM.
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  9. #29
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    Extra-virgin olive oil may prevent Alzheimer's

    http://www.medicalnewstoday.com/articles/318032.php

    New research suggests that extra-virgin olive oil - a key component of the Mediterranean diet - may protect the brain from Alzheimer's disease symptoms. Mouse experiments revealed changes in both cognitive performance and the appearance of nerve cells. Alzheimer's disease is estimated to affect approximately 5 million people in the United States. The neurodegenerative disease is progressive and cannot yet be cured or reversed.

    But new research moves closer to a prevention - and potentially reversing - strategy, by studying the effects of extra-virgin olive oil on the cognitive performance and brain health of mice.

    The new study - published in the journal Annals of Clinical and Translational Neurology - was carried out by a team of researchers from the Lewis Katz School of Medicine at Temple University (LKSOM) in Philadelphia, PA.

    Lead investigator Dr. Domenico Praticò - a professor in the departments of Pharmacology and Microbiology and the Center for Translational Medicine at LKSOM - explains why several studies have singled out olive oil and hailed it as the main reason why the Mediterranean diet is linked to so many health benefits.

    "The thinking is that extra-virgin olive oil is better than fruits and vegetables alone, and as a monounsaturated vegetable fat it is healthier than saturated animal fats," he says.

    Studying the effect of olive oil in mice
    Dr. Praticò and team used a traditional Alzheimer's transgenic mouse model to study the effect of the oil. The rodents were genetically modified to have the three main characteristics of Alzheimer's disease: memory impairment, the buildup of amyloid plaques, and neurofibrillary tangles.

    Neurofibrillary tangles are the result of twisted strands of a protein called tau. In a healthy brain, tau helps with the transportation of nutrients and other molecules that the brain cells need. In Alzheimer's disease, this protein gets tangled up inside the brain cells, which happen to be dying because essential nutrients no longer reach them.

    Amyloid plaques are the result of the excess production and buildup of beta-amyloid, a fragment of the protein called "amyloid precursor protein." In Alzheimer's disease, these plaques build up in the spaces between neurons.

    Dr. Praticò and colleagues split the rodents into two groups: one group was fed a chow diet with extra-virgin olive oil, and the other group received a regular chow diet with no added oil.

    Alzheimer's characteristics begin to develop in a rodent model quite early on, so in this experiment, the oil was added to the diet when the mice were 6 months old, before any symptoms could have appeared.

    The researchers evaluated the mice's cognitive abilities by administering tests for their spatial memory, working memory, and learning skills.

    Olive oil preserves brain cell health
    In terms of general appearance, no differences were noted between the two animal groups.

    But, when the mice were 9 months and 12 months old, the mice that had been fed the extra-virgin olive oil diet performed much better in the cognitive tests.

    Dr. Praticò and his team also analyzed the brain tissue of these mice, and the studies revealed striking differences between the appearance and functioning of the nerve cells.

    Firstly, the integrity of the synapses - which are the parts of the brain cell that facilitate communication among neurons - was preserved much better in the olive oil group. Secondly, the brain tissue in the mice fed olive oil revealed a "dramatic increase" in the autophagy activation of the nerve cells.

    Autophagy is a process that sees nerve cells disintegrate and eliminate the toxic debris that tends to accumulate between the cells.

    In this experiment, the increase in autophagy led to a decrease in the amyloid plaques and phosphorylated tau.

    Dr. Praticò says, "This is an exciting finding for us. Thanks to the autophagy activation, memory, and synaptic integrity were preserved, and the pathological effects in animals otherwise destined to develop Alzheimer's disease were significantly reduced."

    "This is a very important discovery, since we suspect that a reduction in autophagy marks the beginning of Alzheimer's disease."
    Dr. Domenico PraticòNext, the researchers plan to introduce olive oil at a later stage, when Alzheimer's symptoms will have already emerged. In the case of mice, this would mean at 12 months of age.

    "Usually when a patient sees a doctor for suspected symptoms of dementia, the disease is already present," Dr. Praticò explains. "We want to know whether olive oil added at a later time point in the diet can stop or reverse the disease."
    will be very interested to see the results of the follow up study
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  10. #30
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    Every bit helps ...

    It's that time of year again ... when the family rallies together in memory of dad. If you have it in you to donate it would be much appreciated. If not, please offer your thoughts and prayers to those still and those yet to come in their battle with this dreadful disease.

