New Alzheimer's Clues Identified

TUESDAY, July 6 (HealthDay News) -- High concentrations of a blood plasma protein called clusterin may influence the development, severity and progression of Alzheimer's disease, English researchers report.

They conducted clinical assessments and brain imaging scans, and analyzed blood plasma samples from people with either Alzheimer's disease, mild cognitive impairment (precursor to Alzheimer's), or no dementia.

The team at the Institute of Psychiatry at King's College London found an association between levels of clusterin in blood plasma and severity of Alzheimer's disease, rapid progression of the disease, and atrophy in an area of the brain called the entorhinal cortex, which plays a role in memory.

The researchers also concluded that high clusterin levels in blood plasma were linked with increased amyloid-beta (a protein that forms the brain plaques associated with Alzheimer's) in the brain's medial temporal lobe.

The study is published in the June issue of the Archives of General Psychiatry.

Previous studies suggest that clusterins belong to a family of proteins called extracellular chaperones, which regulate the formation and removal of amyloid, said the researchers.

"Although these findings do not support the clinical utility of plasma clusterin concentration as a standalone biomarker for Alzheimer's disease, they reveal a robust peripheral signature of this amyloid chaperone protein that is responsive to key features of disease pathology," they wrote in a news release from the publisher.

"Our findings clearly implicate clusterin, but there may well be other proteins in plasma related to the disease process, and indeed our previous studies and those of others suggest this is the case," they concluded. "These results may have wider implications for the identification of other amyloid chaperone proteins in plasma, both as putative Alzheimer's disease biomarkers as well as drug targets of disease-modifying treatments."

-- Robert Preidt

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SOURCE: JAMA/Archives journals, news release, July 5, 2010