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Thread: Alzheimer's Disease

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    Alzheimer's Disease

    After a 4yr battle with Alzheimer's disease John Thomas O'Grady passed away on 3/29/2013 at 9:23am. We are comforted in the fact that dad passed while resting comfortably, surrounded by family, celebrating his birthday and on Good Friday ... a Catholic couldn't have asked for any better!

    Happy 69th birthday Dad and Godspeed ... I look forward to seeing your smile and shaking your hand again.


    http://www.alz.org/

    https://www.facebook.com/actionalz

    http://www.alz.org/hudsonvalley/
    Last edited by Dog; 03-31-2013 at 09:48 PM.
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    You already know how sorry I am for your loss.

    So let me say this.

    I work in nursing, I see it all.

    I ain't scared of much, but Alzheimers scares the living crap out of me. I won't go into the horror stories, but I'm completely serious when I say that I'd rather have cancer of the junk than to have this horrible disease.

    I'm thinking we need to be looking at a variety of charities, and our servicemen should come first. But second for sure in my book is Alzheimers research.

    Again, I am so sorry for your loss, Spartan.

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    this was a CBS Special Report done just 2 weeks before dad's passing - http://www.cbsnews.com/video/watch/?...43169n&tag=api. The numbers are staggering and rapidly increasing.
    Last edited by Dog; 04-17-2013 at 10:32 AM.
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    Last edited by Dog; 04-17-2013 at 11:01 AM.
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    update ... http://www.sciencedaily.com/releases...-+ScienceDaily)

    Rsearchers at Jacksonville's campus of Mayo Clinic have discovered a defect in a key cell-signaling pathway they say contributes to both overproduction of toxic protein in the brains of Alzheimer's disease patients as well as loss of communication between neurons -- both significant contributors to this type of dementia.

    Their study, in the online issue of Neuron, offers the potential that targeting this specific defect with drugs "may rejuvenate or rescue this pathway," says the study's lead investigator, Guojun Bu, Ph.D., a neuroscientist at Mayo Clinic, Jacksonville, Fla. "This defect is likely not the sole contributor to development of Alzheimer's disease, but our findings suggest it is very important, and could be therapeutically targeted to possibly prevent Alzheimer's or treat early disease," he says.

    The pathway, Wnt signaling, is known to play a critical role in cell survival, embryonic development and synaptic activity -- the electrical and chemical signals necessary for learning and memory. Any imbalance in this pathway (too much or too little activity) leads to disease -- the overgrowth of cells in cancer is one example of overactivation of this pathway.

    While much research on Wnt has focused on diseases involved in overactive Wnt signaling, Dr. Bu's team is one of the first to demonstrate the link between suppressed Wnt signaling and Alzheimer's disease. "Our finding makes sense, because researchers have long known that patients with cancer are at reduced risk of developing Alzheimer's disease, and vice versa," Dr. Bu says. "What wasn't known is that Wnt signaling was involved in that dichotomy."
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    some potentially great news ... http://www.examiner.com/article/alzh...-loss-patients

    Individuals suffering from Alzheimer's had their memory loss reversed in a breakthrough discovery, says UCLA doctors in conjunction with the Buck Institute for Research on Aging. The study and results, though cautioned to be in an infant stage, show promising headway in the battle against the debilitating neurological disease.

    Writes MedicalXpress.com on Oct. 2: “Since its first description over 100 years ago, Alzheimer's disease has been without effective treatment. That may finally be about to change: in the first, small study of a novel, personalized and comprehensive program to reverse memory loss, nine of 10 participants displayed subjective or objective improvement in their memories beginning within 3-to-6 months after the program's start.”

    The findings, released by the University of California, Los Angeles, are the first of their kind that show dementia and memory loss can not only be potentially halted, but reversed to the point where the patients are able to rejoin the workforce and fully recognize friends and family.
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    Stanford Might Have Found A Cure For Alzheimerís Disease

    a potential game changer ... http://www.inquisitr.com/1753543/sta...imers-disease/

    New research at Stanford University could help cure a disease that affects 36 million people worldwide: Alzheimer’s disease.

    According to the Telegraph, Stanford University researchers have discovered the cause of dying nerve cells in the brain, particularly from Alzheimer’s disease. Cells that are designated to clean up harmful bacteria, viruses and damaging deposits stop working, which results in the Alzheimer’s symptom of brain deterioration. These clean-up cells are called “microglia” and they make up about 10 to 15 percent of all brain cells. These essential cells do their job efficiently in the brains of young people; but as humans age, a protein called EP2 can stop the microglia” from functioning. This can lead to Alzheimer’s disease, a neurodegenerative ailment that causes devastating memory loss and eventually death.

