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Targeting PTEN interactions for Alzheimer's disease

Depression of AMPA receptor–mediated synaptic currents and impairment of long-term potentiation, triggered by amyloid-β, are the hallmarks of Alzheimer's pathophysiology. These dysfunctions are now linked to upregulated PDZ domain–dependent PTEN translocation to spines, contributing to cognitive deficits in model mice.

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Figure 1: A proposed model for AD-related synaptic dysfunctions mediated by PIP3-Akt signaling at hippocampal neurons.

Katie Vicari/Nature Publishing Group


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Correspondence to Samuel Frere or Inna Slutsky.

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Frere, S., Slutsky, I. Targeting PTEN interactions for Alzheimer's disease. Nat Neurosci 19, 416–418 (2016).

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