| Glutamate receptor overactivation | Excessive stimulation of NMDA and AMPA receptors leads to calcium influx |
| Intracellular calcium dysregulation | Activates enzymatic degradation of cellular components |
| Mitochondrial dysfunction | Impaired energy production and release of pro-apoptotic factors |
| Oxidative stress | Generation of reactive oxygen species damaging cellular components |
| Inhibitory neuron loss | Specific populations of GABAergic interneurons are selectively vulnerable |
| Reduced GABA synthesis | Decreased glutamic acid decarboxylase (GAD) activity |
| Impaired receptor function | Altered GABA-A receptor subunit composition |
| Microglial activation | Persistent elevation of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) |
| Astrocytic dysfunction | Impaired potassium buffering and glutamate uptake |
| Blood-brain barrier disruption | Allows peripheral immune cell infiltration |
| Entorhinal cortex dysfunction | Primary gateway for hippocampal input/output |
| Databases | OMIMOrphanetClinicalTrialsPubMed |