Alzheimer's protein not restricted to brain.

Alzheimer's protein not restricted to brain

A protein that accumulates in the brains of Alzheimer's patients also resides elsewhere in their bodies, new research indicates. Scientists say the unprecedented finding of beta amyloid protein in non-neural tissue should significantly aid their efforts to understand the disease's underlying biology and may improve their ability to develop and assess experimental treatments. Until now, such research has largely been restricted to postmortem examinations of patients' brains.

"This is a development that puts a new perspective on how we think about Alzheimer's disease," says Dennis J. Selkoe, who performed the research with colleagues at the Brigham and Women's Hospital in Boston. "Since 1906, when Alzheimer first described it, the disease was thought to be a brain-only process. Now we're saying there's a clear signature of this process in other parts of the body."

Beta amyloid is the major ingredients of protein deposits common in the brains of elderly people but abnormally abundant in the brains of Alzheimer's patients. Selkoe, Catherine L. Joachim and Hiroshi Mori produced antibodies to beta amyloid, then used the antibodies as bloodhounds to sniff out and bind to similar protein deposits in biopsy specimens taken from various organs in both Alzheimer's patients and normal elderly people. They found evidence of the protein in skin, blood vessels or intestinal tissues in eight of 10 Alzheimer's patients. Only four of 24 normal patients tested positive for the protein; all four were more than 77 years old.

Scientists, not patients, will reap the finding's first benefits. Long hampered by the difficulties inherent in any research restricted to the brain, they now have a chance to track the natural history of amyloid accumulation in the body with relatively noninvasive biopsy techniques. Moreover, the test may allow researchers to identify Alzhemier's patients more accurately. Such an ability would aid genetic linkage studies and might provide more uniform populations in which to test experimental drugs. "If 20 percent of your test subjects don't really have Alzheimer's, your drug study is not going to be very useful," Selkoe says.

In the long run, therapeutic implications may follow, the researchers conclude in the Sept. 21 NATURE. They say their findings suggest beta amyloid may be produced in non-neural tissue somewhere in the body, then get transported via the circulatory system to the brain, where the protein does its damage. Such a mechanism would open the possibility of using a drug either to mop up the circulating protein or to keep it from crossing the blood-brain barrier.