    Thank you,
    Darren

    http://act.alz.org/site/TR?fr_id=106...al&px=13031810
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  11. #31
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    Disappointing ...

    http://www.latimes.com/science/scien...109-story.html

    One of the most promising drugs for Alzheimer's disease fails in clinical trials

    o the roughly 400 clinical trials that have tested some experimental treatment for Alzheimer’s disease and come up short, we can now add three more.

    An experimental drug called idalopirdine failed to help people with mild to moderate Alzheimer’s disease in a trio of trials that involved 2,525 patients in 34 countries. Not only did the drug fail to bring about any meaningful change in cognitive tests that are widely used in diagnosing and tracking the progress of the disease, it also failed to cause significant improvements in general measures of daily function among those taking it at any of three tested doses.

    Those are relatively modest goals — not to reverse Alzheimer’s disease or block its progress, but simply to slow the loss of function in those who have it. Even that, it turns out, is a humbling challenge.

    The failure of idalopirdine, reported Tuesday in the Journal of the American Medical Assn., probably marks the unraveling of an approach to Alzheimer’s treatment that has long looked promising.

    The experimental drug largely acted to increase the supply of the brain chemical serotonin, which, among other things, regulates mood, sleep and appetite, and ebbs in those with Alzheimer’s disease. Idalopirdine also acts on four other neural transmitters that are affected by Alzheimer’s: glutamate, norepinephrine, acetylcholine and dopamine.

    The drug had looked promising in earlier clinical trials that focused largely on safety. But after 24 weeks, subjects with Alzheimer’s who got idalopirdine fared no better than those who got a sham drug.

    The disappointing results follow the failure, reported last fall, of intepirdine, another experimental drug that acted on many of the same brain systems as idalopirdine.

    Subjects in both trials also took donepezil (long marketed as Aricept) or another Alzheimer’s drug in the same class. Researchers had hoped that the combination therapy might boost the action of several different neurotransmitter systems at once to improve mental function in Alzheimer’s patients.

    Lundbeck, the publicly traded Danish pharmaceutical company that was developing idalopirdine, told investors last year that it would not be asking the Food & Drug Administration to evaluate the drug for the U.S. market. That would have been the next step if the phase 3 trials had succeeded.

    As researchers and government officials have focused on ambitious efforts to reverse or even cure Alzheimer’s, doctors have appealed for therapies that will at least improve the lives of the 5.5 million Americans already living with the disease.

    Yet the new results underscore the diabolical challenge of merely slowing Alzheimer’s disease once its behavioral symptoms become evident, according to Dr. David A. Bennett, a neurologist and director of Rush University’s Alzheimer’s Disease Center in Chicago.

    Given the millions of Americans already afflicted, “better symptomatic therapies must continue to be pursued,” Bennett wrote in an editorial also published in JAMA. “However, from a public health perspective, delaying the onset of Alzheimer disease dementia is the most effective approach to reduce the overall human and economic toll of the disease.”

    That, he wrote, will require earlier diagnosis of Alzheimer’s among a broader range of people, including people with no outward sign of dementia. And those in the disease’s earliest phases will need to be enrolled in clinical trials of preventive strategies faster, and in larger numbers.

    A public hungry for quick fixes and streamlined drug development had better get patient, Bennett added. Citing a recent exploration of why so many Alzheimer’s disease drugs fail, he noted that treatments that could halt or reverse Alzheimer’s might need to be tested for five to 10 years for an effect to be detected. Currently, few such trials last for more than three years.

    And maybe, Bennett added, we’re not seeing that we’re on a trajectory — albeit a long one — to eventual success.

    “Given the series of failures in rigorous attempts to develop an effective treatment for Alzheimer disease, it may seem difficult to be optimistic,” he wrote. “Yet lessons from the past century paint a different picture.”

    With a request for $100 million in added funds for cancer research in 1971, President Nixon began a process of investment and discovery that has brought forth treatments for cancer that were beyond imagination at the time. In 2011, President Obama launched the National Alzheimer’s Project Act with an initial investment of $50 million. By 2017, federal research on Alzheimer’s disease had reached $1.4 billion.

    “It is just a matter of time before that knowledge is translated into effective strategies for the treatment and prevention” of Alzheimer’s, Bennett wrote.

