Literature DB >> 29340929

S-Adenosyl Methionine and Transmethylation Pathways in Neuropsychiatric Diseases Throughout Life.

Jin Gao1,2,3, Catherine M Cahill2, Xudong Huang2, Joshua L Roffman1, Stefania Lamon-Fava4, Maurizio Fava1, David Mischoulon1, Jack T Rogers5.   

Abstract

S-Adenosyl methionine (SAMe), as a major methyl donor, exerts its influence on central nervous system function through cellular transmethylation pathways, including the methylation of DNA, histones, protein phosphatase 2A, and several catecholamine moieties. Based on available evidence, this review focuses on the lifelong range of severe neuropsychiatric and neurodegenerative diseases and their associated neuropathologies, which have been linked to the deficiency/load of SAMe production or/and the disturbance in transmethylation pathways. Also included in this review are the present-day applications of SAMe in the treatment in these diseases in each age group.

Entities:  

Keywords:  Neurodegenerative disease; Pathway; Psychiatric disease; S-Adenosyl-methionine; Transmethylation

Mesh：

Substances：

Year:  2018        PMID： 29340929      PMCID： PMC5794704          DOI： 10.1007/s13311-017-0593-0

Source DB:  PubMed          Journal:  Neurotherapeutics        ISSN： 1878-7479            Impact factor:   7.620


  210 in total

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Review 8.  Polymorphisms in genes involved in folate metabolism and colorectal neoplasia: a HuGE review.

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Journal:  Neuron       Date:  2014-03-05       Impact factor: 17.173
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6.  Prenatal S-Adenosine Methionine (SAMe) Induces Changes in Gene Expression in the Brain of Newborn Mice That Are Prevented by Co-Administration of Valproic Acid (VPA).

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Review 10.  S-Adenosylmethionine (SAMe) in major depressive disorder (MDD): a clinician-oriented systematic review.

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