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Abstract Title:

S-adenosylmethionine reduces the progress of the Alzheimer-like features induced by B-vitamin deficiency in mice.

Abstract Source:

Neurobiol Aging. 2012 Jul ;33(7):1482.e1-16. Epub 2012 Jan 4. PMID: 22221883

Abstract Author(s):

Andrea Fuso, Vincenzina Nicolia, Laura Ricceri, Rosaria A Cavallaro, Elisa Isopi, Franco Mangia, Maria Teresa Fiorenza, Sigfrido Scarpa

Article Affiliation:

Department of Surgery P. Valdoni, Via Antonio Scarpa, 14-00161, Sapienza University of Rome, Italy. andrea.fuso@uniroma1.it

Abstract:

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.

Study Type : Animal Study

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