    The cure for Alzheimer’s disease is simple in concept. Block the EP2 protein that inhibits the microglia. If the protein no longer keeps the microglia from functioning, it can go about its business cleaning up nerve-damaging pathogens like amyloid-beta plaques. Stanford researchers realized the concept by developing an Alzheimer’s drug to block the protein, which they then tested on mice with Alzheimer’s symptoms. The drug effectively reversed memory loss in the rodents and other harmful effects of Alzheimer’s.
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    this article is about my little sister, who has tirelessly raised awareness, 10's of thousands of dollars and helped our mother side-by-side as dad wasted away from Alzhiemrs ... couldn't be more proud of her!


    http://www.rocklandtimes.com/2015/01...ion-volunteer/

    According to the Alzheimer’s Association, progressive mental deterioration in old age has been recognized and described throughout history. In 1906, a German physician, Dr. Alois Alzheimer identified a collection of brain cell abnormalities as a disease. In the 1960s, scientists discovered a link between cognitive decline and the number of plaques and tangles in the brain. In the medical community, this discovery formally recognized Alzheimer’s as a disease and not a normal part of aging.

    Mentally having trouble following instructions, losing one’s orientation, displaying poor judgment and having difficulty managing money are all possible symptoms of Alzheimer’s disease. More than 5 million Americans are living with the disease and every 67 seconds, someone in the United States develops Alzheimer’s. It is estimated that by the year 2050, the number of people aged 65 or older with Alzheimer’s may triple from 5 million to 16 million barring medical breakthroughs.

    Maria Paliotta, Rockland Office Director said, “In Rockland County, there are 5,000 to 6,000 families affected by the disease. As the disease progresses, it becomes a full-time effort for the caregivers to provide the necessary services for their loved ones. The non-profit Alzheimer’s Association of Rockland County offers information and free support services to individuals with Alzheimer’s disease and their families.”

    Siobhan O’Grady is one Rocklander who has dedicated countless hours to helping the afflicted

    Paliotta said, “I met Siobhan two years ago, when she came to the office to find out about services for her father, John, who had Alzheimer’s. Siobhan and her mother became primary caregivers during the long journey from March 2009 to March 2014, when John passed away at the age of 69. Siobhan is a spectacular person, ‘rallied the troops’ and has spent a great deal of effort to raise funds and awareness of the Alzheimer’s support groups. She hit the ground running, became a volunteer and joined the planning committee for The Walk to End Alzheimer’s.”

    Siobhan O’Grady said, “It is important for people to get involved, because the personal and medical costs related to Alzheimer’s disease will make or break this county. The big fundraiser that I held was ‘A Night Out with Team O’Grady.’ We had comedy, music, food and it was an opportunity to raise awareness and celebrate the life of my father John O’Grady. At the event, we raised $10,000 and for the year, the team has raised $14,000. The ‘Second Annual Night Out with Team O’Grady’ will be held in Emmet’s Castle, March 28, 2015 at 8 p.m. at the Blue Hill Golf Course.”

    For additional information about future programs and events, call 845-639-6776 or access www.alz.org
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    Alzheimerís breakthrough ...

    http://www.telegraph.co.uk/news/scie...f-disease.html

    Scientists have found a method which could potentially stop the growth of Alzheimerís disease in its tracks, raising the prospect of a wave of new treatments for the condition.

    A team at Cambridge University, working with partners in Sweden and Estonia, has identified a molecule which can block the progress of Alzheimerís at a crucial stage in its development.

    Not only is it the first time that experts have identified a means of breaking the cycle leading to the development of Alzheimerís but they believe the technique could be used to identify other molecules as future treatments to curb the growth of the condition.

    Charities hailed it as an "exciting" discovery.
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    Alzheimer's Disease study: 'The cure could be in our blood'

    http://www.al.com/news/anniston-gads...f_alzheim.html

    For a northeast Alabama woman and her extended family, losing keys or forgetting names is no laughing matter. In fact, she and her relatives watch with dread for signs that a disease that affects a startling 50 percent or more of her family may be lurking.

    "You wonder every time you misplace something," said Doris Crouse of Gaylesville. "You ask yourself, 'Is this normal or is it beginning?'"

    According to Crouse, researchers have discovered her genetics, as part of the Chastain family tree, mean there is a strong likelihood that her fears are founded.

