{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T18:06:50Z","timestamp":1790014010338,"version":"4.0.1"},"reference-count":27,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2025,7,14]],"date-time":"2025-07-14T00:00:00Z","timestamp":1752451200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,7,14]],"date-time":"2025-07-14T00:00:00Z","timestamp":1752451200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["movementdisorders.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Movement Disord Clin Pract"],"published-print":{"date-parts":[[2025,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Although traditionally recognized for motor impairment, evidence suggests that cognitive deficits may emerge before ataxia onset in autosomal dominant spinocerebellar ataxias (\n                      <jats:styled-content style=\"fixed-case\">SCA<\/jats:styled-content>\n                      ), particularly in nucleotide repeat expansion\n                      <jats:styled-content style=\"fixed-case\">SCAs<\/jats:styled-content>\n                      (\n                      <jats:styled-content style=\"fixed-case\">NRE<\/jats:styled-content>\n                      \u2010\n                      <jats:styled-content style=\"fixed-case\">SCAs<\/jats:styled-content>\n                      ). However, the nature and extent of these early cognitive changes and cognition disorders remain unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      This scoping review maps existing evidence on cognitive alterations in pre\u2010ataxic\n                      <jats:styled-content style=\"fixed-case\">NRE<\/jats:styled-content>\n                      \u2010\n                      <jats:styled-content style=\"fixed-case\">SCAs<\/jats:styled-content>\n                      , focusing on affected cognitive domains, assessment tools, and early biomarkers.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A comprehensive search in PubMed, EMBASE, and CINAHL was performed in accordance with Joanna Briggs Institute guidelines. Studies were included if they assessed cognitive function in genetically confirmed pre\u2010ataxic NRE\u2010SCA individuals using neuropsychological tests, imaging, or biomarkers. Data extraction comprised study design, cognitive domains assessed, and key findings.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Thirteen studies met inclusion criteria, examining pre\u2010ataxic individuals with SCA1, SCA2, SCA3, and SCA36. Executive dysfunction, particularly in cognitive flexibility, inhibitory control, and working memory, was the most frequent finding, assessed using the Trail Making Test, Stroop Test, and phonemic fluency tasks. Processing speed deficits were also commonly reported. Pre\u2010ataxic SCA2 exhibited the most consistent impairments, whereas findings in pre\u2010ataxic SCA1 and pre\u2010ataxic SCA3 were variable. Neuroimaging studies revealed early cerebellar microstructural changes linked to cognitive dysfunction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Cognitive impairments may precede motor symptoms in NRE\u2010SCAs, particularly SCA2. However, methodological heterogeneity and small sample sizes limit definitive conclusions. Standardized assessments and longitudinal studies are needed to clarify cognitive decline trajectories and their potential as early biomarkers.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/mdc3.70215","type":"journal-article","created":{"date-parts":[[2025,7,14]],"date-time":"2025-07-14T11:29:16Z","timestamp":1752492556000},"page":"2071-2079","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Cognitive Changes in Pre\u2010ataxic Spinocerebellar Ataxias: A Scoping Review"],"prefix":"10.1002","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4802-9430","authenticated-orcid":false,"given":"Renata Barreto","family":"Tenorio","sequence":"first","affiliation":[{"name":"Neurological Diseases Group, Postgraduate Program in Internal Medicine, Internal Medicine Department Hospital de Cl\u00ednicas, Federal University of Paran\u00e1  Curitiba Brazil"},{"name":"Neurogenetic Service, Instituto de 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Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3533-0347","authenticated-orcid":false,"given":"Carlos Henrique Ferreira","family":"Camargo","sequence":"additional","affiliation":[{"name":"Neurological Diseases Group, Postgraduate Program in Internal Medicine, Internal Medicine Department Hospital de Cl\u00ednicas, Federal University of Paran\u00e1  Curitiba 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