Epigenetic factors in late-onset alzheimer’s disease: MTHFR and CTH gene polymorphisms, metabolic transsulfuration and methylation pathways, and B vitamins

Gustavo C. Román, Oscar Mancera-Páez, Camilo Bernal

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

DNA methylation and other epigenetic factors are important in the pathogenesis of late-onset Alzheimer’s disease (LOAD). Methylenetetrahydrofolate reductase (MTHFR) gene mutations occur in most elderly patients with memory loss. MTHFR is critical for production of S-adenosyl-L-methionine (SAM), the principal methyl donor. A common mutation (1364T/T) of the cystathionine-γ-lyase (CTH) gene affects the enzyme that converts cystathionine to cysteine in the transsulfuration pathway causing plasma elevation of total homocysteine (tHcy) or hyperhomocysteinemia—a strong and independent risk factor for cognitive loss and AD. Other causes of hyperhomocysteinemia include aging, nutritional factors, and deficiencies of B vitamins. We emphasize the importance of supplementing vitamin B 12 (methylcobalamin), vitamin B 9 (folic acid), vitamin B 6 (pyridoxine), and SAM to patients in early stages of LOAD.

Original languageEnglish (US)
Article number319
JournalInternational journal of molecular sciences
Volume20
Issue number2
DOIs
StatePublished - Jan 2 2019

Keywords

  • Alzheimer’s disease
  • Cystathionine-γ-lyase CTH gene
  • DNA methylation
  • Epigenetics
  • Epigenome-wide association study
  • Methylenetetrahydrofolate reductase MTHFR gene
  • Methylome
  • Nutrition
  • S-adenosylmethionine
  • Vitamin B complex

ASJC Scopus subject areas

  • Catalysis
  • Molecular Biology
  • Spectroscopy
  • Computer Science Applications
  • Physical and Theoretical Chemistry
  • Organic Chemistry
  • Inorganic Chemistry

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