Genetic deletion of Pyk2 prevents amyloid-beta oligomer-induced hippocampal neuronal hyperactivity and synaptic loss while decreasing Tau synaptic localization in the mouse hippocampus.
Functional screening of Alzheimer risk loci identifies PTK2B as an in vivo modulator and early marker of Tau pathology
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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.