Adipose tissue as a systemic modulator of brain aging: mechanistic links between metabolism, inflammation and neurodegeneration.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic, preclinical, and epidemiological literature with no primary data.
PubMed 42229697 · doi:10.1016/j.brainres.2026.150414
What was done
This narrative review synthesized epidemiological, neuroimaging, translational, and molecular evidence evaluating how adipose tissue functions as a systemic endocrine and immune regulator of central nervous system aging, cerebrovascular integrity, and neurodegenerative risk across different fat depots.
What was found
The abstract reports no numerical data. Qualitatively, it reports that visceral adipose tissue expansion and inflammatory remodeling promote chronic low-grade inflammation, impaired insulin signaling, adipokine dysregulation, and senescence-associated secretory activity that lead to microglial dysfunction, blood-brain barrier disruption, and synaptic vulnerability. It also identifies extracellular vesicles and microRNAs as direct molecular mediators, while noting preserved subcutaneous and thermogenic depots support metabolic homeostasis and neurotrophic signaling.
Why it matters
It emphasizes that brain aging is modulated by peripheral metabolic organs, highlighting adipose tissue dysfunction and depot-specific biology as modifiable therapeutic targets for neurodegenerative disease.
Limits
As a narrative review, it presents no original clinical or experimental data and does not follow a systematic search protocol. Most mechanistic pathways described rely on preclinical models, while human associations between adipose distribution and cognitive decline are observational and subject to confounding.
Cited by
- supports Abdominal fat cells produce inflammatory adipocytokines that cross into or affect the brain.