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J\u00f8rgensen and Gunnar Hansens Foundation"},{"DOI":"10.13039\/501100003554","name":"Lundbeck Foundation","doi-asserted-by":"publisher","award":["R389-2021-1596"],"award-info":[{"award-number":["R389-2021-1596"]}],"id":[{"id":"10.13039\/501100003554","id-type":"DOI","asserted-by":"publisher"}]},{"name":"National Hospital"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["J Neurol"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Apathy is a common and debilitating neuropsychiatric symptom in Huntington\u2019s disease (HD), yet its long-term trajectory remains poorly characterized. This study examined changes in apathy in HD gene expansion carriers (HDGECs) over 6\u00a0years, using a multidimensional measure, and investigated associations with cognition, motor symptoms and depression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Eighty-two HDGECs (premanifest and manifest) completed assessments at Time 0 and Time 1 with a mean follow-up interval of 6\u00a0years. Apathy was measured using the Lille Apathy Rating Scale (LARS) and the Problem Behaviors Assessment\u2013short (PBA-s). Depressive symptoms were assessed with the Hamilton Depression Rating Scale, while social cognition and executive functioning were measured using the Emotion Hexagon and Symbol Digit Modalities Test. Within-person changes were examined using paired statistical tests and associations with clinical variables were evaluated using correlation analyses.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Total apathy scores increased significantly over 6\u00a0years, with small changes (LARS: 1.38 points; PBA-s: 1.11 points). Premanifest participants showed a selective decline in Action Initiation, whereas manifest participants exhibited a broader worsening of total apathy. Individual trajectories were variable, with both worsening and improvement observed. An increase in depressive symptoms was significantly correlated with changes in apathy but accounted for little variance.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Apathy in HD shows a small but significant increase over 6\u00a0years, characterized by marked heterogeneity and changes in Action Initiation. The limited association with depression and cognition highlights apathy as an independent neuropsychiatric feature. These findings underscore the heterogeneous nature of apathy progression and the value of multidimensional assessment in longitudinal studies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00415-026-13825-x","type":"journal-article","created":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T09:41:22Z","timestamp":1776764482000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Longitudinal trajectories of apathy in Huntington\u2019s disease: a 6-year follow-up study"],"prefix":"10.1007","volume":"273","author":[{"ORCID":"https:\/\/orcid.org\/0009-0000-7517-2921","authenticated-orcid":false,"given":"Emilie","family":"Poulsen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3899-7665","authenticated-orcid":false,"given":"Rebecca K.","family":"Hendel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Birna","family":"\u00c1sbj\u00f6rnsd\u00f3ttir","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lena E.","family":"Hjermind","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00f8rgen E.","family":"Nielsen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3401-1061","authenticated-orcid":false,"given":"Asmus","family":"Vogel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,4,21]]},"reference":[{"key":"13825_CR1","doi-asserted-by":"publisher","first-page":"971","DOI":"10.1016\/0092-8674(93)90585-e","volume":"72","author":"The Huntington\u2019s Disease Collaborative Research Group","year":"1993","unstructured":"The Huntington\u2019s Disease Collaborative Research Group (1993) A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington\u2019s disease chromosomes. 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