Altered mitochondrial microenvironment at the spotlight of musculoskeletal aging and Alzheimer's disease

Panagiotis Giannos1,2, Konstantinos Prokopidis3,4, Stuart M Raleigh5

  • 1Society of Meta-research and Biomedical Innovation, London, UK. panagiotis.giannos19@imperial.ac.uk.

Scientific Reports
|July 5, 2022
PubMed

Insights

This study identifies five mitochondrial genes in skeletal muscle that are dysregulated in both aging and Alzheimer's disease (AD). These genes may serve as early biomarkers for AD risk in aging individuals.

Area of Science:

  • Mitochondrial biology
  • Neuroscience
  • Gerontology

Background:

  • Alzheimer's disease (AD) onset is increasingly linked to musculoskeletal aging.
  • This connection is mediated by muscle-brain crosstalk involving mitochondrial microenvironment dysregulation.

Purpose of the Study:

  • To identify gene biomarkers in skeletal muscle associated with both aging and AD.
  • To investigate the protein interactome of these potential biomarkers.

Main Methods:

  • Analysis of 12 microarray datasets from musculoskeletal aging and AD studies.
  • Construction of protein-protein interaction networks for differentially expressed genes (DEGs).
  • Identification of overlapping hub genes using 11 topological algorithms.

Main Results:

  • Five mitochondrial microenvironment genes (NDUFAB1, UQCRC1, UQCRFS1, NDUFS3, MRPL15) showed overlapping dysregulated expression in both aging and AD networks.
  • These genes were identified as potential hub genes.

Conclusions:

  • The identified genes may serve as potential biomarkers for Alzheimer's disease occurrence in the context of musculoskeletal aging.
  • Further human studies are needed to confirm their functional role and prognostic value in aging populations with sarcopenia and AD.

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