Epigenetics in Alzheimer’s Disease: Perspective of DNA Methylation
Molecular Neurobiology, ISSN: 1559-1182, Vol: 55, Issue: 2, Page: 1026-1044
2018
- 108Citations
- 260Captures
- 1Mentions
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Metrics Details
- Citations108
- Citation Indexes108
- 108
- CrossRef60
- Captures260
- Readers260
- 260
- Mentions1
- News Mentions1
- News1
Most Recent News
Epigenetics in Alzheimer's Disease: Perspective of DNA Methylation.
Mol Neurobiol. 2017 Jan 14; Authors: Qazi TJ, Quan Z, Mir A, Qing H PubMed: 28092081 Submit Comment
Review Description
Research over the years has shown that causes of Alzheimer’s disease are not well understood, but over the past years, the involvement of epigenetic mechanisms in the developing memory formation either under pathological or physiological conditions has become clear. The term epigenetics represents the heredity of changes in phenotype that are independent of altered DNA sequences. Different studies validated that cytosine methylation of genomic DNA decreases with age in different tissues of mammals, and therefore, the role of epigenetic factors in developing neurological disorders in aging has been under focus. In this review, we summarized and reviewed the involvement of different epigenetic mechanisms especially the DNA methylation in Alzheimer’s disease (AD), late-onset Alzheimer’s disease (LOAD), familial Alzheimer’s disease (FAD), and autosomal dominant Alzheimer’s disease (ADAD). Down to the minutest of details, we tried to discuss the methylation patterns like mitochondrial DNA methylation and ribosomal DNA (rDNA) methylation. Additionally, we mentioned some therapeutic approaches related to epigenetics, which could provide a potential cure for AD. Moreover, we reviewed some recent studies that validate DNA methylation as a potential biomarker and its role in AD. We hope that this review will provide new insights into the understanding of AD pathogenesis from the epigenetic perspective especially from the perspective of DNA methylation.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85009471362&origin=inward; http://dx.doi.org/10.1007/s12035-016-0357-6; http://www.ncbi.nlm.nih.gov/pubmed/28092081; http://link.springer.com/10.1007/s12035-016-0357-6; https://dx.doi.org/10.1007/s12035-016-0357-6; https://link.springer.com/article/10.1007/s12035-016-0357-6
Springer Science and Business Media LLC
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