Top Researchers Believe Prevention is the Future of Alzheimer’s Research

Top Researchers Believe Prevention is the Future of Alzheimer’s Research
The Alzheimer’s disease scientific community is changing its research focus from treatment to prevention, according to researchers from the University of Alabama at Birmingham (UAB). The shift has been driven by increased insights into the mechanisms of the disease, as well as better tools to study Alzheimer’s-associated brain changes in living people. “In my experience, Alzheimer’s disease is the most feared disease in people over 65,” said David Geldmacher, MD, the director of the Division of Memory Disorders in the Department of Neurology at the UAB. Geldmacher's remarks were made to Bob Shepard of UAB News in an article about the University's research efforts. “And while it’s true that efforts to find a cure for AD [Alzheimer’s disease] have not yet proved successful, much of that fear may be misplaced, since we have learned so much about the disease in the last several decades,” he said. According to Geldmacher, these insights suggest that prevention is a more likely scenario than a cure. One of the developments that has changed Alzheimer’s research is the development of a tool for detection of amyloid-beta buildup in the brain of living humans. Only a decade ago, the only way to diagnose Alzheimer’s disease was by an autopsy after the patient died. Meanwhile, research suggested that amyloid-beta starts aggregating in the brain decades before a person starts developing cognitive symptoms. Now, a brain-imaging method called positron emission tomography (PET) has been ada
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  1. Lance Packer says:

    The essence of the message here is that most researchers still can’t drop the Amyloid hypothesis for Alzheimer’s. They refuse to give up on 20+ years of trying to prove it is the key to all Alzheimer’s causation, in spite of 100% clinical trial failures, increasing evidence of multiple disease pathways, new avenues of treatment (especially repurposing existing drugs), and the simple fact that about half of all people having concentrations of amyloid plaque do not express Alzheimer’s symptoms. I get suspicious of motivation for such blind adherence at many levels of the research process given these stark facts.

    Yes, prevention is important, but so is my wife and millions of other Alzheimer’s sufferers. Are they to be so cavalierly discarded to the wayside of symptom management because they don’t benefit from the past myopic infatuation with amyloid? This is immoral and scientifically illogical. There are lots of alternatives being discovered which must be examined and developed; they must brought into the mainstream of major research centers and funded just like those in the history of amyloid failures.

  2. Marcus Wood says:

    “Alzheimer’s Disease” unfortunately is a catch-all term, like “cancer.” My wife is third generation suffering a distinct pattern that is genetic based with noticeable on-set in early 60s. Until the various forms of dementia that even researchers call AD are differentiated we will continue with flawed research results.

  3. Considering the nature of this disease, it makes sense to focus on prevention. The question is, focus on what? The most promising approach, i.e. immune therapy, despite of the support provided by aducanumab, is practically death. A casualty of an endless series of ill fated clinical studies; yet, those failures were the result of using the wrong strategies to develop effective products. But, the recent successful clinical studies from AXON Neurosciences with a tau vaccine have shown promising results; an outcome that should reinvigorate R&D in active immune therapy or vaccination to prevent AD. Hence, the new R&D efforts should recognize that the past activities were due to incomplete information defective, and start new studies taking into consideration the available body of new information, rather than ignoring it. Indeed, both aducanumab and AXON clinical studies provide strong support to active immune therapy of AD as a preventive approach. Hence, those efforts should end in success, assuming that the experimental designs are well thought and correct. Otherwise, we would see another 20 years of chasing unachievable AD drugs.

  4. While rather new to this (my wife 64, is 2 years into AD), I have been following this and of course, I like others, would rather the weight of research be towards treatment sooner, I can’t dismiss preventive research altogether. When electricity was first developed there were 2 different delivery methods, AC or DC. It didn’t take long for the U.S. to choose which was better. 20+ years into Amyloid brushes on excessive waste. I think a re-focusing is needed.

  5. Robert Lovell says:

    My wife is in stage 7 of this awful affliction. I don’t like the term “disease” – she is not infected. Throughout her life she has been fit, agile and an accomplished skier. She watched her weight, never used much alcohol, had low blood pressure and a great sense of humour. She drank more than three cups of tea per day and was superb at crossword puzzles and general knowledge quizzes.

    All that is gone now, and she has just turned 60. She is now in permanent high care in a hospital for the treatment of mental health.

    Her mother died from AD four years after diagnosis. Five years later, my partner of 25 years presented with the condition. Too young, far too young.

    I would like to think that early diagnosis might lead to better treatment regimes, but I see no evidence that any intervention either ameliorates or slows the advance. So why would you want to know that this affliction is going to rob you of your faculties by. It’s inexorable advance? Why put yourself through the horror and mental agony of the years of knowing your fate? I see no benefit in early diagnosis.

    This is a geneticically inherited condition, and I suspect that only through gene therapy will any solution be found to halt it. I hope for all sufferers that a solution is found soon. For us, it will all be too late.

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