In ALS, TBK1 loss-of-function traps microglia in a senescence-like, SASP-producing state that drives neurodegeneration. By analogy, partial TBK1 insufficiency in AD microglia may similarly lock cells into an aged, pro-inflammatory transcriptional program, shifting them from a protective amyloid-clearance phenotype toward a destructive,tau-propagating one. This predicts that microglial TBK1 activity inversely correlates with AD severity, and that restoring TBK1 signaling attenuates neuroinflammat
Radar Chart — 10 Dimensions
Score Comparison Bars
Mechanistic
0.60
Evidence
0.55
Novelty
0.75
Feasibility
0.00
Impact
0.00
Druggability
0.00
Safety
0.00
Competition
0.00
Data
0.00
Reproducible
0.00
KG Connect
0.50
Score Breakdown
Dimension
TBK1 Insufficiency in Alzheime
Mechanistic
0.600
Evidence
0.550
Novelty
0.750
Feasibility
0.000
Impact
0.000
Druggability
0.000
Safety
0.000
Competition
0.000
Data
0.000
Reproducible
0.000
KG Connect
0.500
Evidence
TBK1 Insufficiency in Alzheimer Microglia Drives a Senescenc