beta-amyloid triggers neuronal hyper-activation and results in Alzheimer's-related epilepsy

What is it about?

In this study we showed, for the first time, that the ApDE9/PS1 mouse model of Alzheimer’s Disease exhibits progressive epilepsy, and that this epilepsy is underlain by cortical and dentage gyrus principal cells being hyperexcitable (depolarized). We also showed that increased levels of the pathogenic peptide Amyloid beta is responsible for the hyperexcitability, as acute application of fibrillar Aβ in wild-type brain slices resulted in similar effects. Our results indicated that epilepsy and its underlying neuronal hyperexcitability are early pathological changes in AD, preceding any cognitive changes.

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