Description

Alzheimer's disease (AD) is the most frequent global cause of severe cognitive impairment. Epileptic seizures have always been thought to be a late complication in a minority of AD patients. We hypothesise that subclinical epileptic phenomena do however occur in a considerable part of AD patients much earlier in the disease course which aggravates cognitive decline. We will test this hypothesis in a prospective, longitudinal observational clinical study. Moreover, we will investigate the onset and frequency of epileptiform discharges in well-established transgenic AD mouse models and how their cognitive performance in memory tasks is influenced.
Next we propose an early intervention with antiseizure drugs as a possible disease modifying therapy. To this end, AD mice will be chronically treated with a clinically used antiseizure drug levetiracetam or with a ghrelin receptor agonist in development. Levetiracetam was previously shown to exhibit antiepileptogenic properties, while ghrelin receptor agonism inhibits cognitive deficits in AD models 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. If successful, we could set up future clinical investigations with chronic treatment of levetiracetam in patients with mild cognitive impairment due to AD.
AcronymFWOAL927
StatusActive
Effective start/end date1/01/1931/12/22

    Research areas

  • Alzheimer

    Flemish discipline codes

  • Neurological and neuromuscular diseases

ID: 44199319