    "They are doing a study on the Chastain blood, because we have an extra Alzheimer's gene," she said. "They're trying to find a cure and think it's real possible it could be in our blood. They say we're the only family in America who has this extra gene and there are only two other families in the world who do."

    It's a remarkable assertion confirmed by Dr. Allan Levey, chair of the Department of Neurology at Emory University School of Medicine in Atlanta and director of Emory's Alzheimer's Disease Research Center.

    "There is a horrible crisis with more and more people developing Alzheimer's disease, because more people are aging and living longer," he said. "It's really a tsunami ahead of us with horrendous personal and family impact."

    Levey said the disease has a devastating societal impact and is a major threat to the global economy.

    "Years ago, when people didn't live past an average lifespan of 50 or 60 years, it wasn't a problem," he said. "The likelihood of Alzheimer's starts doubling every year as people get older. It turns out 40 to 50 percent of those past the age of 85 have Alzheimers. More and people are living that long. Currently, over 5 million Americans are affected and that number will grow.

    "Currently, there's not a single treatment which is able to slow or prevent the disease," said Levey. "It's the only one of the major causes of death that has no known treatment to stop it.
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    http://www.sciencealert.com/new-alzh...emory-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 move in. Microglila cells are basically waste-removal cells, so once they get past the blood-brain barrier, they’re able to clear out the toxic beta-amyloid clumps before the blood-brain barrier is restored within a few hours.

    The team reports fully restoring the memories 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, JŁrgen GŲtz, 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.

    You can hear an ABC radio interview with the team here.
    could be a ray of hope
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    And the work goes on ...

    http://www.webmd.com/alzheimers/news...rly-alzheimers

    WEDNESDAY, May 27, 2015 (HealthDay News) -- Damage to the brain's white matter may be an early sign of certain types of Alzheimer's disease, according to a new study.

    Researchers used a specialized MRI technique called diffusion tensor imaging (DTI) to assess white matter in 53 people with three different types of Alzheimer's. Some patients had atypical forms of the disorder that affect localized parts of the brain (called focal AD syndromes). These atypical forms may cause vision and language problems.


    Other patients in the study had early onset Alzheimer's, which affects several areas of the brain and interferes with thinking skills such as reasoning, planning and problem solving. This is different than late-onset Alzheimer's, which develops after age 65 and is marked by progressive memory loss.

    All of the patients had extensive white matter damage, along with regional gray matter damage, according to the study published May 27 in the journal Radiology.

    "Alzheimer's is a gray matter disease. However, white matter damage has a central role in how the disease strikes and progresses," study co-author Dr. Federica Agosta, from the Neuroimaging Research Unit at the San Raffaele Scientific Institute in Milan, Italy, said in a news release from the Radiological Society of North America.

    "The white matter damage in patients with focal AD syndromes was much more severe and widespread than expected," she said. Changes in gray matter occurred in more limited areas, she added.

    The findings support the theory that Alzheimer's disease may travel along white matter fibers from one area of the brain to another, according to Agosta.
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    Get your rest ...

    http://www.usnews.com/news/science/n...lzheimers-risk

    WASHINGTON (AP) ó To sleep, perchance to... ward off Alzheimer's? New research suggests poor sleep may increase people's risk of Alzheimer's disease, by spurring a brain-clogging gunk that in turn further interrupts shut-eye.

    Disrupted sleep may be one of the missing pieces in explaining how a hallmark of Alzheimer's, a sticky protein called beta-amyloid, starts its damage long before people have trouble with memory, researchers reported Monday at the Alzheimer's Association International Conference.

    "It's very clear that sleep disruption is an underappreciated factor," said Dr. Matthew Walker of the University of California, Berkeley, who presented data linking amyloid levels with people's sleep and memory performance. "It's a new player on the scene that increases risk of Alzheimer's disease."
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    http://www.theguardian.com/society/2...velop-dementia

    One in three people born this year will develop dementia, according to new figures.

    The Alzheimer’s Research UK charity warned of a “looming national health crisis” as the population ages.

    It called for greater efforts across the globe to help develop new treatments.
    Dementia affects 850,000 people in the UK, resulting in the loss of brain cells. The most common type is Alzheimer’s disease.

    Early symptoms include problems with memory and thinking. As the disease progresses, people can experience difficulty with walking, balance and swallowing.

    Alzheimer’s Research UK said age was the biggest risk factor for developing dementia.

    As people live longer than ever before, the numbers with dementia will rise. The latest analysis, commissioned by the charity and carried out by the Office of Health Economics, was released to mark World Alzheimer’s Day.

