Research Paper Volume 13, Issue 16 pp 20716—20737
N6-methyladenosine (m6A) modification and its clinical relevance in cognitive dysfunctions
- 1 Department of Neurology, Shanghai Changhai Hospital, The Second Military Medical University, Shanghai, PR China
- 2 Department of Psychiatry, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada
- 3 Faculty of Basic Medical Sciences, The Second Military Medical University, Shanghai, PR China
- 4 Department of Biochemistry and Cell Biology, Geisel School of Medicine, Dartmouth College, Hanover, NH 03755, USA
- 5 Department of Oral and Maxillofacial-Head Neck Oncology, Shanghai Ninth People’s Hospital College of Stomatology, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China
Received: March 18, 2021 Accepted: August 2, 2021 Published: August 30, 2021https://doi.org/10.18632/aging.203457
How to Cite
Copyright: © 2021 Du et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: N6 adenosine methylation (m6A) is the most abundant internal RNA modification in eukaryotic cells. Dysregulation of m6A has been associated with the perturbations of cell proliferation and cell death in different diseases. However, the roles of m6A in the neurodegenerative process and cognitive dysfunction are unclear.
Methods: We systematically investigated the molecular alterations of m6A regulators and their clinical relevance with cognitive dysfunctions using published datasets of Alzheimer's Disease (AD), vascular dementia, and mild cognitive impairment (MCI).
Findings: The expressions of m6A regulators vary in different tissues and closely correlate with neurodegenerative pathways. We identified co-expressive m6A regulators SNRPG and SNRPD2 as potential biomarkers to predict transformation from MCI to AD. Moreover, we explored correlations between Apolipoprotein E4 and m6A methylations.
Interpretation: Collectively, these findings suggest that m6A methylations as potential biomarkers and therapeutic targets for cognitive dysfunction.
Funding: This work was supported by the National Natural Science Foundation of China (81871040) and the Shanghai Health System Talent Training Program (2018BR29).