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

Neurotherapeutics. 2018 Jan;15(1):156-175. doi: 10.1007/s13311-017-0593-0.

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.

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

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • DNA Methylation
  • Epigenesis, Genetic
  • Humans
  • Mental Disorders / genetics
  • Mental Disorders / metabolism*
  • Methylation
  • Neurodegenerative Diseases / genetics
  • Neurodegenerative Diseases / metabolism*
  • S-Adenosylmethionine / metabolism*
  • Signal Transduction

Substances

  • S-Adenosylmethionine