- The Washington Times - Monday, July 10, 2006

Early signs of Alzheimer’s disease risk can be seen in the cerebrospinal fluid of middle-age adults genetically predisposed to the condition, suggesting prevention strategies should be applied at earlier ages, a study finds.

The multicenter study, published in this week’s issue of Archives of Neurology, concluded that the presence of a gene known as APOE epsilon 4 substantially increases the risk for later-onset Alzheimer’s, by accelerating “brain deposition of a pathogenic form of a protein known as AB42 starting in late middle age.”

AB42, a beta-amyloid protein, forms the plaques indicative of Alzheimer’s disease in the brain. Amyloid plaque is a clump of dead nerve cells containing a gummy insoluble substance known as amyloid, which is thought responsible for much of the brain cell destruction in Alzheimer’s patients.

In an interview yesterday, Dr. Elaine R. Peskind, the study’s lead investigator, said the ongoing research began three years ago and involves nearly 200 people ages 21 to 88. Their average age is 50.

Dr. Peskind is associate director of the Alzheimer’s Disease Research Center at the University of Washington at Seattle and a professor of psychiatry at the university.

Alzheimer’s typically strikes people in their 60s or later. As many as half of all Americans 85 or older are thought to have Alzheimer’s, according to the National Institute on Aging.

Aging and the presence of the APOE epsilon 4 gene are the strongest risk factors for Alzheimer’s. Those with APOE epsilon 4 tend to develop clinical dementia 10 to 15 years earlier than those without the gene, the authors noted.

In their research, the scientists wanted to determine whether adults confirmed as having APOE epsilon 4 have lower levels of AB42 in their spinal fluid. They found such a correlation.

“There is an inverse relationship” between levels of AB42 in the fluid surrounding the brain and spinal cord and the risk for developing Alzheimer’s, Dr. Peskind said.

That’s because these amyloid proteins clump together in the brains of those with Alzheimer’s, so fewer are available to circulate throughout the nervous system. Previous research had shown that the plaques that form in the brain during Alzheimer’s begin forming years before the onset of symptoms.

At this time, Dr. Peskind said, primary prevention for Alzheimer’s is not available. “But primary prevention trials targeting elderly persons may be too late to affect the early stages of disease pathology,” she wrote.

In an accompanying editorial, Dr. Roger N. Rosenberg of the University of Texas Southwestern Medical Center and editor of Archives of Neurology, wrote: “Peskind and colleagues offer an additional means to identify the earliest phase of Alzheimer’s disease, when the effectiveness of future agents will have the most benefit.”

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