Abstract
Recent epigenome-wide association studies have confirmed the importance of epigenetic effects mediated by DNA methylation in late-onset Alzheimer's disease (LOAD). Metabolic folate pathways and methyl donor reactions facilitated by B-group vitamins may be critical in the pathogenesis of LOAD. Methylenetetrahydrofolate reductase (MTHFR) gene mutations were studied in consecutive Alzheimer's Disease & Memory Clinic patients up to December 2014. DNA analyses of MTHFR-C667T and -A1298C homozygous and heterozygous polymorphisms in 93 consecutive elderly patients revealed high prevalence of MTHFR mutations (92.5%). Findings require confirmation in a larger series, but MTHFR mutations may become a LOAD marker, opening novel possibilities for prevention and treatment.
Original language | English (US) |
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Pages (from-to) | 323-327 |
Number of pages | 5 |
Journal | Journal of Alzheimer's Disease |
Volume | 47 |
Issue number | 2 |
DOIs | |
State | Published - Jul 24 2015 |
Keywords
- Alzheimer's disease
- DNA methylation
- MTHFR gene
- epigenetics
- vitamins B-group
ASJC Scopus subject areas
- Neuroscience(all)
- Clinical Psychology
- Geriatrics and Gerontology
- Psychiatry and Mental health