    And none too soon: The Alzheimer’s Assn. estimates that an American is newly diagnosed with the disease every 66 seconds.
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  12. #32
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    Failure of Alzheimer's drugs in trials makes researchers wonder what is going wrong

    https://www.upi.com/Health_News/2018...5521516912572/

    In recent weeks, a pair of high-profile disappointments have been reported, including one just announced on a trial of the Eli Lilly drug solanezumab.

    THURSDAY, Jan. 25, 2018 -- As more experimental drugs fail to stop Alzheimer's from destroying human memory, experts now wonder whether research into the devastating brain disease has been marching in the wrong direction.

    In recent weeks, a pair of high-profile disappointments have been reported, including one just announced on a trial of the Eli Lilly drug solanezumab.

    Now, researchers are trying to figure out what might have been missed in the search for an Alzheimer's cure.

    Did errors occur in the clinical trials of these drugs, creating the failure of potentially promising therapies? Or has there been a fundamental misunderstanding of the complex nature of Alzheimer's disease?

    Until now, research has focused mainly on treating or preventing Alzheimer's by attacking the clumps of amyloid beta protein that form in patients' brains, potentially blocking signals sent between brain synapses. Amyloid plaques are one of the hallmarks of the disease.

    "The overriding hypothesis for many years has been the amyloid hypothesis -- the idea if you can stop, slow or clear the formation of amyloid plaques from the brain you will be able to treat the disease and see marked improvements in cognition," said James Hendrix, director of global science initiatives for the Alzheimer's Association. "So far, that hasn't worked out."

    Solanezumab binds with amyloid beta, and was intended to help the body flush the protein out of the brain before it could form damaging plaques.

    But the drug failed to significantly slow thinking declines, Columbia University researchers reported in the Jan. 25 issue of the New England Journal of Medicine.

    Those results came on the heels of a trio of failed trials of the drug idalopirdine, which was intended to help treat Alzheimer's by promoting production of serotonin and other essential brain chemicals. A team of researchers reported in the Journal of the American Medical Association earlier this month that the drug failed to improve thinking or memory in Alzheimer's patients.
    frustrating ... we were right here in this exact same spot back in the 90's. So much time lost
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  13. #33
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    New evidence that viruses may play a role in Alzheimer’s

    https://apnews.com/8e4ebccd8f09446d982eb63b85aafa9c

    WASHINGTON (AP) — Viruses that sneak into the brain just might play a role in Alzheimer’s, scientists reported Thursday in a provocative study that promises to re-ignite some long-debated theories about what triggers the mind-robbing disease.

    The findings don’t prove viruses cause Alzheimer’s, nor do they suggest it’s contagious.

    But a team led by researchers at New York’s Mount Sinai Health System found that certain viruses — including two extremely common herpes viruses — affect the behavior of genes involved in Alzheimer’s.

    The idea that infections earlier in life might somehow set the stage for Alzheimer’s decades later has simmered at the edge of mainstream medicine for years. It’s been overshadowed by the prevailing theory that Alzheimer’s stems from sticky plaques that clog the brain.

    Thursday’s study has even some specialists who never embraced the infection connection saying it’s time for a closer look, especially as attempts to block those so-called beta-amyloid plaques have failed.

    “With an illness this terrible, we cannot afford to dismiss all scientific possibilities,” said Dr. John Morris, who directs the Alzheimer’s research center at Washington University School of Medicine in St. Louis. He wasn’t involved in the new research but called it impressive.

    The study also fits with mounting evidence that how aggressively the brain’s immune system defends itself against viruses or other germs may be riskier than an actual infection, said Alzheimer’s specialist Dr. Rudolph Tanzi of Massachusetts General Hospital. With Harvard colleague Dr. Robert Moir, Tanzi has performed experiments showing that sticky beta-amyloid captures invading germs by engulfing them — and that’s why the plaque starts forming in the first place.

    “The question remained, OK, in the Alzheimer brain what are the microbes that matter, what are the microbes that trigger the plaque?” explained Tanzi, who also had no role in the new research.

    The team from Mount Sinai and Arizona State University came up with some viral suspects — by accident. The study, funded by the National Institutes of Health, wasn’t hunting viruses but was looking for new drug targets for Alzheimer’s. The researchers were using complex genetic data from hundreds of brains at several brain banks to compare differences between people who’d died with Alzheimer’s and the cognitively normal.


