☆ 4.5 Article

Alzheimer disease pathology in cognitively healthy elderly: A genome-wide study

NEUROBIOLOGY OF AGING (2011)

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NEUROBIOLOGY OF AGING
卷 32, 期 12, 页码 2113-2122

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ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2010.01.010

关键词

Genome-wide association study; Alzheimer disease; Non-demented elderly with AD neuropathology; Non-demented elderly without AD neuropathology; Reelinneurofibrillary tangles

类别

Geriatrics & Gerontology Neurosciences

资金

  1. National Institute on Aging of National Institutes of Health [R01-AG026916, P30-AG028377, P50-AG005146, P30-AG028383, P50-AG16574, U01-AG06786, P30-AG008017, P30-AG10161, R01-AG17917, P30-AG10129, P50-AG05131, P50-AG08671, P50-AG05681, P01-AG03991, U01-AG016976]
  2. Natural Science Foundation of China NSFC [30700442]

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Many elderly individuals remain dementia-free throughout their life. However, some of these individuals exhibit Alzheimer disease neuropathology on autopsy, evidenced by neurofibrillary tangles (NFTs) in AD-specific brain regions. We conducted a genome-wide association study to identify genetic mechanisms that distinguish non-demented elderly with a heavy NFT burden from those with a low NFT burden. The study included 299 non-demented subjects with autopsy (185 subjects with low and 114 with high NFT levels). Both a genotype test, using logistic regression, and an allele test provided consistent evidence that variants in the RELN gene are associated with neuropathology in the context of cognitive health. Immunohistochemical data for reelin expression in AD-related brain regions added support for these findings. Reelin signaling pathways modulate phosphorylation of tau, the major component of NFTs, either directly or through beta-amyloid pathways that influence tau phosphorylation. Our findings suggest that up-regulation of reelin may be a compensatory response to tau-related or beta-amyloid stress associated with AD even prior to the onset of dementia. (C) 2010 Elsevier Inc. All rights reserved.

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