Abstract Spatial Protein Quality Control (sPQC) sequesters misfolded proteins into specific, organelle-associated inclusions within the cell to control their toxicity. To approach the role of
Abstract Early and progressive cortico-striatal circuit alterations have been widely characterized in Huntington’s disease (HD) patients. Cortical premotor area, M2 cortex in rodents, is the
Summary Background Valbenazine is a highly selective vesicular monoamine transporter 2 (VMAT2) inhibitor approved for treatment of tardive dyskinesia. To address the ongoing need for
Abstract Huntington’s disease is a neurodegenerative disorder caused by a CAG expansion in the first exon of the HTT gene, resulting in an extended polyglutamine (poly-Q) tract
Abstract Huntington’s disease (HD) is a neurodegenerative disorder caused by poly-Q expansion in the Huntingtin (HTT) protein. Here, we delineate elevated mutant HTT (mHTT) levels
In the mid-1950s, Sam Clark Jr. of the School of Medicine at Washington University in St. Louis looked through his electron microscope at newborn-mouse kidneys
Armed with a modified version of CRISPR-Cas9, scientists have removed nucleotide repeats from RNA in vitro that are known to cause diseases, namely, Huntington’s, ALS,
Journal of Cell Biology, July 18, 2011 DOI: 10.1083/jcb.201105010. Ju, T.-C., et al. “Nuclear translocation of AMPK-α1 potentiates striatal neurodegeneration in Huntington’s disease.” A new
Journal of Cell Biology, July 18, 2011 DOI: 10.1083/jcb.201105010. Ju, T.-C., et al. “Nuclear translocation of AMPK-α1 potentiates striatal neurodegeneration in Huntington’s disease.” A new
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