All the Alzheimer’s Research We Didn’t Do

What if a preposterous failed treatment for Covid-19 — the arthritis drug hydroxychloroquine — could successfully treat another dreaded disease, Alzheimer’s?

Dr. Madhav Thambisetty, a neurologist at the National Institute on Aging, thinks the drug’s suppression of inflammation, commonly associated with neurodegenerative disorders, might provide surprising benefits for dementia.

It’s an intriguing idea. Unfortunately, we won’t know for quite a while, if ever, whether Dr. Thambisetty is right. That’s because unconventional ideas that do not offer fealty to the dominant approach to study and treat Alzheimer’s — what’s known as the amyloid hypothesis — often find themselves starved for funds and scientific mind share.

Such shortsighted rigidity may have slowed progress toward a cure — a tragedy for a disease projected to affect more than 11 million people in the United States by 2040.

The amyloid hypothesis holds that sticky plaques and other so-called amyloid-beta proteins build up in the brain and prompt changes that cause Alzheimer’s disease’s cruel decline, gradually stealing a person’s mastery of everyday life, cherished memories and, finally, their sense of self.

In the early 1990s, legions of researchers began to sign on to the idea that removing amyloid from the brain could stop or reverse that process. But anti-amyloid drugs failed time and again. Then, in 2006, an animal experiment published in the journal Nature identified a specific type of amyloid protein as the first substance found in brain tissue to directly cause symptoms associated with Alzheimer’s. Top scientists called it a breakthrough that provided a key target for treatments. The paper became one of the most cited in the field, and funds to explore similar proteins skyrocketed.