Genetic deletion of Pyk2 prevents amyloid-beta oligomer-induced hippocampal neuronal hyperactivity and synaptic loss while decreasing Tau synaptic localization in the mouse hippocampus.
Postsynaptic clustering and activation of Pyk2 by PSD-95
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Pyk2 plays a critical role in synaptic dysfunction during the early stages of Alzheimer's disease
Genetic deletion of Pyk2 prevents amyloid-beta oligomer-induced hippocampal neuronal hyperactivity and synaptic loss while decreasing Tau synaptic localization in the mouse hippocampus.