Amyloid β precursor protein regulates neuron survival and maturation in the adult mouse brain.

摘要: The amyloid-β precursor protein (APP) is a transmembrane that widely expressed within the central nervous system (CNS). While pathogenic dysfunction of this has been extensively studied in context Alzheimer's disease, its normal function poorly understood, and reports have often appeared contradictory. In study we examined role APP regulating neurogenesis adult mouse brain by comparing neural stem cell proliferation, as well new neuron number morphology between knockout mice C57bl6 controls. Short-term EdU administration revealed proliferating EdU+ progenitor cells PSA-NCAM+ neuroblasts produced SVZ dentate gyrus were not affected life-long absence APP. However, labelling newborn with then following their fate over-time, determined ~48% more newly generated NeuN+ neurons accumulated granule layer olfactory bulb ~57% young relative to Furthermore, proportionally fewer adult-born calretinin+. To determine whether was having an effect on neuronal maturation, administered tamoxifen Nestin-CreERT2::Rosa26-YFP Nestin-CreERT2::Rosa26-YFP::APP-knockout mice, fluorescently ~80% (EdU+) formed P75 P105. Our analysis added hippocampus shorter dendritic arbors only half branch points those mice. We conclude reduces survival hippocampus, but it does influence all subtypes equally. Additionally, influences acting robust regulator extension arborisation.