What molecular mechanisms drive the transition from acute to persistent neuroinflammation in pediatric TBI?
Analysis ID: SDA-2026-04-15-gap-pubmed-20260411-075425-2feffb0c | Domain: neuroinflammation | Status: failed | Created: 2026-04-15T04:23:20.656737
Knowledge Graph: 2 edges — View JSON
Top Hypotheses (2 total)
#1 STING Antagonism Prevents Acute-to-Chronic Neuroinflammation Transition via Interruption of IFN-I Feedback Looping
0.605
TMEM173 (STING)
The transition from acute to persistent neuroinflammation is driven by mitochondrial DNA leakage activating the cGAS-STING pathway, which establishes a chronic type I interferon (IFN-I) response signa
#2 Timed Senolytic Therapy Eliminates p16^Ink4a/p21^Cip1-Senescent Microglia to Prevent SASP-Driven Complement Cascade Amplification
0.587
CDKN2A (p16^Ink4a), CDKN1A (p21^Cip1/Waf1)
Senescent microglia expressing p16^Ink4a and p21^Cip1/Waf1 constitute the cellular substrate driving persistent neuroinflammation months after pediatric TBI. These cells secrete SASP factors including