Huntington's Disease: Nuclear Gatekeepers Under Attack

Matthew B Veldman; X William Yang

doi:10.1016/j.neuron.2017.03.032

Huntington's Disease: Nuclear Gatekeepers Under Attack

Neuron. 2017 Apr 5;94(1):1-4. doi: 10.1016/j.neuron.2017.03.032.

Authors

Matthew B Veldman¹, X William Yang²

Affiliations

¹ Center for Neurobehavioral Genetics and Semel Institute for Neuroscience & Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
² Center for Neurobehavioral Genetics and Semel Institute for Neuroscience & Human Behavior, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA; Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA. Electronic address: xwyang@mednet.ucla.edu.

PMID: 28384467
DOI: 10.1016/j.neuron.2017.03.032

Abstract

In this issue of Neuron, Gasset-Rosa et al. (2017) and Grima et al. (2017) describe defects in the nuclear pore complex and impaired nucleocytoplasmic transport in Huntington's disease (HD). The findings suggest that erosion of nuclear gatekeeping function, which is found in normal brain aging, may play an important role in the pathogenesis of multiple neurodegenerative disorders, including HD.

Keywords: Huntington’s disease; aging; neurodegeneration; nucleocytoplasmic transport.

MeSH terms

Aging
Brain*
Humans
Huntington Disease*
Neurons
Nuclear Proteins

Substances

Nuclear Proteins