Breakthroughs in our understanding of Alzheimer's

Dark brown amyloid plaques

A surprising new study is part of a wave of unexpected findings that are enriching scientists’ views of the genesis of Alzheimer’s disease.

For years, it seemed, the problem in Alzheimer’s was that brain cells were making too much of a small, sticky protein fragment, beta amyloid. The latest research proves that wrong: It turns out that most people with Alzheimer’s seem to make perfectly normal amounts of amyloid. They just can’t get rid of it.

If researchers could find a way to speed up disposal, perhaps they could slow down or halt the disease. Researchers have also found that amyloid, in its normal small amounts, seems to have a purpose in the brain — it may be acting like a circuit breaker to prevent nerve firing from getting out of control. But too much amyloid can shut down nerves, eventually leading to cell death. That means that if amyloid levels were reduced early in the disease, when excess amyloid is stunning nerve cells but has not yet killed them, the damage might be reversed. 

About all the new research:

The result of all this work is a renewed vigor in the field. After years in which it was not clear how to attack this devastating disease, scientists have almost an embarrassment of riches. The research is in early stages, of course, and there are many questions about which discoveries and insights will lead to prevention or a treatment that works. 

There is a new hopefulness that this terrible disease may eventually be conquered. “We are much closer and quite optimistic that we will be able to do it,” Dr. Richard Mohs, Alzheimer’s group team leader at Eli Lilly, said.