{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T23:09:56Z","timestamp":1785884996503,"version":"3.56.0"},"reference-count":59,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T00:00:00Z","timestamp":1769558400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T00:00:00Z","timestamp":1769558400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000864","name":"Michael J. 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To further dissect this biological variability, we explored spatial neuroimaging differences in S+ versus S\u2013 patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>The study aim was to investigate how SAA status influences imaging measures of dopamine denervation and atrophy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We compare SAA status with CSF proteinopathy markers,\n                      <jats:sup>123<\/jats:sup>\n                      I\u2010Ioflupane dopamine transporter (DAT), and magnetic resonance imaging (MRI) in participants with sporadic (n\u2009=\u2009490),\n                      <jats:italic>LRRK2<\/jats:italic>\n                      \u2010associated (n\u2009=\u2009158), and\n                      <jats:italic>GBA<\/jats:italic>\n                      \u2010associated (n\u2009=\u200980) PD from the Parkinson's Progression Markers Initiative (PPMI).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Between 64% and 95% of participants in these groups have S+ status. For all groups, S+ participants have decreased putamen DAT neurotransmission compared to S\u2013 participants, whereas S\u2013 participants have reduced MRI volume in basal ganglia structures relative to S+ participants. With striatal DAT\/MRI ratios, S+ participants have disproportionately lower putamen DAT uptake relative to atrophy. In exploratory analyses, participants with cognitive impairment or hyposmia are associated with worse DAT\/MRI discordance. By CSF markers, S\u2013 participants with sporadic PD have higher CSF pTau\n                      <jats:sub>181<\/jats:sub>\n                      \/amyloid\u2010\u03b2\n                      <jats:sub>42<\/jats:sub>\n                      ratio, suggesting Alzheimer's copathology.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      S+ patients exhibit more dopaminergic deficit, whereas S\u2013 patients have more subcortical atrophy across sporadic and genetic PD. Together, our findings reveal structure\/function and DAT\/MRI discordance, providing insight into biomarkers and pathophysiology of synucleinopathy and PD. \u00a9 2026 The Author(s).\n                      <jats:italic>Movement Disorders<\/jats:italic>\n                      published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/mds.70186","type":"journal-article","created":{"date-parts":[[2026,1,28]],"date-time":"2026-01-28T14:03:25Z","timestamp":1769609005000},"page":"1101-1113","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Discordance of Dopaminergic Dysfunction and Subcortical Atrophy by \u03b1\u2010Synuclein Status in Sporadic and Genetic Parkinson's Disease"],"prefix":"10.1002","volume":"41","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0312-5530","authenticated-orcid":false,"given":"Michael Tran","family":"Duong","sequence":"first","affiliation":[{"name":"Department of Radiology, Perelman School of Medicine University of Pennsylvania  Philadelphia Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandhitsu R.","family":"Das","sequence":"additional","affiliation":[{"name":"Department of Neurology, Perelman School of Medicine University of Pennsylvania  Philadelphia Pennsylvania USA"},{"name":"Departments of Medicine, Neurology and Psychiatry, Alzheimer's Disease Research Center, Perelman School of Medicine University of Pennsylvania  Philadelphia Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pulkit","family":"Khandelwal","sequence":"additional","affiliation":[{"name":"Department of Radiology, Perelman School of Medicine University of Pennsylvania  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