    The first clues that viruses were around “came screaming out at us,” said Mount Sinai geneticist Joel Dudley, a senior author of the research published Thursday in the journal Neuron.

    The team found viral genetic material at far higher levels in Alzheimer’s-affected brains than in normal ones. Most abundant were two human herpes viruses, known as HHV6a and HHV7, that infect most people during childhood, often with no symptoms, and then lie dormant in the body.

    That wasn’t unusual. Since 1980, other researchers have linked a variety of bacteria and viruses, including another type of herpes that causes cold sores, to an increased risk of Alzheimer’s. But it was never clear if germs were merely bystanders, or actively spurring Alzheimer’s.

    The new study went farther: Researchers used computer models to check how the viral genes interacted with human genes, proteins and amyloid buildup, almost like the viruses’ social media connections, Dudley explained.

    “We’re able to see if viral genes are friending some of the host genes and if they tweet, who tweets back,” Dudley said.

    They found a lot of interactions, suggesting the viruses could even switch on and off Alzheimer’s-related genes. To see if those interactions mattered, the researchers bred mice lacking one molecule that herpes seemed to deplete. Sure enough, the animals developed more of those amyloid plaques.

    “I look at this paper and it makes me sit up and say, ’Wow,’” said Alzheimer’s Association scientific programs director Keith Fargo.

    He said the research makes a viral connection much more plausible but cautioned that the study won’t affect how today’s patients are treated.

    If the findings pan out, they could change how scientists look for new ways to treat or prevent Alzheimer’s, said Dr. Miroslaw Mackiewicz of NIH’s National Institute on Aging. Already, NIH is funding a first-step study to see if an antiviral drug benefits people who have both mild Alzheimer’s and different herpes viruses.

    Just having a herpes virus “does not mean you’re going to get Alzheimer’s,” Mass General’s Tanzi stressed. It may not even have penetrated the brain.

    But in another study soon to be published, Tanzi showed biologically how both HHV6 and a cold sore-causing herpes virus can trigger or “seed” amyloid plaque formation, supporting the Mount Sinai findings.

    Still, he doesn’t think viruses are the only suspects.

    “The Mount Sinai paper tells us the viral side of the story. We still have to work out the microbe side of the story,” said Tanzi, who is looking for bacteria and other bugs in what’s called the Brain Microbiome Project. “The brain was always thought to be a sterile place. It’s absolutely not true.”
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    The 'Big Bang' of Alzheimer's: Scientists ID genesis of disease

    https://medicalxpress.com/news/2018-...d-genesis.html

    Scientists have discovered a "Big Bang" of Alzheimer's disease – the precise point at which a healthy protein becomes toxic but has not yet formed deadly tangles in the brain.

    A study from UT Southwestern's O'Donnell Brain Institute provides novel insight into the shape-shifting nature of a tau molecule just before it begins sticking to itself to form larger aggregates. The revelation offers a new strategy to detect the devastating disease before it takes hold and has spawned an effort to develop treatments that stabilize tau proteins before they shift shape.

    "This is perhaps the biggest finding we have made to date, though it will likely be some time before any benefits materialize in the clinic. This changes much of how we think about the problem," said Dr. Marc Diamond, Director for UT Southwestern's Center for Alzheimer's and Neurodegenerative Diseases and a leading dementia expert credited with determining that tau acts like a prion – an infectious protein that can self-replicate.

    The study published in eLife contradicts the previous belief that an isolated tau protein has no distinct shape and is only harmful after it begins to assemble with other tau proteins to form the distinct tangles seen in the brains of Alzheimer's patients.

    Scientists made the discovery after extracting tau proteins from human brains and isolating them as single molecules. They found that the harmful form of tau exposes a part of itself that is normally folded inside. This exposed portion causes it to stick to other tau proteins, enabling the formation of tangles that kill neurons.

    "We think of this as the Big Bang of tau pathology," said Dr. Diamond, referring to the prevailing scientific theory about the formation of the universe. "This is a way of peering to the very beginning of the disease process. It moves us backward to a very discreet point where we see the appearance of the first molecular change that leads to neurodegeneration in Alzheimer's. This work relied on a close collaboration with my colleague, Dr. Lukasz Joachimiak."
    this is potentially huge!
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