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Biomarkers May Predict Alzheimer's
Proteins in spinal fluid may help diagnose disease early, study shows
By Steven Reinberg
HealthDay Reporter
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TUESDAY, July 21 (HealthDay News) -- Certain proteins found in cerebrospinal fluid may accurately identify the people with mild cognitive impairment who are most likely to develop Alzheimer's disease, a new study finds.
Changes in the chemistry of cerebrospinal fluid have been identified as early signs of Alzheimer's disease. If and when treatments are available for Alzheimer's, diagnosing the disease early may help prevent it from developing, experts say.
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"We confirmed, in a large multi-center study, that proteins in cerebrospinal fluid identify early-stage Alzheimer's disease, as suggested by previous smaller studies," said lead researcher Dr. Niklas Mattsson, from the Institute of Neuroscience and Physiology, Clinical Neurochemistry Laboratory at Sahlgrenska University Hospital in Molndal, Sweden.
"These proteins may be used in research, in particular in drug trials, and also as a complement to clinical diagnostics, in particular when disease-modifying drugs become available," he said.
The report is published in the July 22/29 issue of the Journal of the American Medical Association.
For the study, Mattsson's team studied the accuracy of using three biomarkers found in spinal fluid in predicting Alzheimer's diseases. The biomarkers are beta-amyloid1-42 (Aβ42), total tau protein (T-tau), and tau phosphorylated at position threonine 181 (P-tau).
The researchers tested for these biomarkers in 750 people with mild cognitive impairment, 529 people with Alzheimer's disease and 304 healthy people. After two years, 271 of those with mild cognitive impairment progressed to Alzheimer's disease and 59 developed other dementias.
The researchers found that people who developed Alzheimer's had lower levels of Aβ42 and higher levels of P-tau and T-tau compared with patients with mild cognitive impairment who did not develop Alzheimer's.
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Copyright © 2009 ScoutNews, LLC. All rights reserved.
Last updated 7/21/2009
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SOURCES: Niklas Mattsson, M.D., Institute of Neuroscience and Physiology, Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Molndal, Sweden; Maria Carrillo, Ph.D., director, medical and scientific relations, Alzheimer's Association; Samuel Gandy, M.D., Ph.D., Mount Sinai Professor in Alzheimer's Disease Research, Mount Sinai School of Medicine, New York City; July 22/29, 2009, Journal of the American Medical Association
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