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Evidence for a novel late-onset Alzheimer disease locus on chromosome 19p13.2.

Wijsman, Ellen M., Daw, E. Warwick, Yu, Change-En, Payami, Haydeh, Steinbart, Ellen J., Nochlin, David, Conlon, Erin M., Bird, Thomas D., Schellenberg, Gerard D.·2004·The American Journal of Human Genetics
DOI 10.1086/423393
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  • Several groups identified a potential contribution of LDLR to AD and investigated potential links, with some apparently opposing results.

    “Several groups identified a potential contribution of LDLR to AD and investigated potential links, for example by crossing AD transgenic mice with the LDLR−/− mouse model of hypercholesterolemia to investigate the effects of LDLR deficiency [30]–[40]. Some apparently opposing results were obtained.”

    From LDLR Expression and Localization Are Altered in Mouse and Human Cell Culture Models of Alzheimer's Disease (2010) · cites this paper as [35]

    The Discussion identifies LDLR as near a chromosome 19p linkage signal and calls its possible connection to Alzheimer disease suggestive. It does not report crossing AD transgenic mice with LDLR-deficient mice or opposing results from such experiments; the mouse evidence mentioned elsewhere concerns LRP, a different receptor. (LLM, conf=0.86)

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Metadata

Authors
Wijsman, E. M., Daw, E. W., Yu, C.-E., Payami, H., Steinbart, E. J., Nochlin, D., Conlon, E. M., Bird, T. D., & Schellenberg, G. D.
Venue
The American Journal of Human Genetics
Publisher
Elsevier BV
Published
2004-09
Volume
75
Issue
3
Pages
398-409
ISSN
0002-9297
DOI
10.1086/423393
Cited by
71
References
6
Language
en
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