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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Frere, S., Slutsky, I. Targeting PTEN interactions for Alzheimer's disease. Nat Neurosci 19, 416–418 (2016). https://doi.org/10.1038/nn.4248
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DOI: https://doi.org/10.1038/nn.4248
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