title: Huntington's Disease: Nuclear Gatekeepers Under Attack.
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.
authors.affiliation: 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.
authors.forename: Matthew B
authors.initials: MB
authors.lastname: Veldman
authors.affiliation: 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.
authors.forename: X William
authors.initials: XW
authors.lastname: Yang
mesh_terms: D000375:Aging; D001921:Brain; D006801:Humans; D006816:Huntington Disease; D009474:Neurons; D009687:Nuclear Proteins
chemical_list: D009687:Nuclear Proteins
keywords: Huntington’s disease; aging; neurodegeneration; nucleocytoplasmic transport