کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
330346 1433643 2008 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Genetic loci modulating amyloid-beta levels in a mouse model of Alzheimer's disease
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی سالمندی
پیش نمایش صفحه اول مقاله
Genetic loci modulating amyloid-beta levels in a mouse model of Alzheimer's disease
چکیده انگلیسی

Genetic studies have demonstrated very high heritability for Alzheimer's disease (AD) risk in humans; however, these genetic contributions have proven extremely challenging to map in large studies of AD patients. Processing of the amyloid precursor protein (APP) to produce amyloid-beta (Aβ) peptide is increasingly believed to be of central importance in AD pathogenesis. Intriguingly, mice from the C57BL/6J and DBA2/J inbred strains carrying the R1.40 APP transgene produce identical levels of unprocessed APP, but demonstrate significant, heritable differences in Aβ levels. To identify specific loci responsible for the observed genetic control of Aβ metabolism in this model system, we have performed a whole-genome quantitative trait locus (QTL) mapping experiment on a total of 516 animals from a C57BL/6J × DBA/2J intercross using a dense set of SNP genetic markers. Our studies have identified three loci on mouse chromosomes 1, 2, and 7 showing significant or suggestive associations with brain Aβ levels, several of which contain regions syntenic to previous reports of linkage in human AD.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Aging - Volume 29, Issue 8, August 2008, Pages 1190–1198
نویسندگان
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