A Neuroinflammatory Crosstalk Between Alzheimer's Disease And Alzheimer's Disease-Associated Epilepsy

Alzheimer’s Disease (AD) and epilepsy are common comorbidities. This study investigated how disease origin influences seizure impact using familial AD (fAD; 5xFAD mice) and sporadic AD (sAD; Intracerebroventricular-streptozotocin (STZ) rats) models. In the fAD model, status epilepticus induced spontaneous seizures but did not significantly alter cognitive performance, amyloid burden, or neuroinflammation compared to controls. Conversely, in the sAD model, STZ and seizures independently impaired spatial memory and triggered region-specific neuroinflammation, particularly within the hippocampal CA2 subfield. Study concludes that seizure impact is profoundly dictated by underlying AD etiology, necessitating origin-specific therapeutic approaches and monitoring to address these parallel neurological trajectories.