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Association studies between risk for late-onset Alzheimer's disease and variants in insulin degrading enzyme

✍ Scribed by Petra Nowotny; Anthony L. Hinrichs; Scott Smemo; John S.K. Kauwe; Taylor Maxwell; Peter Holmans; Marian Hamshere; Dragana Turic; Luke Jehu; Paul Hollingworth; Pamela Moore; Leslie Bryden; Amanda Myers; Lisa M. Doil; Kristina M. Tacey; Alison M. Gibson; Ian G. McKeith; Robert H. Perry; Chris M. Morris; Leon Thal; John C. Morris; Michael C. O'Donovan; Simon Lovestone; Andrew Grupe; John Hardy; Michael J. Owen; Julie Williams; Alison Goate


Publisher
John Wiley and Sons
Year
2005
Tongue
English
Weight
161 KB
Volume
136B
Category
Article
ISSN
1552-4841

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## Abstract Linkage studies have suggested a susceptibility locus for late‐onset Alzheimer's disease (LOAD) on chromosome 21. A functional candidate gene in this region is the β‐amyloid precursor protein (APP) gene. Previously, coding mutations in APP have been associated with early onset Alzheimer

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Butyrylcholinesterase (BChE) as well as acetylcholinesterase has been suggested to be associated with Alzheimer's disease (AD). : Hum Mol Genet 6: 1933-1936] recently reported the synergism between the gene for the K variant of BChE (BCHE-K) and the 4 allele of apolipoprotein E (APOE 4) in late-onse

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It is now commonly known that possession of one of the three common alleles of the apolipoprotein E (APOE) gene (allele epsilon 4) confers an increased risk for both familial and sporadic Alzheimer's disease (AD), and that this risk is dose-dependent. Other genes that may play a role in AD, either t