Preprint Review Version 1 This version is not peer-reviewed

Epigenetic Factors in Late-Onset Alzheimer’s Disease: MTHFR and CTH Gene Polymorphisms, Metabolic Trans-sulfuration and Methylation Pathways, and B Vitamins

Version 1 : Received: 21 December 2018 / Approved: 24 December 2018 / Online: 24 December 2018 (04:48:53 CET)

A peer-reviewed article of this Preprint also exists.

Román, G.C.; Mancera-Páez, O.; Bernal, C. Epigenetic Factors in Late-Onset Alzheimer’s Disease: MTHFR and CTH Gene Polymorphisms, Metabolic Transsulfuration and Methylation Pathways, and B Vitamins. Int. J. Mol. Sci. 2019, 20, 319. Román, G.C.; Mancera-Páez, O.; Bernal, C. Epigenetic Factors in Late-Onset Alzheimer’s Disease: MTHFR and CTH Gene Polymorphisms, Metabolic Transsulfuration and Methylation Pathways, and B Vitamins. Int. J. Mol. Sci. 2019, 20, 319.

Journal reference: Int. J. Mol. Sci. 2019, 20, 319
DOI: 10.3390/ijms20020319

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 trans-sulfuration 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.

Subject Areas

Alzheimer’s disease; CTH gene; DNA methylation; epigenetics; epigenome-wide association study; methylome; MTHFR gene; nutrition; S-adenosylmethionine; vitamin B complex

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