Rethinking Alzheimer’s

Alzheimer’s disease has been a known condition since it was discovered, in 1906, by a German doctor, and it has been the focus of lots of attention and research for decades.  It ranks as one of the top causes of death in the United States and is the third leading cause of death among people 60 and older, just behind heart disease and cancer.

So, after more than a hundred years, why haven’t we figured out how to treat this dread and deadly disease that robs people of their minds and personalities and leaves them empty shelves of their former selves?  Why, for example, have doctors and drug companies been able to develop effective treatments for HIV and AIDS, but not Alzheimer’s?

alzheimer_brainIt’s not that the scientific and medical community isn’t trying — but identifying the real cause of Alzheimer’s, and then devising a meaningful treatment, is proving to be an incredibly elusive challenge.  A brain with Alzheimer’s is like a car crash with no witnesses, where the accident reconstruction expert tries to find clues from the physical evidence.  Do those skid marks indicate that the driver was going too fast, or do they suggest that the driver was distracted, or was the driver paying attention when something like a deer unexpectedly came onto the road?  In the case of Alzheimer’s the brain is mangled and distorted and physically changed, both chemically and structurally.  Are those changes what caused the disease, or are they mere byproducts of the active agent that does the real harm?

For more than a quarter century, Alzheimer’s researchers and drug companies have been focusing on the “amyloid hypothesis,” which posits that an increase in amyloid deposits causes the disease, and have worked to develop drugs to target amyloid.  The hypothesis was devised because Alzheimer’s patients have an unusual buildup of amyloid in their brains, amyloid buildups have been found to be harmful in other bodily organs, and people with a genetic history of Alzheimer’s in their families also have been found to have mutations in the genes responsible for amyloid production.  With this kind of evidence, it’s not surprising that amyloid production has been the focus of treatment efforts.

Unfortunately, though, the trials of drugs that address amyloid production haven’t been successful — and after repeated failures, some scientists are wondering whether the amyloid hypothesis should be scrapped, and the disease should be examined afresh.  The amyloid hypothesis remains the prevailing view, but a minority of researchers think that the focus on amyloid buildup is like trying to close the barn door after the livestock have already escaped.  And they wonder whether the amyloid hypothesis has become entrenched with so many people, who invested so much time and money in developing amyloid-based treatments, that work on alternative approaches is being undercut.

It’s a classic test for the scientific method.  Over the years, there are countless examples of instances where prevailing views on medical, or physical, problems were overturned in favor of new approaches that turned out to accurately identify cause and effect.  The scientific method is supposed to objectively find the right answers.  For Alzheimer’s disease, maybe it is just a matter of tweaking how to develop the right treatment for the amyloid build-up — or maybe it’s something else entirely.

Those of us who have dealt with Alzheimer’s in our families hope the scientific and medical community put aside preconceived notions, dispassionately assess the evidence, and explore every avenue for developing a successful treatment.  This disease is just too devastating to go unaddressed.

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