Aging-related dysregulation of energy metabolism and mitochondrial dynamics in microglia.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic concepts without primary human data or systematic review methodology
PubMed 40510394 · doi:10.3164/jcbn.24-202
What was done
This narrative review synthesized recent findings on microglial energy metabolism, mitochondrial dysfunction, metabolic shifting toward glycolysis, mitochondrial DNA leakage, and potential metabolic therapeutic targets in aging and neurodegenerative diseases such as Alzheimer's disease.
What was found
The abstract reports no numerical data or quantitative effect sizes. It describes that aging and neurodegenerative diseases involve impaired mitochondrial function, mitochondrial DNA leakage into the cytoplasm, and a shift from oxidative phosphorylation to glycolysis that sustains microglial activation and neuroinflammation.
Why it matters
It outlines how targeting microglial metabolic pathways or mitochondrial quality control (such as mitophagy) could serve as therapeutic strategies against age-related neurodegeneration.
Limits
This is a narrative review with no systematic search methodology, meta-analytic data, or new primary experimental findings presented in the abstract. Clinical applicability and specific effect magnitudes are not documented.
Cited by
- supports As ATP demand on a cell increases, aging and disease lead to an earlier shift from oxidative phosphorylation to glycolysis.