{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,10]],"date-time":"2026-10-10T04:35:30Z","timestamp":1791606930719,"version":"4.3.4"},"reference-count":67,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T00:00:00Z","timestamp":1768521600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T00:00:00Z","timestamp":1768521600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2026,4]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      Whether cognitive decline in patients with Parkinson's disease (PD) carrying\n                      <jats:italic>GBA1<\/jats:italic>\n                      variants is accelerated after subthalamic deep brain stimulation (STN\u2010DBS) remains controversial. Clarifying long\u2010term cognitive outcomes is essential for informed decision making.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We assembled matched cohorts of patients carrying\n                      <jats:italic>GBA1<\/jats:italic>\n                      variants with STN\u2010DBS (PD\n                      <jats:sub>GBA1+DBS+<\/jats:sub>\n                      , n\u2009=\u200928) and without (PD\n                      <jats:sub>G BA1+DBS\u2212<\/jats:sub>\n                      , n\u2009=\u200928). Additional cohorts included non\u2010carriers with STN\u2010DBS (PD\n                      <jats:sub>GBA1\u2212DBS+<\/jats:sub>\n                      , n\u2009=\u200940) and without (PD\n                      <jats:sub>GBA1\u2013DBS\u2212<\/jats:sub>\n                      , n\u2009=\u200943). Clinical, genetic, and cerebrospinal fluid (CSF) biomarkers (A\n                      <jats:italic>\u03b2<\/jats:italic>\n                      1\u201342, h\u2010Tau, p181\u2010Tau, and neurofilament light chain) were analyzed. Cognition was assessed using the Montreal Cognitive Assessment (MoCA). Cognitive slopes were estimated using linear mixed models and the minimally detectable slope difference at 3\u2010year follow\u2010up was 1.33 MoCA points enabling sensitivity to clinically meaningful changes. Secondarily, conversion to dementia was analyzed with Kaplan\u2013Meier\u2010analysis once the MoCA was &lt;\u200921.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      There was no significant difference in cognitive decline between PD\n                      <jats:sub>GBA1+DBS+<\/jats:sub>\n                      and PD\n                      <jats:sub>GBA1+DBS\u2212<\/jats:sub>\n                      (\u22120.24 MoCA points\/year; 95% confidence interval [CI]\u2009=\u2009\u20131.11 to 0.70) projecting to \u22120.72 MoCA points at 3\u2010year\u2010follow\u2010up (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.583). Secondarily, the risk for conversion to dementia did not differ between PD\n                      <jats:sub>GBA1+DBS+<\/jats:sub>\n                      and PD\n                      <jats:sub>GBA1+DBS\u2212<\/jats:sub>\n                      (HR\u2009=\u20090.55, 95% CI\u2009=\u20090.23\u20131.34,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.119) or between PD\n                      <jats:sub>GBA1\u2212DBS+<\/jats:sub>\n                      and PD\n                      <jats:sub>GBA1\u2212DBS\u2212<\/jats:sub>\n                      (HR\u2009=\u20091.22, 95% CI\u2009=\u20090.53\u20132.83,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.897). Dementia risk was associated with\n                      <jats:italic>GBA1<\/jats:italic>\n                      status (HR\u2009=\u20093.04, 95% CI\u2009=\u20091.05\u20138.79,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.041), baseline MoCA &lt;\u200926 (HR\u2009=\u20093.05, 95% CI\u2009=\u20091.29\u20137.21,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.011), and baseline age &gt;\u200969\u2009years (HR\u2009=\u20094.42, 95% CI\u2009=\u20091.79\u201310.89,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.001). In\n                      <jats:italic>GBA1<\/jats:italic>\n                      carriers, a visuospatial\/executive domain score &lt;\u20094\/5 predicted dementia (HR\u2009=\u20094.71, 95% CI\u2009=\u20091.25\u201317.86,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.022).