The Reason There’s Been No Cure for Alzheimer’s
https://www.thefp.com/p/where-is-the-cure-for-alzheimers
In 1984, researchers from the University of California, San Diego, published one of the first reports on what those plaques were made of—a protein fragment called beta-amyloid. In 1987, Dr. Rachael Neve, then an assistant professor and molecular biologist at Boston Children’s Hospital, with colleagues, cloned the amyloid precursor protein gene, as did several other labs. Meanwhile, other scientists around the world were associating amyloid proteins with Alzheimer’s as well, characterizing the proteins, and finding genetic defects related to amyloid in people with an inherited form of the disease.
It looked pretty clear: the amyloid clumps must be causing the disease. So it would make sense that clearing this debris would return a brain to health.
But there was a problem with this theory. Some people with Alzheimer’s disease didn’t have discernible plaques. And some people had discernible plaques without symptoms of the disease. Neve herself didn’t believe that there was enough evidence to blame the plaques. And it turned out that once drugs were developed to clear the plaques, when they were given to patients in clinical trials, the patients didn’t improve.
Still, the amyloid believers persisted. Not just persisted. The goal of mitigating amyloid in the brain has held a vise-like grip on Alzheimer’s research for decades, despite the fact that, one by one, the drugs designed to address amyloid—around twentyof them— have shown virtually no beneficial effects on patients.
https://www.thefp.com/p/where-is-the-cure-for-alzheimers
In 1984, researchers from the University of California, San Diego, published one of the first reports on what those plaques were made of—a protein fragment called beta-amyloid. In 1987, Dr. Rachael Neve, then an assistant professor and molecular biologist at Boston Children’s Hospital, with colleagues, cloned the amyloid precursor protein gene, as did several other labs. Meanwhile, other scientists around the world were associating amyloid proteins with Alzheimer’s as well, characterizing the proteins, and finding genetic defects related to amyloid in people with an inherited form of the disease.
It looked pretty clear: the amyloid clumps must be causing the disease. So it would make sense that clearing this debris would return a brain to health.
But there was a problem with this theory. Some people with Alzheimer’s disease didn’t have discernible plaques. And some people had discernible plaques without symptoms of the disease. Neve herself didn’t believe that there was enough evidence to blame the plaques. And it turned out that once drugs were developed to clear the plaques, when they were given to patients in clinical trials, the patients didn’t improve.
Still, the amyloid believers persisted. Not just persisted. The goal of mitigating amyloid in the brain has held a vise-like grip on Alzheimer’s research for decades, despite the fact that, one by one, the drugs designed to address amyloid—around twentyof them— have shown virtually no beneficial effects on patients.