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Huntington's disease: easing the NMDAR traffic jam

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Excitatory neurotransmission through NMDA receptors (NMDARs) has a pivotal role in healthy brain function, and its dysfunction has long been implicated in the pathogenesis of neurodegenerative disorders, including Huntington's disease. A new study uncovers a molecular link between mutant huntingtin and aberrant trafficking of an unconventional NDMAR subunit (GluN3A). Targeting this disease mechanism in a Huntington's disease mouse model had multiple therapeutic benefits (pages 1030–1038).

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Figure 1: Aberrant mHtt interaction with PACSIN1 impairs endocytosis of the NMDAR subunit GluN3A at synapses in Huntington's disease.

Marina Corral Spence

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Authors and Affiliations

  1. Department of Psychiatry & Biobehavioral Sciences, Anthony Daggett and X. William Yang are at the Center for Neurobehavioral Genetics, Semel Institute for Neuroscience & Human Behavior, David Geffen School of Medicine, University of California–Los Angeles, Los Angeles, California, USA.,

    Anthony Daggett & X William Yang

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  1. Anthony Daggett
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  2. X William Yang
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Correspondence to X William Yang.

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The authors declare no competing financial interests.

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Daggett, A., Yang, X. Huntington's disease: easing the NMDAR traffic jam. Nat Med 19, 971–973 (2013). https://doi.org/10.1038/nm.3283

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