Topic: network hyperexcitability

During early stages of Alzheimer’s disease (AD) gradual accumulation and aggregation of Aβ oligomers (AβO) occurs prior to cognitive decline. This preclinical stage of AD is further characterized by synaptic dysfunction and network hyperexcitability. We recently discovered that 24-hour treatment of AβO​​​​​ to hippocampal slices impairs release at GABAergic synapses, most prominently at dendritic inhibitory synapses. This suggests that inhibitory synapses are particularly vulnerable to AβO toxicity.We currently use advanced imaging approaches in vitro to further investigate the mechanisms that

Network hyperexcitability in Alzheimer’s Disease (AD) is claimed to be an important and potentially treatable pathophysiological mechanism. Empirical and modeling studies suggest that functional connectivity (FC) are promising quantitative neurophysiological markers for network hyperexcitability. This study examines how robust FC measures differ between AD patients with and without interictal epileptiform discharges (IEDs). We obtained eyes closed source-level magnetoencephalography recordings from demographically matched biomarker confirmed AD patients in the mild cognitive impairment and dem