Gap Debate: Aging Mouse Brain v3

0.790

CGAS, STING1

Age-related activation of the cGAS-STING pathway drives microglial senescence and neuroinflammation, creating a feed-forward loop of neurodegeneration vulnerability. Selective cGAS-STING inhibitors co

0.703

CXCL10

Aging-specific white matter vulnerability involves microglial CXCL10 production driving CD8+ T cell recruitment and oligodendrocyte damage. Targeted inhibition of CXCL10 signaling or enhancement of ol

0.625

Mitochondrial respiratory complexes and inflammatory cytokine receptors

Age-related cytokine secretion specifically suppresses neuronal mitochondrial metabolism, creating vulnerability to energy stress. Targeted modulation of this cytokine-mitochondria axis through select

0.539

TNFRSF25

Brain-derived exosomes from aged mice accelerate cognitive decline through neuronal TNFRSF25 activation. Blocking this age-related exosome-receptor pathway could prevent the propagation of aging-relat

0.532

AP1S1

Age-related downregulation of AP1S1 (adaptor protein complex 1 sigma 1) disrupts clathrin-mediated vesicular transport, creating vulnerability to amyloid-β and oxidative stress. Therapeutic restoratio

0.528

Cell-type specific vulnerability markers

Aging creates differential neuronal vulnerability patterns based on network connectivity and metabolic demands. Therapeutic approaches targeting the most vulnerable neuronal populations (such as choli

0.452

PFN1

Age-related decline in microglial profilin-1 disrupts cytoskeletal checkpoints that prevent senescence and synaptic decline. Therapeutic enhancement of PFN1 expression or function could maintain micro