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We previously reported that pathophysiological concentrations of amyloid β protein (Aβ25–35, 0.1–10nM) directly inhibited type II phosphatidylinositol 4-kinase (PI4KII) activity in neuronal plasma membranes, which resulted in the enhanced glutamate neurotoxicity. In the present study, we examined the effects of Aβ fragments, Aβ20–29 and Aβ31–35, on the 10nM Aβ25–35- or Aβ1–42-induced inhibition of...
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