Late Onset Alzheimer's Disease Risk Variants in Cognitive Decline: The PATH Through Life Study
Journal of Alzheimer's disease : JAD, ISSN: 1875-8908, Vol: 57, Issue: 2, Page: 423-436
2017
- 23Citations
- 53Captures
- 1Mentions
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Metrics Details
- Citations23
- Citation Indexes23
- CrossRef23
- 21
- Captures53
- Readers53
- 53
- Mentions1
- News Mentions1
- 1
Most Recent News
Late Onset Alzheimer's Disease Risk Variants in Cognitive Decline: The PATH Through Life Study.
J Alzheimers Dis. 2017 Feb 28; Authors: Andrews SJ, Das D, Anstey KJ, Easteal S PubMed: 28269768 Submit Comment
Article Description
Recent genome wide association studies have identified a number of single nucleotide polymorphisms associated with late onset Alzheimer's disease (LOAD). We examined the associations of 24 LOAD risk loci, individually and collectively as a genetic risk score, with cognitive function. We used data from 1,626 non-demented older Australians of European ancestry who were examined up to four times over 12 years on tests assessing episodic memory, working memory, vocabulary, and information processing speed. Linear mixed models were generated to examine associations between genetic factors and cognitive performance. Twelve SNPs were significantly associated with baseline cognitive performance (ABCA7, MS4A4E, SORL1), linear rate of change (APOE, ABCA7, INPP5D, ZCWPW1, CELF1), or quadratic rate of change (APOE, CLU, EPHA1, HLA-DRB5, INPP5D, FERMT2). In addition, a weighted genetic risk score was associated with linear rate of change in episodic memory and information processing speed. Our results suggest that a minority of AD related SNPs may be associated with non-clinical cognitive decline. Further research is required to verify these results and to examine the effect of preclinical AD in genetic association studies of cognitive decline. The identification of LOAD risk loci associated with non-clinical cognitive performance may help in screening for individuals at greater risk of cognitive decline.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85014446306&origin=inward; http://dx.doi.org/10.3233/jad-160774; http://www.ncbi.nlm.nih.gov/pubmed/28269768; http://dx.doi.org/10.1101/067694; http://www.medra.org/servlet/aliasResolver?alias=iospress&doi=10.3233/JAD-160774; https://journals.sagepub.com/doi/full/10.3233/JAD-160774; https://doi.org/10.7490%2Ff1000research.1112173.1; http://dx.doi.org/10.7490/f1000research.1112173.1; https://dx.doi.org/10.7490/f1000research.1112173.1; https://f1000research.com:443/posters/5-1208; https://dx.doi.org/10.3233/jad-160774; https://content.iospress.com:443/articles/journal-of-alzheimers-disease/jad160774; https://dx.doi.org/10.1101/067694; https://www.biorxiv.org/content/10.1101/067694v1; https://content.iospress.com:443/download/journal-of-alzheimers-disease/jad160774?id=journal-of-alzheimers-disease%2Fjad160774; http://biorxiv.org/lookup/doi/10.1101/067694; https://www.biorxiv.org/content/10.1101/067694v1.abstract; https://www.biorxiv.org/content/biorxiv/early/2016/08/04/067694.full.pdf; https://f1000research.com/posters/5-1208
Cold Spring Harbor Laboratory
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