کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6808925 | 1433593 | 2012 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
S-adenosylmethionine reduces the progress of the Alzheimer-like features induced by B-vitamin deficiency in mice
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
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![عکس صفحه اول مقاله: S-adenosylmethionine reduces the progress of the Alzheimer-like features induced by B-vitamin deficiency in mice S-adenosylmethionine reduces the progress of the Alzheimer-like features induced by B-vitamin deficiency in mice](/preview/png/6808925.png)
چکیده انگلیسی
Methylation reactions linked to homocysteine in the one-carbon metabolism are increasingly elicited in Alzheimer's disease, although the association of hyperhomocysteinemia and of low B vitamin levels with the disease is still debated. We previously demonstrated that hyperhomocysteinemia and DNA hypomethylation induced by B vitamin deficiency are associated with PSEN1 and BACE1 overexpression and amyloid production. The present study is aimed at assessing S-adenosylmethionine effects in mice kept under a condition of B vitamin deficiency. To this end, TgCRND8 mice and wild-type littermates were assigned to control or B vitamin deficient diet, with or without S-adenosylmethionine supplementation. We found that S-adenosylmethionine reduced amyloid production, increased spatial memory in TgCRND8 mice and inhibited the upregulation of B vitamin deficiency-induced PSEN1 and BACE1 expression and Tau phosphorylation in TgCRND8 and wild-type mice. Furthermore, S-adenosylmethionine treatment reduced plaque spreading independently on B vitamin deficiency. These results strengthen our previous observations on the possible role of one-carbon metabolism in Alzheimer's disease, highlighting hyperhomocysteinemia-related mechanisms in dementia onset/progression and encourage further studies aimed at evaluating the use of S-adenosylmethionine as a potential candidate drug for the treatment of the disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neurobiology of Aging - Volume 33, Issue 7, July 2012, Pages 1482.e1-1482.e16
Journal: Neurobiology of Aging - Volume 33, Issue 7, July 2012, Pages 1482.e1-1482.e16
نویسندگان
Andrea Fuso, Vincenzina Nicolia, Laura Ricceri, Rosaria A. Cavallaro, Elisa Isopi, Franco Mangia, Maria Teresa Fiorenza, Sigfrido Scarpa,