Title : Amyloid β oligomers suppress excitatory transmitter release via presynaptic depletion of phosphatidylinositol-4,5-bisphosphate.

Pub. Date : 2019 Mar 13

PMID : 30867420






5 Functional Relationships(s)
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1 This Abeta-induced suppression of Pr is mainly due to an mGluR5-mediated depletion of phosphatidylinositol-4,5-bisphosphate (PIP2) in axons. Phosphatidylinositol 4,5-Diphosphate amyloid beta (A4) precursor protein Mus musculus
2 This Abeta-induced suppression of Pr is mainly due to an mGluR5-mediated depletion of phosphatidylinositol-4,5-bisphosphate (PIP2) in axons. Phosphatidylinositol 4,5-Diphosphate amyloid beta (A4) precursor protein Mus musculus
3 Selectively inhibiting Abeta-induced PIP2 hydrolysis in the CA3 region of the hippocampus strongly prevents oligomeric Abeta-induced suppression of Pr at the SC-CA1 synapse and rescues synaptic and spatial learning and memory deficits in APP/PS1 mice. Phosphatidylinositol 4,5-Diphosphate amyloid beta (A4) precursor protein Mus musculus
4 Selectively inhibiting Abeta-induced PIP2 hydrolysis in the CA3 region of the hippocampus strongly prevents oligomeric Abeta-induced suppression of Pr at the SC-CA1 synapse and rescues synaptic and spatial learning and memory deficits in APP/PS1 mice. Phosphatidylinositol 4,5-Diphosphate amyloid beta (A4) precursor protein Mus musculus
5 These results first reveal the presynaptic mGluR5-PIP2 pathway whereby oligomeric Abeta induces early synaptic deficits in AD. Phosphatidylinositol 4,5-Diphosphate amyloid beta (A4) precursor protein Mus musculus