Comparative logic of cellular state transitions across neuroimmune disorders.
| Disorder | Primary initiating context | Dominant state-transition pattern | Shared principle | Boundary of interpretation |
|---|---|---|---|---|
| Alzheimer’s disease | Chronic protein aggregation and age-associated tissue stress | Plaque-associated microglial and astrocyte remodeling, metabolic adaptation, synaptic disruption [139, 228] | Chronic glial state transitions can reshape the local degenerative niche | Plaque-associated states may not generalize directly to acute injury or autoimmune disease |
| Multiple sclerosis | Autoimmune infiltration and demyelination | Infiltrating immune-cell activation, microglia/macrophage activation, astrocyte remodeling, remyelination failure or repair [214, 229] | Peripheral immune entry can reorganize resident glial states and lesion evolution | MS lesions differ by stage, region, and inflammatory activity; not all glial activation is damaging |
| Stroke | Acute ischemia, hypoxia, and tissue necrosis | Rapid microglial activation, peripheral immune recruitment, vascular disruption, later repair/remodeling states [230, 231] | Timing determines whether inflammatory states support clearance or amplify injury | Acute ischemic responses should not be directly equated with chronic neurodegeneration |
| Traumatic brain injury | Mechanical injury, barrier disruption, and secondary inflammatory cascades | Early damage sensing, glial activation, immune-cell recruitment, persistent astrocyte/microglial changes in some cases [227, 232] | Acute injury can transition into chronic neuroimmune remodeling | TBI is heterogeneous; focal, diffuse, mild, and severe injury may produce different state trajectories |
MMN: Conceptualization, Methodology, Investigation, Resources, Data curation, Formal analysis, Visualization, Writing—original draft, Writing—review & editing. The author read and approved the submitted version.
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