Preliminary research on Alzheimer's disease suggests a protein that accumulates in the brain at very high levels in Alzheimer's patients is not being overproduced, it's just not being cleared efficiently from the brain.
The study, published in Science, measured beta-amyloid levels in the cerebrospinal fluid of twelve 74-year old patients with late-onset Alzheimer's and twelve without. Researchers looked at how fast beta-amyloid was produced and how quickly it cleared the brain.
"These findings may help point us toward better diagnostic tests and effective therapies," said study author Dr. Randall Bateman. "The next question is what is causing the decreased clearance rate."
Researchers say the study is significant because it's the first to measure beta-amyloid production and clearance–long thought to be an underlying cause of the disease–and could lead to an easier test–possibly a blood test–that will measure the protein early enough to detect Alzheimer's before symptoms begin.
"Abnormal protein deposits within the brain are a hallmark not only of Alzheimer's disease, but of many neurological disorders," said Roderick Corriveau, a program director at the National Institute of Neurological Disorders and Stroke (NINDS) at the National Institutes of Health. "With knowledge about how these proteins accumulate, we may be able to slow that process and reduce the damage to the brain."
"For years scientists believed that it was the overproduction of beta-amyloid that led to its accumulation in the brain," said Marcelle Morrison-Bogorad, director of the Division of Neuroscience at the NIA. "These new findings shift the emphasis to clearance of beta-amyloid. This may lead to development of a diagnostic test as well as identification of new therapeutic targets."
More than 5 million Americans have Alzheimer's disease, the most common cause of dementia in the elderly. According to the Alzheimer's Association's Dr. Ralph Nixon, Vice Chair, Medical & Scientific Advisory Council, this research adds human validation to the puzzle of how amyloid beta accumulates in the brain. "It is the first data of this kind in a human," and, as such, provides key preliminary validation to studies in animal models, which are incomplete and often give conflicting information."
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