A perfect storm: Converging paths of epilepsy and Alzheimer's dementia intersect in the hippocampal formation.

摘要: Seizures in the human temporal lobe transiently impair cognition and steadily damage hippocampal circuitry, leading to progressive memory loss. Similarly, toxic accumulation of Aβ peptides underlying Alzheimer's disease (AD) triggers synaptic degeneration, circuit remodeling, abnormal synchronization within same networks. Because neuronal hyperexcitability amplifies release Aβ, seizures create a vicious spiral that accelerates cell death cognitive decline AD brain. The confluence excitotoxicity, combined with challenge seizure detection hippocampus, make epilepsy these individuals extremely important correctly diagnose treat. Emerging clinical evidence reveals an elevated comorbidity AD, particularly when linked mutations APP/Aβ gene pathway. Experimental models genetically engineered mice confirm extend findings, highlighting presence subclinical overlapping pathophysiologic cascades. There is urgent need for more basic investigation improve early recognition arising during course dementing disorders, validate molecular blockers Aβ-induced aberrant excitability can slow potentially reverse progression decline.