Alzheimer’s disease is the most common form of dementia among older people. The condition is characterized by memory decline that includes difficulty remembering events as well as recognizing family and friends.
When an Alzheimer’s sufferer’s brain is biopsied, the tissue contains many abnormal clumps of protein called amyloid plaques, as well as other tangled bundles of fibers. Scientists have been searching for a cure for decades.
The drug Verubecestat works by inhibiting an enzyme (BACE1) that reduces amyloid in the brain. The results of a phase 3 trial were published in JAMA, showing that Verubecestat reduced amyloid in the cerebrospinal fluid and the brain of subjects, but the clinical outcomes were not changed.
In other words, Alzheimer’s disease progressed among those treated with the medication to reduce amyloid levels.
The authors of the study wrote, “. . . disease progression [in Alzheimer’s disease] may be independent of [amyloid] production or, alternatively, the amyloid hypothesis of Alzheimer’s disease may not be correct.”
This study showed that altering a clinical marker — amyloid levels — in Alzheimer’s did nothing to slow the disease’s progression.
When I first heard about this study, I predicted it would fail. By the time the brain is being remodeled with amyloid plaques and tangles, it may be too late to save it.
Hopefully, this study will spur Alzheimer’s researchers to search for the real underlying mechanism of the disease.
I have maintained for years that toxic exposures coupled with nutritional deficiencies set the stage for chronic diseases like Alzheimer’s. Only when we find the real cause of the illness will we make progress toward curing it.
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