Protein deposits may cause Alzheimer's

CHICAGO (AP) -- A new study supports the notion that certain protein deposits found in the brains of Alzheimer's victims are a cause of the mind-robbing disease, and not just a symptom. Autopsies on 79 nursing home patients confirmed that beta-amyloid protein plays a role in the earliest stages of Alzheimer's -- even before symptoms of dementia appear, the researchers reported in today's Journal of the American Medical Association. Sticky plaques of beta-amyloid in the brain and tangles of a protein known as tau inside brain nerve fibres are two of the distinguishing features of Alzheimer's. Scientists disagree over which feature may play a more central role in the destruction of brain cells. And some believe that the plaques and tangles are actually markers left by nerve cells killed by some other unknown cause. The study's authors favour the beta-amyloid theory because they found that the presence of beta-amyloid preceded development of tau protein in the brain's frontal cortex. In an accompanying editorial, Dr. Dennis J. Selkoe, a neurologist at Harvard's Brigham and Women's Hospital, called the conclusion exciting and said it could lead to new ways to diagnose and treat Alzheimer's. "This work, coupled with early work, clearly points to amyloid build-up as the cause," said Selkoe, who holds a stake in Elan Corp., which is testing a vaccine aimed at preventing beta-amyloid accumulation. But an executive at the Alzheimer's Association said the study does not prove what causes the disease. "What it doesn't tell us is which comes first, the chicken or the egg -- the disease or beta-amyloid," said William Theis, vice-president for medical and scientific affairs at the Alzheimer's Association. The authors, led by neuroscientist Jan Naslund of Rockefeller University in New York, studied autopsy results on 63 patients with mild to severe dementia believed to be caused by Alzheimer's and 16 mentally healthy patients. Increases of beta-amyloid in brain tissue were associated with increasing severity of mental decline, with the highest levels of beta-amyloid found in the brains of patients with the greatest degree of dementia. Abnormal beta-amyloid levels were also found even in patients without dementia. The researchers said those patients would have gone on to develop full-blown Alzheimer's had they lived. There were already significant levels of beta-amyloid found in early dementia patients with no tangles in the frontal cortex, said Dr. Joseph Buxbaum, a co-author and head of the molecular neuropsychiatry laboratory at Mount Sinai School of Medicine in New York. Buxbaum said that suggests beta-amyloid "must be a cause." Buxbaum said his study is a boost to research aimed at finding ways to block accumulation of beta-amyloid.