Alzheimer's disease (AD) is the most frequent global cause of severe cognitive impairment. Epilepsy, characterised by repetitive unprovoked seizures, is more prevalent in AD patients than in healthy controls.

We hypothesise that subclinical epileptic phenomena occur in a considerable part of AD patients which aggravates cognitive decline. We therefore propose an intervention with antiseizure drugs early in the disease course as a possible disease modifying therapy. We will test this hypothesis in well-established transgenic AD mouse models.

First, we will investigate the onset and frequency of epileptiform discharges in AD mice and how cognitive performance in memory tasks is influenced. Next, AD mice will be
chronically treated with a clinically used antiseizure drug levetiracetam or with a ghrelin receptor agonist in development. Ghrelin is an endogenous mediator, mainly involved in metabolism. Research has indicated that ghrelin inhibits cognitive deficits in AD and reduces seizures in epilepsy mouse models. We will assess the effect of both treatments on epileptiform biomarkers, cognitive performance and various markers indicative of AD progression.
Effective start/end date1/10/1830/09/22

    Flemish discipline codes

  • Biomedical modelling

    Research areas

  • Alzheimer

ID: 38838647