کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10956940 | 1099465 | 2005 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
S-adenosylmethionine/homocysteine cycle alterations modify DNA methylation status with consequent deregulation of PS1 and BACE and beta-amyloid production
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
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چکیده انگلیسی
Few diseases are characterized by high homocysteine (HCY) and low folate and vitamin B12 blood levels. Alzheimer disease (AD) is among these. It has already been shown that DNA methylation is involved in amyloid precursor protein (APP) processing and β-amyloid (Aβ) production through the regulation of Presenilin1 (PS1) expression and that exogenous S-adenosylmethionine (SAM) can silence the gene reducing Aβ production. Here we demonstrate that BACE (β-secretase), as well as PS1, is regulated by methylation and that the reduction of folate and vitamin B12 in culture medium can cause a reduction of SAM levels with consequent increase in presenilin1 and BACE levels and with increase in Aβ production. The simultaneous administration of SAM to the deficient medium can restore the normal gene expression, thus reducing the Aβ levels. The use of deprived medium was intended to mimic a mild nutritional deficit involved in the onset of AD.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular and Cellular Neuroscience - Volume 28, Issue 1, January 2005, Pages 195-204
Journal: Molecular and Cellular Neuroscience - Volume 28, Issue 1, January 2005, Pages 195-204
نویسندگان
Andrea Fuso, Laura Seminara, Rosaria A. Cavallaro, Fabrizio D'Anselmi, Sigfrido Scarpa,