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Targeting PTEN interactions for Alzheimer's disease

Nature Neuroscience volume 19, pages 416–418 (2016)Cite this article

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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.

Phosphatase and tensin homolog located on chromosome 10 (PTEN) is a lipid and protein phosphatase that was originally characterized as a tumor suppressor. Eventually, it became clear that PTEN regulates a diverse range of functions in the CNS. Today we know that deregulation of PTEN affects neurogenesis, neurite outgrowth, synaptogenesis, synaptic transmission and plasticity1. Human PTEN mutations or conditional deletions of Pten in mice have provided insights into pathogenesis of various neurological disorders, such as macrocephaly, ataxia, seizures, autism and mental retardation1.

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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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Authors and Affiliations

  1. Samuel Frere and Inna Slutsky are in the Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel,

    Samuel Frere & Inna Slutsky

  2. Inna Slutsky is at the Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel.,

    Inna Slutsky

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  1. Samuel Frere
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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). https://doi.org/10.1038/nn.4248

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