{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T16:48:52Z","timestamp":1791564532934,"version":"4.3.4"},"reference-count":80,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,1,15]],"date-time":"2026-01-15T00:00:00Z","timestamp":1768435200000},"content-version":"vor","delay-in-days":14,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"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":["Brain and Behavior"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>The study utilized MRI\u2010derived brain structure age (BSA) to compare global and regional subcortical BSA among healthy controls (HCs), Parkinson's disease (PD) patients with normal cognition (PD\u2010NC), and mild cognitive impairment (PD\u2010MCI), identifying regions with accelerated aging and linking altered BSA to native volumes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We analyzed structural MRI data from 55 participants (22 HCs, 18 PD\u2010NC, 15 PD\u2010MCI) using the volBrain platform to estimate global and regional subcortical BSA. Group differences in age, global, and regional BSA were tested via Kruskal\u2010Wallis. Follow\u2010up analyses included Pearson correlations for significant regions and ANOVAs where assumptions were met.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      No significant group differences were found for chronological age (\n                      <jats:italic>p<\/jats:italic>\n                      = 0.111) or global BSA (\n                      <jats:italic>p<\/jats:italic>\n                      = 0.143). However, at the regional level, non\u2010parametric analyses revealed significant group differences in the predicted age of the left amygdala (H = 6.42,\n                      <jats:italic>p<\/jats:italic>\n                      = 0.040) and the left basal forebrain (H = 6.01,\n                      <jats:italic>p<\/jats:italic>\n                      &lt; 0.05), though effect sizes were small (\u03b5\n                      <jats:sup>2<\/jats:sup>\n                      \u2264 0.07). The predicted ages of these two regions were highly collinear (\n                      <jats:italic>r<\/jats:italic>\n                      = 0.992). Subsequent parametric tests and Bonferroni\u2010corrected pairwise comparisons on other subcortical regions did not yield any significant differences.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Accelerated aging appears to be a localized and asymmetric process confined to the limbic\u2010cholinergic network, specifically involving the left amygdala and basal forebrain. Accelerated brain aging in PD is not global but a localized, asymmetric process in the left limbic\u2010cholinergic network. Regional brain\u2010age metrics offer a sensitive biomarker for detecting the specific neurodegeneration linked to cognitive decline.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/brb3.71202","type":"journal-article","created":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T07:00:16Z","timestamp":1768546816000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Subcortical Brain\u2010Age Gaps Reveal Asymmetric Aging Patterns in Parkinson's Disease With Cognitive Impairment"],"prefix":"10.1002","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1334-8826","authenticated-orcid":false,"given":"Sadegh","family":"Ghaderi","sequence":"first","affiliation":[{"name":"Neuromuscular Research Center, Department of Neurology, Shariati Hospital Tehran University of Medical Sciences  Tehran Iran"},{"name":"Department of Neuroscience and Addiction Studies, School of Advanced Technologies in Medicine Tehran University of Medical Sciences  Tehran Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6838-929X","authenticated-orcid":false,"given":"Ali Fathi","family":"Jouzdani","sequence":"additional","affiliation":[{"name":"School of Cognitive Sciences Institute For Research in Fundamental Sciences (IPM)  Tehran Iran"},{"name":"Neuroscience and Neoplasia AI Research Group (NAIRG), Neurophysiology Research Center, Institute of Neuroscience and Cognition, School of Medicine Shahid Beheshti University of Medical Sciences  Tehran Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4462-9890","authenticated-orcid":false,"given":"Ali Mohammad","family":"Pourbagher\u2010Shahri","sequence":"additional","affiliation":[{"name":"Neuroscience Research Center Mashhad University of Medical Sciences  Mashhad Iran"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2286-9052","authenticated-orcid":false,"given":"Sana","family":"Mohammadi","sequence":"additional","affiliation":[{"name":"Neuromuscular Research Center, Department of Neurology, Shariati Hospital Tehran University of Medical Sciences  Tehran Iran"},{"name":"Department of Medical Sciences, School of Medicine Iran University of Medical Sciences  Tehran Iran"},{"name":"School of Medicine Hamadan University of Medical Sciences  Hamadan 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