{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T06:50:31Z","timestamp":1777877431629,"version":"3.51.4"},"reference-count":32,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2025,4,13]],"date-time":"2025-04-13T00:00:00Z","timestamp":1744502400000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,4,13]],"date-time":"2025-04-13T00:00:00Z","timestamp":1744502400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"name":"Parkinson's United Kingdom","award":["Project grant J-2101- \u2018Understanding Parkinson\u2019s Progression"],"award-info":[{"award-number":["Project grant J-2101- \u2018Understanding Parkinson\u2019s Progression"]}]}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Parkinson\u2019s Disease"],"published-print":{"date-parts":[[2025,5]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Parkinson's disease (PD) has marked phenotypic variability. Increased lipids have been suggested as being neuroprotective whilst hyperglycemia may increase \u03b1-synuclein aggregation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>We have tested whether high total cholesterol and high-density lipoprotein cholesterol (HDL-C) and low levels of fructosamine are associated with better PD phenotypes and predict less rapid progression<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Non-fasting serum HDL-C, total cholesterol, and fructosamine were measured at baseline in 866 patients with early PD (median duration, 0.96; IQR, 0.43\u20131.98 years) from the Oxford Discovery cohort. These biomarkers were compared against our data-derived PD subtypes using multinomial logistic regression. We used multilevel models to predict longitudinal motor and non-motor outcomes (e.g., cognition, mood).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>HDL-C and total cholesterol differed across baseline PD phenotype clusters, with reduced levels associated with the most severe motor and non-motor phenotypes (psychological well-being, cognitive impairment, REM sleep behavior disorder, and daytime sleepiness). Higher HDL-C and total cholesterol, although the latter was attenuated after adjustment for statin use, were associated with better baseline activities of daily living (e.g., UPDRS-II score with 1 SD increase in HDL-C \u22120.74, 95%CI \u22121.22 to \u22120.26, p\u2009=\u20090.002) and non-motor features. Neither predicted the rate of motor or non-motor progression. Fructosamine levels were not associated with phenotypic variability or rate of disease progression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Hypercholesterolemia was associated with a better motor\/non-motor disease subtype and daily living impairment at presentation, but did not predict longitudinal change. Future research needs to determine if these associations are causally related or secondary to disease onset by examining prodromal subjects.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1877718x251323914","type":"journal-article","created":{"date-parts":[[2025,4,13]],"date-time":"2025-04-13T11:17:46Z","timestamp":1744543066000},"page":"522-530","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Association of cholesterol and glycemic state biomarkers with phenotypic variation and Parkinson's disease progression: The Oxford Discovery cohort"],"prefix":"10.1177","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9012-8010","authenticated-orcid":false,"given":"Nicholas Kwan","family":"Ho Chiu","sequence":"first","affiliation":[{"name":"Margaret K. L. Cheung Research Centre for Management of Parkinsonism, Department of Medicine and Therapeutics, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China"},{"name":"Oxford Parkinson's Disease Centre, University of Oxford, \rOxford, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3419-0354","authenticated-orcid":false,"given":"Michael","family":"Lawton","sequence":"additional","affiliation":[{"name":"Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4672-5619","authenticated-orcid":false,"given":"Tanja","family":"Zerenner","sequence":"additional","affiliation":[{"name":"Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5832-7992","authenticated-orcid":false,"given":"Alireza","family":"Morovat","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry, Oxford University Hospital NHS Foundation Trust, Oxford, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jessica","family":"Welch","sequence":"additional","affiliation":[{"name":"Oxford Parkinson's Disease Centre, University of Oxford, \rOxford, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6700-1177","authenticated-orcid":false,"given":"Jamil","family":"Razzaque","sequence":"additional","affiliation":[{"name":"Oxford Parkinson's Disease Centre, University of Oxford, \rOxford, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6382-5841","authenticated-orcid":false,"given":"Michele T","family":"Hu","sequence":"additional","affiliation":[{"name":"Oxford Parkinson's Disease Centre, University of Oxford, \rOxford, UK"},{"name":"Nuffield Department of Clinical Neurosciences, Division of Clinical Neurology, University of Oxford, Oxford, UK"},{"name":"Department of Clinical Neurology, Oxford University Hospital NHS Foundation Trust, Oxford, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6648-3007","authenticated-orcid":false,"given":"Yoav","family":"Ben-Shlomo","sequence":"additional","affiliation":[{"name":"Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2025,4,13]]},"reference":[{"key":"e_1_3_5_2_2","doi-asserted-by":"publisher","DOI":"10.1136\/jnnp-2018-318337"},{"key":"e_1_3_5_3_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.0000000000011553"},{"key":"e_1_3_5_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/mds.26698"},{"key":"e_1_3_5_5_2","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2377-13-35"},{"key":"e_1_3_5_6_2","doi-asserted-by":"publisher","DOI":"10.1002\/mds.27492"},{"key":"e_1_3_5_7_2","doi-asserted-by":"publisher","DOI":"10.1002\/mds.27413"},{"key":"e_1_3_5_8_2","doi-asserted-by":"publisher","DOI":"10.1002\/mds.27888"},{"key":"e_1_3_5_9_2","doi-asserted-by":"publisher","DOI":"10.1186\/s12944-020-01284-w"},{"key":"e_1_3_5_10_2","first-page":"836962","article-title":"Total cholesterol and the risk of Parkinson's disease: a review for some new findings","volume":"2010","author":"Hu G","year":"2009","unstructured":"Hu G. 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