{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T23:56:18Z","timestamp":1789689378732,"version":"4.0.1"},"reference-count":61,"publisher":"Wiley","license":[{"start":{"date-parts":[[2016,1,1]],"date-time":"2016-01-01T00:00:00Z","timestamp":1451606400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2016]]},"abstract":"<jats:p>\n                    Huntington\u2019s disease (HD) is a neurodegenerative disorder characterized by selective loss of neurons in the striatum and cortex, which leads to progressive motor dysfunction, cognitive decline, and psychiatric disorders. Although the cause of HD is well described\u2014HD is a genetic disorder caused by a trinucleotide (CAG) repeat expansion in the gene encoding for huntingtin (\n                    <jats:italic>HTT<\/jats:italic>\n                    ) on chromosome 4p16.3\u2014the ultimate cause of neuronal death is still uncertain. Apart from impairment in systems for handling abnormal proteins, other metabolic pathways and mechanisms might contribute to neurodegeneration and progression of HD. Among these, inflammation seems to play a role in HD pathogenesis. The current review summarizes the available evidence about immune and\/or inflammatory changes in HD. HD is associated with increased inflammatory mediators in both the central nervous system and periphery. Accordingly, there have been some attempts to slow HD progression targeting the immune system.\n                  <\/jats:p>","DOI":"10.1155\/2016\/8653132","type":"journal-article","created":{"date-parts":[[2016,8,8]],"date-time":"2016-08-08T17:02:05Z","timestamp":1470675725000},"page":"1-10","source":"Crossref","is-referenced-by-count":82,"title":["Neuroimmunology of Huntington\u2019s Disease: Revisiting Evidence from Human Studies"],"prefix":"10.1155","volume":"2016","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2616-8082","authenticated-orcid":true,"given":"Natalia P.","family":"Rocha","sequence":"first","affiliation":[{"name":"Neuropsychiatry Program, Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77054, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabiola M.","family":"Ribeiro","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and 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