Next Article in Journal
c-Src Recruitment is Involved in c-MET-Mediated Malignant Behaviour of NT2D1 Non-Seminoma Cells
Next Article in Special Issue
Sleep Disturbance as a Potential Modifiable Risk Factor for Alzheimer’s Disease
Previous Article in Journal
Silkworm Storage Protein 1 Inhibits Autophagy-Mediated Apoptosis
Previous Article in Special Issue
Imaging and Molecular Mechanisms of Alzheimer’s Disease: A Review
Open AccessReview

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

1
Department of Neurology, Methodist Neurological Institute, Institute for Academic Medicine Houston Methodist Research Institute, Houston Methodist Hospital, Houston, TX 77030, USA
2
Weill Cornell Medical College, Department of Neurology, Cornell University, New York, NY 10065, USA
3
Universidad Nacional de Colombia, Hospital Universitario Nacional, Faculty of Medicine, Department of Neurology, Bogotá ZC 57, Colombia
4
David Cabello International Alzheimer Disease Scholarship Fund, Houston Methodist Hospital, Houston, TX77030, USA
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2019, 20(2), 319; https://doi.org/10.3390/ijms20020319
Received: 20 December 2018 / Revised: 10 January 2019 / Accepted: 11 January 2019 / Published: 14 January 2019
(This article belongs to the Special Issue Molecular Mechanism of Alzheimer's Disease)
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. View Full-Text
Keywords: Alzheimer’s disease; cystathionine-γ-lyase CTH gene; DNA methylation; epigenetics; epigenome-wide association study; methylome; methylenetetrahydrofolate reductase MTHFR gene; nutrition; S-adenosylmethionine; vitamin B complex Alzheimer’s disease; cystathionine-γ-lyase CTH gene; DNA methylation; epigenetics; epigenome-wide association study; methylome; methylenetetrahydrofolate reductase MTHFR gene; nutrition; S-adenosylmethionine; vitamin B complex
Show Figures

Figure 1

MDPI and ACS Style

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.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map

1
Back to TopTop