title: It's not necessarily all about the delivery in Huntington's disease.
abstract: Existing models of Huntington's disease posit that deficits in BDNF delivery to the striatum contribute to atrophy and motor impairment. In this issue of Neuron, Plotkin et al. (2014) show that BDNF delivery is normal but downstream signaling via TrkB and p75 is impaired, leading to corticostriatal synaptic dysfunction.
authors.affiliation: Department of Psychiatry, Brain Research Centre and Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, BC V6T 1Z3, Canada.
authors.forename: Matthew P
authors.initials: MP
authors.lastname: Parsons
authors.affiliation: Department of Psychiatry, Brain Research Centre and Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, BC V6T 1Z3, Canada; Department of Medicine, Brain Research Centre and Djavad Mowafaghian Centre for Brain Health, University of British Columbia, Vancouver, BC V6T 1Z3, Canada. Electronic address: lynn.raymond@ubc.ca.
authors.forename: Lynn A
authors.initials: LA
authors.lastname: Raymond
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000503:physiopathology*; D003342:Corpus Striatum / Q000503:physiopathology*; D004195:Disease Models, Animal; D006816:Huntington Disease / Q000503:physiopathology*; D020813:Receptor, trkB / Q000172:deficiency*; D015398:Signal Transduction / Q000235:genetics*
chemical_list: D020813:Receptor, trkB