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The\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    pathology resulting from the mutation is most prominent in the striatal part of the basal ganglia, and progressive differential dysfunction and loss of striatal projection neurons and interneurons account for the progression of motor deficits seen in this disease. The present review summarizes current understanding regarding the progression in striatal neuron dysfunction and loss, based on studies both in human\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    victims and in genetic mouse models of\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    . We review evidence on early loss of inputs to striatum from cortex and thalamus, which may be the basis of the mild premanifest bradykinesia in\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    , as well as on the subsequent loss of indirect pathway striatal projection neurons and their outputs to the external pallidal segment, which appears to be the basis of the chorea seen in early symptomatic\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    . Later loss of direct pathway striatal projection neurons and their output to the internal pallidal segment account for the severe akinesia seen late in\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    . Loss of parvalbuminergic striatal interneurons may contribute to the late dystonia and rigidity.\n                  <\/jats:p>","DOI":"10.1111\/cns.12844","type":"journal-article","created":{"date-parts":[[2018,4,6]],"date-time":"2018-04-06T11:03:30Z","timestamp":1523012610000},"page":"250-280","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":97,"title":["Disrupted striatal neuron inputs and outputs in Huntington's disease"],"prefix":"10.1111","volume":"24","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2146-5232","authenticated-orcid":false,"given":"Anton","family":"Reiner","sequence":"first","affiliation":[{"name":"Department of Anatomy &amp; Neurobiology The University of Tennessee Health Science Center  Memphis TN USA"},{"name":"Department of Ophthalmology The University of Tennessee Health Science Center  Memphis TN 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