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Three new targets in Alzheimer\'s diseaseAdd to my bookmarks

Nature Genetics

September 7, 2009

Three new genetic associations to late onset Alzheimer\'s disease are reported in two papers online this week in Nature Genetics. These are among the first robustly replicated genetic associations to the disease since the now well established association to APOE. Alzheimer\'s disease (AD) is the most common form of dementia worldwide.

Philippe Amouyel, Julie Williams and their respective colleagues report two independent genome-wide association studies to late onset AD. In addition to replicating the well established genetic association to APOE, they report three new genetic loci associated with progression of the disease. Two of the newly associated genes ― CLU (Clusterin) and CR1 ― have been shown to play a role in clearance of the amyloid beta peptide, a major component of the plaques that form in the brain of patients with AD. Clusterin, a major brain apolipoprotein, has been shown to interact with amyloid beta proteins, and is found in amyloid plaques.

The genetic risk for AD has been estimated to account for as much as 80% of the overall risk of progression to AD. While the genetic association to APOE has been robustly established through numerous studies over the past decade, the current studies are amongst the first well powered genetic association studies that are able to identify and replicate additional common genetic variants associated with late onset AD.

DOI:10.1038/ng.439 | Original article

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