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>\n                      <jats:italic>GBA1<\/jats:italic>\n                      variant carriers meeting general STN\u2010DBS indication criteria did not show accelerated cognitive decline in the presence of STN\u2010DBS. In addition, exploratory predictors of dementia could support counseling of DBS candidates. ANN NEUROL 2026;99:976\u2013988\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ana.78139","type":"journal-article","created":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T10:21:32Z","timestamp":1768558892000},"page":"976-988","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Clinical and Biological Determinants of Longitudinal Cognitive Function in Patients With\n                    <scp>\n                      <i>GBA1<\/i>\n                    <\/scp>\n                    Variants and Subthalamic Deep Brain Stimulation"],"prefix":"10.1002","volume":"99","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0267-2762","authenticated-orcid":false,"given":"Moritz A.","family":"Loeffler","sequence":"first","affiliation":[{"name":"Centre for Neurology, Department of Neurodegenerative Diseases University of T\u00fcbingen  T\u00fcbingen Germany"},{"name":"Hertie\u2010Institute for Clinical Brain Research University of T\u00fcbingen  T\u00fcbingen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philipp","family":"Klocke","sequence":"additional","affiliation":[{"name":"Centre for Neurology, Department of Neurodegenerative Diseases University of T\u00fcbingen  T\u00fcbingen Germany"},{"name":"Hertie\u2010Institute for Clinical Brain Research University of T\u00fcbingen  T\u00fcbingen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isabel","family":"Wurster","sequence":"additional","affiliation":[{"name":"Centre for Neurology, Department of Neurodegenerative Diseases University of T\u00fcbingen  T\u00fcbingen Germany"},{"name":"Hertie\u2010Institute for Clinical Brain Research University of T\u00fcbingen  T\u00fcbingen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5508-004X","authenticated-orcid":false,"given":"Stefanie","family":"Lerche","sequence":"additional","affiliation":[{"name":"Centre for Neurology, Department of Neurodegenerative Diseases University of T\u00fcbingen  T\u00fcbingen Germany"},{"name":"Hertie\u2010Institute for Clinical Brain Research University of T\u00fcbingen  T\u00fcbingen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Idil","family":"Cebi","sequence":"additional","affiliation":[{"name":"Centre for Neurology, Department of Neurodegenerative Diseases University of T\u00fcbingen  T\u00fcbingen Germany"},{"name":"Hertie\u2010Institute for Clinical Brain Research University of T\u00fcbingen  T\u00fcbingen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Gasser","sequence":"additional","affiliation":[{"name":"Centre for Neurology, Department of Neurodegenerative Diseases University of T\u00fcbingen  T\u00fcbingen Germany"},{"name":"Hertie\u2010Institute for Clinical Brain Research University of T\u00fcbingen  T\u00fcbingen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9782-5281","authenticated-orcid":false,"given":"Alireza","family":"Gharabaghi","sequence":"additional","affiliation":[{"name":"Institute for Neuromodulation and Neurotechnology University of T\u00fcbingen  T\u00fcbingen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7515-8596","authenticated-orcid":false,"given":"Kathrin","family":"Brockmann","sequence":"additional","affiliation":[{"name":"Centre for Neurology, Department of Neurodegenerative Diseases University of T\u00fcbingen  T\u00fcbingen Germany"},{"name":"Hertie\u2010Institute for Clinical Brain Research University of T\u00fcbingen  T\u00fcbingen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0447-7132","authenticated-orcid":false,"given":"Daniel","family":"Weiss","sequence":"additional","affiliation":[{"name":"Centre for Neurology, Department of Neurodegenerative Diseases University of T\u00fcbingen  T\u00fcbingen Germany"},{"name":"Hertie\u2010Institute for Clinical Brain Research University of T\u00fcbingen  T\u00fcbingen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,1,16]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.3390\/cells11081261"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.256.5058.794"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuron.2019.12.004"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1002\/mds.26071"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMoa1205158"},{"key":"e_1_2_9_7_1","first-page":"309","article-title":"Are patients with GBA\u2010Parkinson disease good candidates for deep brain stimulation? 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