{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"medRxiv"}],"indexed":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T04:57:08Z","timestamp":1784005028150,"version":"3.55.0"},"posted":{"date-parts":[[2026,3,26]]},"group-title":"Neurology","reference-count":42,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T00:00:00Z","timestamp":1774483200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,3,26]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:sec>\n                  <jats:title>Importance<\/jats:title>\n                  <jats:p>\n                    Accurate diagnosis of neurodegenerative movement disorders is challenging because of a lack of\n                    <jats:italic>in vivo<\/jats:italic>\n                    biomarkers, overlapping clinical features and a delay in the emergence of pathognomonic features.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>To evaluate clinicopathological correlation, diagnostic accuracy, genetic association with pathology, and ancestry-related differences in a multi-ancestry brain bank cohort.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Design<\/jats:title>\n                  <jats:p>Multicentre retrospective autopsy cohort study on donors enrolled between 1985 - 2024.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Setting<\/jats:title>\n                  <jats:p>11 academic brain banks in the UK, US and Australia<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Participants<\/jats:title>\n                  <jats:p>Brain donors identified from participating brain banks with available brain tissue and a clinical diagnosis of Parkinson\u2019s disease, Parkinson\u2019s disease dementia, dementia with Lewy bodies, progressive supranuclear palsy, corticobasal syndrome, multiple system atrophy, or neurologically normal controls.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Exposure<\/jats:title>\n                  <jats:p>Genetic variant carrier status and clinical diagnostic category.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Main outcome<\/jats:title>\n                  <jats:p>Clinical diagnostic accuracy; Lewy body and Alzheimer\u2019s disease pathology burden; survival; association with genetic variants and genetically inferred ancestry.<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>\n                    We studied 3,353 brain donors (1281 [38.2%] female, mean [SD] age at death, 76.8 [10.6] years). Misdiagnosis rates for movement disorders ranged approximately from 10% - 20%. Clinical diagnoses of dementia with parkinsonism (PDD\/DLB) were more strongly associated with Lewy body pathology than Parkinson\u2019s disease without dementia (OR = 1\u00b796, 95% CI = 1\u00b730 - 3\u00b704, p = 7\u00b72e-04). Lewy pathology was identified in 4% of neurologically normal controls. Alzheimer\u2019s disease co-pathology was present in 40% of cases with Lewy body disease.\n                    <jats:italic>GBA1<\/jats:italic>\n                    variant carriers exhibited greater Lewy body burden compared with noncarriers (OR = 1\u00b794, 95% CI = 1\u00b724 - 3\u00b703, p = 0\u00b701) or\n                    <jats:italic>LRRK2<\/jats:italic>\n                    carriers (OR = 7\u00b744, 95% CI = 2\u00b716 - 25\u00b764, p = 0\u00b701). Pathological diagnoses differed by ancestry, with South Asian donors more likely to have progressive supranuclear palsy pathology and Ashkenazi Jewish donors more likely to have Lewy body disease (p &lt; 0.0001), independent of\n                    <jats:italic>GBA1<\/jats:italic>\n                    and\n                    <jats:italic>LRRK2<\/jats:italic>\n                    mutation status.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Conclusion and Relevance<\/jats:title>\n                  <jats:p>\n                    Our findings highlight the value of integrating genetic and pathological data to improve diagnostic accuracy. The high prevalence of Alzheimer\u2019s disease co-pathology and ancestry-related differences in pathology point to the need for biologically informed diagnostic tools. These results support the integration of genetically and pathologically stratified approaches, correlating pathology with\n                    <jats:italic>in vivo<\/jats:italic>\n                    biomarkers, for future therapeutic trials.\n                  <\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Funding<\/jats:title>\n                  <jats:p>Medical Research Council, Global Parkinson\u2019s Genetic Program\/Aligning Science Across Parkinson\u2019s<\/jats:p>\n                <\/jats:sec>\n                <jats:sec>\n                  <jats:title>Key Points<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Question<\/jats:title>\n                    <jats:p>How do genetic variants and neuropathology influence clinical features and diagnostic accuracy in movement disorders?<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Findings<\/jats:title>\n                    <jats:p>\n                      In this multi-ancestry brain bank series including over 3000 individuals, clinical misdiagnosis was common. Dementia with parkinsonism was more strongly associated with Lewy body (LB) pathology than Parkinson\u2019s disease without dementia, and Alzheimer\u2019s disease co-pathology was frequent. Genetic variation was associated with pathological differences.\n                      <jats:italic>GBA1<\/jats:italic>\n                      carriers had greater LB burden, while\n                      <jats:italic>LRRK2<\/jats:italic>\n                      pathogenic variant carriers had a lower LB burden and longer survival. Pathological diagnosis differed by ancestry.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Meaning<\/jats:title>\n                    <jats:p>Integrating genetics and neuropathology may improve diagnosis and support pathology-informed therapeutic trials.<\/jats:p>\n                  <\/jats:sec>\n                <\/jats:sec>","DOI":"10.64898\/2026.03.23.26348322","type":"posted-content","created":{"date-parts":[[2026,3,26]],"date-time":"2026-03-26T18:20:18Z","timestamp":1774549218000},"source":"Crossref","is-referenced-by-count":1,"title":["Pathology and genetics in a global cohort of Parkinsonian Disorders"],"prefix":"10.64898","author":[{"given":"Lesley Y.","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tessa","family":"du 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