{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T01:08:31Z","timestamp":1792112911888,"version":"4.4.0"},"reference-count":80,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2020,7,24]],"date-time":"2020-07-24T00:00:00Z","timestamp":1595548800000},"content-version":"vor","delay-in-days":205,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"name":"Australian Government National Health"},{"DOI":"10.13039\/501100000265","name":"Medical Research Council","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000265","id-type":"DOI","asserted-by":"publisher"}]},{"name":"The Fox Family Foundation"},{"name":"Torquay Coasters Cycling Group"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Huntington\u2019s disease is characterized by a triad of motor, cognitive and psychiatric impairments, as well as unintended weight loss. Although much of the research has focused on cognitive, motor and psychiatric symptoms, the extent of peripheral pathology and the relationship between these factors, and the core symptoms of Huntington\u2019s disease, are relatively unknown. Gut microbiota are key modulators of communication between the brain and gut, and alterations in microbiota composition (dysbiosis) can negatively affect cognition, behaviour and affective function, and may be implicated in disease progression. Furthermore, gut dysbiosis was recently reported in Huntington\u2019s disease transgenic mice. Our main objective was to characterize the gut microbiome in people with Huntington\u2019s disease and determine whether the composition of gut microbiota are significantly related to clinical indicators of disease progression. We compared 42 Huntington\u2019s disease gene expansion carriers, including 19 people who were diagnosed with Huntington\u2019s disease (Total Functional Capacity &amp;gt; 6) and 23 in the premanifest stage, with 36 age- and gender-matched healthy controls. Participants were characterized clinically using a battery of cognitive tests and using results from 16S V3 to V4 rRNA sequencing of faecal samples to characterize the gut microbiome. For gut microbiome measures, we found significant differences in the microbial communities (beta diversity) based on unweighted UniFrac distance (P\u2009=\u20090.001), as well as significantly lower alpha diversity (species richness and evenness) between our combined Huntington\u2019s disease gene expansion carrier group and healthy controls (P\u2009=\u20090.001). We also found major shifts in the microbial community structure at Phylum and Family levels, and identified functional pathways and enzymes affected in our Huntington\u2019s disease gene expansion carrier group. Within the Huntington\u2019s disease gene expansion carrier group, we also discovered associations among gut bacteria, cognitive performance and clinical outcomes. Overall, our findings suggest an altered gut microbiome in Huntington\u2019s disease gene expansion carriers. These results highlight the importance of gut biomarkers and raise interesting questions regarding the role of the gut in Huntington\u2019s disease, and whether it may be a potential target for future therapeutic intervention.<\/jats:p>","DOI":"10.1093\/braincomms\/fcaa110","type":"journal-article","created":{"date-parts":[[2020,7,24]],"date-time":"2020-07-24T17:26:53Z","timestamp":1595611613000},"source":"Crossref","is-referenced-by-count":202,"title":["Gut dysbiosis in Huntington\u2019s disease: associations among gut microbiota, cognitive performance and clinical outcomes"],"prefix":"10.1093","volume":"2","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1830-2862","authenticated-orcid":false,"given":"Cory I","family":"Wasser","sequence":"first","affiliation":[{"name":"Ageing and Neurodegeneration Program, School of Psychological Sciences, Turner Institute for Brain and Mental Health, Monash University, Clayton, Victoria 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8162-0679","authenticated-orcid":false,"given":"Emily-Clare","family":"Mercieca","sequence":"additional","affiliation":[{"name":"Ageing and Neurodegeneration Program, School of Psychological Sciences, Turner Institute for Brain and Mental Health, Monash University, Clayton, Victoria 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9277-8650","authenticated-orcid":false,"given":"Geraldine","family":"Kong","sequence":"additional","affiliation":[{"name":"Florey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, Parkville, Victoria 3010, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7532-8922","authenticated-orcid":false,"given":"Anthony J","family":"Hannan","sequence":"additional","affiliation":[{"name":"Florey Institute of Neuroscience and Mental Health, Melbourne Brain Centre, University of Melbourne, Parkville, Victoria 3010, Australia"},{"name":"Department of Anatomy and Neuroscience, University of Melbourne, Parkville, Victoria 3010, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7318-116X","authenticated-orcid":false,"given":"Sonja J","family":"McKeown","sequence":"additional","affiliation":[{"name":"Department of Anatomy & Developmental Biology, Monash University, Clayton, Victoria 3800, Australia"},{"name":"Development and Stem Cells Program, Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6128-7768","authenticated-orcid":false,"given":"Yifat","family":"Glikmann-Johnston","sequence":"additional","affiliation":[{"name":"Ageing and Neurodegeneration Program, School of Psychological Sciences, Turner Institute for Brain and Mental Health, Monash University, Clayton, Victoria 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9637-8590","authenticated-orcid":false,"given":"Julie C","family":"Stout","sequence":"additional","affiliation":[{"name":"Ageing and Neurodegeneration Program, School of Psychological Sciences, Turner Institute for Brain and Mental Health, Monash University, Clayton, Victoria 3800, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2020,7,24]]},"reference":[{"key":"2020092609544202700_fcaa110-B1","doi-asserted-by":"crossref","first-page":"398","DOI":"10.1038\/ng0893-398","article-title":"The relationship between trinucleotide (CAG) repeat length and clinical features of Huntington's disease","volume":"4","author":"Andrew","year":"1993","journal-title":"Nat 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