Alzheimer’s, as America’s sixth-leading cause of death, has been the subject a lot of research, and much of this has focused on a protein called beta amyloid. Identified in 1906 by Alois Alzheimer, it has long been believed that when this protein accumulates in the brain, it can cause Alzheimer’s disease. Scientists have theorized that the sticky protein forms a plaque that essentially strangles healthy brain cells.
It’s understandable that this protein has been shouldering the blame for the disease, which affects more than 5 million Americans. Mice that develop amyloid plaque go on to develop Alzheimer’s-like behavior, and rare genes in people that boost the production of beta amyloid practically guarantee the individual will develop Alzheimer’s. In addition, people who have Down Syndrome actually have three copies of the gene carrying beta amyloid, and many of them develop Alzheimer’s by the time they reach middle age.
Despite this convincing evidence, the long-standing theory of beta amyloid’s crucial role is being called into question as more than 100 drugs that attack the protein have failed to treat and prevent Alzheimer’s, including several high-profile recent Alzheimer’s drug failures from big pharmaceutical names such as Eli Lilly, AstraZeneca, and Merck.
Beta amyloid therapies can clear amyloid plaque, yet patients continue to suffer from Alzheimer’s and progress further into the disease's clutches. This spectacular failure lends a lot of credence to the idea that the beta amyloid protein was never really the problem in the first place.
Some experts have expressed concerns that expensive trials are being launched with little evidence and that researchers have been putting all their eggs into one basket and wasted the last three decades chasing the amyloid hypothesis.
If beta amyloid protein isn’t the problem, what is?
Amyloid protein could still be a factor in that disease, but some experts believe that a different one, such as tau, or even the apolipoprotein E (ApoE) gene could play a more important role; it could even turn out that a complex interplay is taking place between various abnormal brain proteins and other factors.
It’s clear that researchers have been barking up the wrong tree for many years, and perhaps these failures will lead them to start considering other possibilities. For example, diet and environment likely play a bigger role than the prevailing theory allows for. Why does vitamin D deficiency more than double a person’s risk of Alzheimer’s? Why does taking turmeric reduce your risk of developing the disease? And why is it that those who follow a Mediterranean diet can reduce their risk of cognitive decline? Not only are researchers failing to pin down what causes Alzheimer’s in the first place, but they’re also largely ignoring the growing body of evidence that other factors can have a big influence on the disease.
See PharmaceuticalFraud.com for more stories on the failures of pharmaceuticals.
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