Epigenetic Factors in Late-Onset Alzheimer's Disease: MTHFR and CTH Gene Polymorphisms, Metabolic Transsulfuration and Methylation Pathways, and B Vitamins Article Report uri icon

Overview

MeSH Major

  • Alzheimer Disease
  • Cognition
  • Cytidine Diphosphate Choline
  • Dementia, Vascular
  • Nootropic Agents
  • Stroke

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 B12 (methylcobalamin), vitamin B₉ (folic acid), vitamin B₆ (pyridoxine), and SAM to patients in early stages of LOAD.

publication date

  • January 14, 2019

Research

keywords

  • Report

Identity

Digital Object Identifier (DOI)

  • 10.3390/ijms20020319

PubMed ID

  • 30646578

Additional Document Info

volume

  • 20

number

  • 2