Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
Add more filters










Database
Language
Publication year range
1.
Am J Obstet Gynecol ; 230(1S): S46, 2024 Jan.
Article in English | MEDLINE | ID: mdl-38355237

ABSTRACT

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/policies/article-withdrawal). This meeting abstract has been retracted at the request of the authors. The team determined further analysis is warranted before the formal presentation of the results.

2.
Int J Mol Sci ; 20(2)2019 Jan 14.
Article in English | MEDLINE | ID: mdl-30646578

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.


Subject(s)
Alzheimer Disease/genetics , Cystathionine gamma-Lyase/genetics , Epigenesis, Genetic , Methylenetetrahydrofolate Reductase (NADPH2)/genetics , Age of Onset , Alzheimer Disease/metabolism , Alzheimer Disease/pathology , Genetic Predisposition to Disease , Humans , S-Adenosylmethionine/metabolism
SELECTION OF CITATIONS
SEARCH DETAIL
...