Therapeutic strategies targeting cellular state transitions in neurological disease.
| Therapeutic strategy | Molecular target | Target cell population | Mechanism of action | Disease context |
|---|---|---|---|---|
| Complement pathway inhibition | Complement proteins C1q, C3 | Microglia, synapse-associated immune signaling pathways | Reduces complement-mediated synaptic pruning and inflammatory activation | Alzheimer’s disease, multiple sclerosis [241, 242] |
| Immune checkpoint modulation | PD-1/PD-L1 signaling axis | T lymphocytes, microglia | Modulates immune activation and inflammatory signaling by regulating immune checkpoint pathways | Stroke, neuroinflammatory disorders [243, 244] |
| Triggering receptor expressed on myeloid cells 2 (TREM2) modulation | TREM2 | Microglia | Enhances microglial metabolic activity, phagocytosis, and responses to neurodegenerative pathology | Alzheimer’s disease and related neurodegenerative diseases [245, 246] |
| Colony-stimulating factor 1 receptor (CSF1R) inhibition | CSF1R | Microglia | Alters microglial survival and proliferation, thereby modulating microglial population dynamics and inflammatory responses | Neurodegenerative disease models, neuroinflammation [247, 248] |
| Cytokine pathway inhibition | IL-6, TNF, interferon signaling pathways | Microglia, astrocytes, immune cells | Reduces inflammatory signaling and downstream neuroimmune activation | Stroke, neuroinflammatory disorders [249, 250] |
MMN: Conceptualization, Methodology, Investigation, Resources, Data curation, Formal analysis, Visualization, Writing—original draft, Writing—review & editing. The author read and approved the submitted version.
The author declares no conflicts of interest.
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