    It showed 27% of boys born in 2015 will develop the condition in their lifetime, alongside 37% of girls. Previous research from the same team has estimated that the development of a drug that could delay the onset of dementia by five years would cut the number of cases by a third.
    If Alzheimer's were a genetic-based disease than life span would have zero effect on the percentages of the inflicted
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    http://www.brightfocus.org/news/brig...rly-alzheimers

    In a major discovery, BrightFocus-funded scientists have made significant progress in understanding how tau tangles may spread in the earliest stages of Alzheimerís disease (AD), adding crucial insight toward learning how to slow or prevent the disease.

    The new research findings, published in Nature Neuroscience, show that a damaged, toxic form of tau protein may spread from neurons in exosomes, or minute particles that are released from microglia, the brainís innate immune cells. While it's quite possible this is not the only way tau tangles grow and spread, the research team provides compelling evidence that microglial cells may play a role by secreting exosomes that contain diseased tau in ADís early stages.

    Exosomes are small, fluid-filled sacs that are released by microglia into the intracellular space, and from there they can be taken up by neurons.
    i
    They are believed to have specialized functions, including waste management and intracellular signaling to invoke an immune response. However, it appears that in this situation, microglia may be spreading tau rather than clearing it from the brain. The experiments published in Nature Neuroscience on October 5 (Asai et al, 2015) showed that stopping this process helped prevent tauís spread.

    The work stems from a 2013-15 BrightFocus grant to first author Hirohide Asai, MD, PhD, which was completed while he was in residence at Boston University. Senior author, Tsuneya Ikezu, MD, PhD, was Asaiís mentor on the project. Another Boston University colleague, Benjamin Wolozin, MD, PhD, a 2015-18 BrightFocus grantee for a different project, is coauthor and drafted the manuscript.

    The researchers were able, in two different experiments, to significantly halt tauís spread by reducing microglia and by inhibiting exosome synthesis. Their work suggests that these tau-carrying exosomes are a promising area for future work toward a new therapeutic treatment. Earlier results of their experiments were publicized at the 2014 Society for Neuroscience meeting and covered in a BrightFocus Science report.

    The work by Ikezu's team brings up most closer to understanding the "disease mechanism," where the disease begins and how it spreads. In the healthy brain, tau protein serves a useful role. However, early in the course of AD, tau undergoes biochemical changes that cause it to change shape and collect in neurofibrillary tangles (NFTs) known as ďtau tangles.Ē These tangles first form in a brain region called the entorhinal cortex (EC), before memory loss or other AD symptoms occur.
    that would be a huge breakthrough
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    Protein in aspirin may reduce Alzheimer's disease risk

    http://www.foxnews.com/health/2015/1...-suggests.html

    Researchers have found that a key protein in aspirin may help pulverize an enzyme linked to neurodegenerative conditions like Alzheimerís, Parkinsonís and Huntingtonís diseasesó suggesting that taking the common drug may help reduce Americansí disease risk. In their research, published this week in the journal PLOS One, study authors at Johns Hopkins University and Boyce Thompson Institute discovered that salicylic acid, a byproduct of aspirin, binds to the enzyme GAPDH (Glyceraldehyde 3-Phosphate Dehydrogenase), preventing it from moving into a cellís nucleus where it would cause cell death.

    During oxidative stress, GAPDH is affected then enters the nucleus of neurons, where it affects protein turnover and leads to cell death, causing neurodegenerative loss. The anti-Parkinson's drug deprenyl already demonstrates GAPDH's ability to prevent entry into the nucleus and the corresponding cell death, according to a news release.

    "The new study establishes that GAPDH is a target for salicylate drugs related to aspirin, and hence may be relevant to the therapeutic actions of such drugs,Ē co-author Solomon Snyder, professor of neuroscience at Johns Hopkins University in Baltimore, said in the release.

    Snyder, along with senior author Daniel Klessig, a professor at Boyce Thompson Institute and Cornell University, used high-throughput screens to find proteins in the human body that bind to salicylic acid. GAPDH primarily plays a role in glucose metabolism, but it also helps regulate plantsí immune systems. Past research suggests several targets in plants are affected by salicylic acid and that many are translatable to humans, according to the release.

    In the current study, scientists also observed that a natural derivative of salicylic acid from the Chinese medical herb licorice and a lab-synthesized derivative bind to GAPDH more effectively than salicylic acid.
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    3rd Annual Night Out w/ Team O'Grady to benefit the Alzheimer's Association

    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
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