By GINA KOLATA
Alzheimer’s researchers are obsessed with a small, sticky protein fragment, beta amyloid, that clumps into barnaclelike balls in the brains of patients with this degenerative neurological disease.
It is a normal protein. Everyone’s brain makes it. But the problem in Alzheimer’s is that it starts to accumulate into balls — plaques. The first sign the disease is developing — before there are any symptoms — is a buildup of amyloid. And for years, it seemed, the problem in Alzheimer’s was that brain cells were making too much of it.
But now, a surprising new study has found that that view appears to be 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. It’s like an overflowing sink caused by a clogged drain instead of a faucet that does not turn off.
That discovery is part of a wave of unexpected findings that are enriching scientists’ views of the genesis of Alzheimer’s disease. In some cases, like the story of amyloid disposal, the work points to new ways to understand and attack the disease. 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.