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N6-methyladenosine (m6A) modification and its clinical relevance in cognitive dysfunctions

Bingying Du1, Yanbo Zhang2, Meng Liang1

  • 1Department of Neurology, Shanghai Changhai Hospital, The Second Military Medical University, Shanghai, PR China.

Aging
|August 30, 2021
PubMed
Abstract

Insights

N6 adenosine methylation (m6A) is crucial in cell regulation. This study identifies m6A regulators as potential biomarkers for predicting cognitive decline and Alzheimer's disease progression.

Area of Science:

  • Epigenetics and Molecular Biology
  • Neuroscience
  • Biomarker Discovery

Background:

  • N6 adenosine methylation (m6A) is the most prevalent internal RNA modification in eukaryotes.
  • m6A dysregulation is linked to cell proliferation and death, but its role in neurodegeneration and cognitive dysfunction remains unclear.

Purpose of the Study:

  • To investigate molecular alterations of m6A regulators in neurodegenerative diseases.
  • To assess the clinical relevance of m6A regulators in cognitive dysfunction, including Alzheimer's Disease (AD), vascular dementia, and mild cognitive impairment (MCI).

Main Methods:

  • Systematic investigation of m6A regulators using published datasets.
  • Analysis of gene expression data from AD, vascular dementia, and MCI cohorts.
  • Exploration of correlations between Apolipoprotein E4 and m6A methylations.

Main Results:

  • m6A regulator expression varies across tissues and correlates with neurodegenerative pathways.
  • SNRPG and SNRPD2 identified as co-expressive m6A regulators.
  • Potential biomarkers for predicting MCI to AD transformation and links to Apolipoprotein E4 established.

Conclusions:

  • m6A methylations show promise as biomarkers for cognitive dysfunction.
  • m6A regulators represent potential therapeutic targets for neurodegenerative diseases and cognitive impairment.
Keywords:
KEGG pathwaysWGCNAapolipoprotein Ecognitive impairmentm6A regulator

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