Network dysfunction and cognitive deficits in a mouse model of Alzheimer's disease

TL;DRAbstract

Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline and severe impairments of memory, especially memory dependent on the hippocampus. It is becoming increasingly clear that network dysfunction, manifested as seizures and epileptiform activity, is not only prevalent in the hippocampus and other brain regions of AD patients and mouse models, but that it directly contributes to hippocampus-dependent cognitive deficits. However, the precise mechanisms governing how this epileptiform activity arises, develops, and contributes to cognitive deficits in AD remains unknown. This dissertation addresses these questions by studying molecular, physiological, and behavioral abnormalities in a well-characterized mouse model of AD (henceforth referred to as APP mice). One alteration observed in AD that is hypothesized to contribute to the generation of network dysfunction is reduced expression of functional Nav1.1&agr;, a voltage-gated sodium channel.

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