期刊
NEURODEGENERATIVE DISEASES
卷 5, 期 2, 页码 60-64出版社
KARGER
DOI: 10.1159/000110789
关键词
Sorl1; Alzheimer's disease; predisposition gene; APOE gene; sortilin-related receptor
资金
- Intramural NIH HHS Funding Source: Medline
- Medical Research Council [G0701075] Funding Source: Medline
- NHLBI NIH HHS [U01HL084744] Funding Source: Medline
- NIA NIH HHS [P50-AG08671, AG05128, P30 AG19610, P50 AG16570, U01 AG016976, P30-AG13846] Funding Source: Medline
- NIMH NIH HHS [MH60451] Funding Source: Medline
- NINDS NIH HHS [U24NS051872, NS39764] Funding Source: Medline
- NATIONAL INSTITUTE OF MENTAL HEALTH [P50MH060451] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [U24NS051872, P50NS039764] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P50AG008671, P30AG019610, P50AG016570, U01AG016976, P30AG013846] Funding Source: NIH RePORTER
- MRC [G0701075] Funding Source: UKRI
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressively disabling impairments in memory, cognition, and non-cognitive behavioural symptoms. Sporadic AD is multifactorial and genetically complex. While several monogenic mutations cause early-onset AD and gene alleles have been suggested as AD susceptibility factors, the only extensively validated susceptibility gene for late-onset AD is the apolipoprotein E (APOE) epsilon 4 allele. Alleles of the APOE gene do not account for all of the genetic load calculated to be responsible for AD predisposition. Recently, polymorphisms across the neuronal sortilin-related receptor (SORL1) gene were shown to be significantly associated with AD in several cohorts. Here we present the results of our large case-control whole-genome scan at over 500,000 polymorphisms which presents weak evidence for association and potentially narrows the association interval. Copyright (C) 2007 S. Karger AG, Basel.
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