From:  Cellular state transitions in neuroimmune disorders

 Comparative logic of cellular state transitions across neuroimmune disorders.

DisorderPrimary initiating contextDominant state-transition patternShared principleBoundary of interpretation
Alzheimer’s diseaseChronic protein aggregation and age-associated tissue stressPlaque-associated microglial and astrocyte remodeling, metabolic adaptation, synaptic disruption [139, 228]Chronic glial state transitions can reshape the local degenerative nichePlaque-associated states may not generalize directly to acute injury or autoimmune disease
Multiple sclerosisAutoimmune infiltration and demyelinationInfiltrating immune-cell activation, microglia/macrophage activation, astrocyte remodeling, remyelination failure or repair [214, 229]Peripheral immune entry can reorganize resident glial states and lesion evolutionMS lesions differ by stage, region, and inflammatory activity; not all glial activation is damaging
StrokeAcute ischemia, hypoxia, and tissue necrosisRapid microglial activation, peripheral immune recruitment, vascular disruption, later repair/remodeling states [230, 231]Timing determines whether inflammatory states support clearance or amplify injuryAcute ischemic responses should not be directly equated with chronic neurodegeneration
Traumatic brain injuryMechanical injury, barrier disruption, and secondary inflammatory cascadesEarly damage sensing, glial activation, immune-cell recruitment, persistent astrocyte/microglial changes in some cases [227, 232]Acute injury can transition into chronic neuroimmune remodelingTBI is heterogeneous; focal, diffuse, mild, and severe injury may produce different state trajectories