{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T11:18:08Z","timestamp":1793186288750,"version":"4.5.0"},"reference-count":62,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2021,10,11]],"date-time":"2021-10-11T00:00:00Z","timestamp":1633910400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,4,29]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The gating of movement depends on activity within the cortico-striato-thalamic loops. Within these loops, emerging from the cells of the striatum, run two opponent pathways\u2014the direct and indirect basal ganglia pathways. Both are complex and polysynaptic, but the overall effect of activity within these pathways is thought to encourage and inhibit movement, respectively. In Huntington\u2019s disease, the preferential early loss of striatal neurons forming the indirect pathway is thought to lead to disinhibition, giving rise to the characteristic motor features of the condition. But early Huntington\u2019s disease is also associated with apathy, a loss of motivation and failure to engage in goal-directed movement. We hypothesized that in Huntington\u2019s disease, motor signs and apathy may be selectively correlated with indirect and direct pathway dysfunction, respectively.<\/jats:p>\n                  <jats:p>We used spectral dynamic casual modelling of resting-state functional MRI data to model effective connectivity in a model of these cortico-striatal pathways. We tested both of these hypotheses in vivo for the first time in a large cohort of patients with prodromal Huntington\u2019s disease. Using an advanced approach at the group level we combined parametric empirical Bayes and Bayesian model reduction procedures to generate a large number of competing models and compare them using Bayesian model comparison. With this automated Bayesian approach, associations between clinical measures and connectivity parameters emerge de novo from the data.<\/jats:p>\n                  <jats:p>We found very strong evidence (posterior probability &amp;gt; 0.99) to support both of our hypotheses. First, more severe motor signs in Huntington\u2019s disease were associated with altered connectivity in the indirect pathway components of our model and, by comparison, loss of goal-direct behaviour or apathy, was associated with changes in the direct pathway component.<\/jats:p>\n                  <jats:p>The empirical evidence we provide here demonstrates that imbalanced basal ganglia connectivity may play an important role in the pathogenesis of some of commonest and disabling features of Huntington\u2019s disease and may have important implications for therapeutics.<\/jats:p>","DOI":"10.1093\/brain\/awab367","type":"journal-article","created":{"date-parts":[[2021,10,8]],"date-time":"2021-10-08T16:50:07Z","timestamp":1633711807000},"page":"991-1000","source":"Crossref","is-referenced-by-count":32,"title":["Imbalanced basal ganglia connectivity is associated with motor deficits and apathy in Huntington\u2019s disease"],"prefix":"10.1093","volume":"145","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0779-9439","authenticated-orcid":false,"given":"Akshay","family":"Nair","sequence":"first","affiliation":[{"name":"Huntington\u2019s Disease Centre, UCL Queen Square Institute of Neurology, University College London, Russell Square House, London WC1B 5EH, UK"},{"name":"Max Planck UCL Centre for Computational Psychiatry and Ageing Research, UCL Queen Square Institute of Neurology, University College London, Russell Square House, London WC1B 5EH, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adeel","family":"Razi","sequence":"additional","affiliation":[{"name":"Turner Institute for Brain and Mental Health, Monash Biomedical Imaging, Monash University, Clayton 3800, Australia"},{"name":"Wellcome Centre for Human Neuroimaging, UCL Queen Square Institute of Neurology, University College London, London WC1N 3AR, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Gregory","sequence":"additional","affiliation":[{"name":"Huntington\u2019s Disease Centre, UCL Queen Square Institute of Neurology, University College London, Russell Square House, London WC1B 5EH, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robb B","family":"Rutledge","sequence":"additional","affiliation":[{"name":"Max Planck UCL Centre for Computational Psychiatry and Ageing Research, UCL Queen Square Institute of Neurology, University College London, Russell Square House, London WC1B 5EH, UK"},{"name":"Wellcome Centre for Human Neuroimaging, UCL Queen Square Institute of Neurology, University College London, London WC1N 3AR, UK"},{"name":"Department of Psychology, Yale University, New Haven, CT 06511, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Geraint","family":"Rees","sequence":"additional","affiliation":[{"name":"Huntington\u2019s Disease Centre, UCL Queen Square Institute of Neurology, University College London, Russell Square House, London WC1B 5EH, UK"},{"name":"Wellcome Centre for Human Neuroimaging, UCL Queen Square Institute of Neurology, University College London, London WC1N 3AR, UK"},{"name":"UCL Institute of Cognitive Neuroscience, University College London, Alexandra House, Bloomsbury, London WC1N 3AZ, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah J","family":"Tabrizi","sequence":"additional","affiliation":[{"name":"Huntington\u2019s Disease Centre, UCL Queen Square Institute of Neurology, University College London, Russell Square House, London WC1B 5EH, UK"},{"name":"Wellcome Centre for Human Neuroimaging, UCL Queen Square Institute of Neurology, University College London, London WC1N 3AR, 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