Ageing research reviewsSep 5, 2026

Contacts Between Cell Energy and Protein Factories May Influence Aging of Brain Immune Cells in Alzheimer's Disease

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Sep 6, 2026

Abstract

Microglial senescence may link biological aging to Alzheimer's disease pathology.

Senescent microglia experience permanent cell-cycle arrest and upregulate specific markers associated with aging.
These microglia secrete a pro-inflammatory profile that contributes to chronic neuroinflammation.
Mitochondria-endoplasmic reticulum contact sites (MERCS) are crucial for various cellular functions, including calcium management and response to stress.
The role of MERCS dysfunction in driving microglial senescence in living organisms is not yet fully understood.

Simplified

Alzheimer's disease (AD) is an age-dependent neurodegenerative syndrome in which microglial senescence bridges biological ageing and Aβ-tau pathology. Senescent microglia undergo permanent cell-cycle arrest, upregulate p16^INK4a and SA-β-gal, and secrete a pro-inflammatory senescence-associated secretory phenotype (SASP) that sustains chronic neuroinflammation. Mitochondria-endoplasmic reticulum contact sites (MERCS) are dynamic physical junctions between the endoplasmic reticulum (ER) and mitochondria, whereas mitochondria-associated membranes (MAM) are biochemically enriched ER subdomains located at MERCS. MERCS coordinate calcium shuttling, mitochondrial dynamics, lipid trafficking and the unfolded protein response (UPR); however, whether their dysfunction drives microglial senescence in vivo remains largely untested.

Full Text

Full text is available at the source.

View Full Text ↗

Contacts Between Cell Energy and Protein Factories May Influence Aging of Brain Immune Cells in Alzheimer's Disease

Abstract

Full Text

You found one interesting study. We’ll send the next 7.

What Lands in Your Inbox Each Week:

Recent issues from the longevity & aging brief