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Biofluid biomarkers are needed to monitor disease progression, but may also provide insights into pathogenic mechanisms and support the development of disease-modifying therapies (DMTs).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      To identify dysregulated cerebrospinal fluid (CSF) proteins in\n                      <jats:italic>HTT<\/jats:italic>\n                      gene expansion carriers (HDGECs), and to evaluate their relationship with disease progression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>CSF was collected from a discovery and a validation cohort, both comprising HDGECs and neurologically unaffected controls (HCs). A total of 734 proteins were quantified using a high-sensitive Proximity Extension Assay (PEA) (Olink Neuro Explore panel 1 and 2). Protein association with disease progression was evaluated using the composite Unified HD Rating Scale (cUHDRS). Disease stage was classified according to the HD Integrated Staging System (HD-ISS).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In total, samples included HDGECs (\n                      <jats:italic>n<\/jats:italic>\n                      =61), HCs (\n                      <jats:italic>n<\/jats:italic>\n                      =54), and longitudinal HDGEC samples (\n                      <jats:italic>n<\/jats:italic>\n                      =21). Sixteen proteins were nominally dysregulated in HDGECs vs. HCs. Most pronounced was a twofold decrease of TNFRSF8 (sCD30) in HDGECs, and longitudinally declining levels were found. TNFRSF8 correlated significantly with cUHDRS, after adjustment for age, sex, and CAG. Levels of TNFRSF8 were similarly reduced in the validation cohort, and correlated with Total Functional Capacity (TFC).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>TNFRSF8 recently emerged as a biomarker of neuroimmune dysfunction in HD. The results indicate and confirm that it is highly dysregulated in HDGECs and also tracks clinical disease progression. This pathway may be a promising potential target for DMTs.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s00415-026-14112-5","type":"journal-article","created":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T17:17:28Z","timestamp":1789233448000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Decreased cerebrospinal fluid TNFRSF8 (sCD30) confirmed as a biomarker of Huntington\u2019s disease progression"],"prefix":"10.1007","volume":"273","author":[{"given":"Helga Maria","family":"Gr\u00e9tarsd\u00f3ttir","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janet L.","family":"Cunningham","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annica","family":"Rasmusson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joachim","family":"Burman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kim","family":"Kultima","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Paucar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Per","family":"Svenningsson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Radu","family":"Constantinescu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2576-9938","authenticated-orcid":false,"given":"Valter","family":"Niemel\u00e4","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,9,12]]},"reference":[{"issue":"12","key":"14112_CR1","doi-asserted-by":"publisher","first-page":"1193","DOI":"10.1016\/S1474-4422(14)70238-8","volume":"13","author":"JS Paulsen","year":"2014","unstructured":"Paulsen JS, Long JD, Ross CA et al (2014) Prediction of manifest Huntington\u2019s disease with clinical and imaging measures: a prospective observational study. 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