Topic: APLP2

The full-length amyloid precursor protein (APP), a key player in Alzheimer’s disease (AD), is ubiquitously expressed in a large majority of neurons, including GABAergic interneurons (INTs). Recent studies showed evidence of disrupted hippocampal plasticity in conditional APP KO of GABAergic forebrain neurons (Mehr et al, 2020). However, the physiological functions of APP at inhibitory synapses remain to be defined. We to study the role of APP at inhibitory synapses onto CA3 pyramidal cells (PCs) as well as on the overall inhibitory balance within the CA3 network. We combine slice electrophysio

The full-length amyloid precursor protein (APP), a key player in Alzheimer’s disease (AD), is ubiquitously expressed throughout the brain. It is known to be abundantly expressed in presynaptic compartments where it interacts with proteins of the presynaptic release machinery. However, the physiological functions of APP in the CNS still remain to be investigated. Here we study the physiological role of APP in presynaptic plasticity and information transfer within the hippocampus. We deleted APP and the related protein APLP2 in dentate gyrus granular cells (GCs) using a viral gene transfer strat