{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,27]],"date-time":"2026-04-27T11:45:39Z","timestamp":1777290339575,"version":"3.51.4"},"reference-count":96,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2026,2,5]],"date-time":"2026-02-05T00:00:00Z","timestamp":1770249600000},"content-version":"vor","delay-in-days":35,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100015659","name":"Cure Parkinson's Trust","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100015659","id-type":"DOI","asserted-by":"publisher"}]},{"name":"National Institute for Health and Care Research, Efficacy & Mechanism Evaluation","award":["16\/167\/19"],"award-info":[{"award-number":["16\/167\/19"]}]},{"name":"Janet Owens Bequest"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,3,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>There are currently no validated peripheral biomarkers for the diagnosis, differentiation or progression of the neurodegenerative synucleinopathies, Parkinson\u2019s disease and multiple system atrophy. Diagnostic biomarkers that reflect the disease mechanisms or progression biomarkers that change with disease severity would be extremely valuable for assessing disease-modifying therapies. Our objective was to explore putative protein biomarkers of Parkinson\u2019s disease and multiple system atrophy, in relation to clinical disease severity, using the nucleic acid-linked immuno-sandwich assay central nervous system disease panel for biomarker quantification. We used the nucleic acid-linked immuno-sandwich assay CNS disease panel to test plasma from 161 Parkinson\u2019s disease patients collected at three time points (0, 48, 96 weeks) and serum from 43 multiple system atrophy patients at three time points (0, 24, 48 weeks) and compared results to paired plasma and serum samples collected from (n = 39) age-matched healthy control individuals at a single time point. We also tested paired CSF samples collected on two occasions, separated by 96 weeks from a subgroup of Parkinson\u2019s disease participants (n = 51) and after an interval of 48 weeks in a subgroup of multiple system atrophy participants (n = 23). All samples were taken contemporaneously with objective clinical assessments of disease severity. Biomarker comparisons were made across disease status and in relation to disease severity using linear modelling. Multiple proteins showed significantly different quantitative levels (false discovery rate-corrected P value &amp;lt; 0.05) between peripheral samples from Parkinson\u2019s disease and healthy controls and multiple system atrophy and healthy controls. For Parkinson\u2019s disease, we identified three key classes of proteins that showed significant differences between Parkinson\u2019s disease and controls: (i) amyloidogenic proteins, specifically, oligomeric alpha-synuclein was significantly higher in Parkinson\u2019s disease compared to controls. A number of other aggregating proteins also exhibited differences. (ii) Metabolic pathways, including the adipokine (chemokine-like protein TAFA-5), were associated with Parkinson\u2019s disease diagnosis, and (iii) inflammatory pathways (interleukin-7) were associated with Parkinson\u2019s disease diagnosis. Importantly, some of these same proteins were significantly associated with Parkinson\u2019s disease severity including oligomeric and phosphorylated forms of alpha-synuclein and insulin-like growth factor-1 receptor. We also confirmed as expected that neurofilament light levels strongly distinguish multiple system atrophy patients from healthy controls, while also demonstrating that serum inflammatory proteins (interleukin-6) as well as the phosphorylated alpha-synuclein ratio are strongly associated with multiple system atrophy severity. These results from the nucleic acid-linked immuno-sandwich assay multiplex platform provide additional insights into the complex pathogenetic mechanisms associated with alpha-synucleinopathy related neurodegeneration. Individual protein levels or the combination of multiple protein candidates may usefully serve as diagnostic biomarkers, or as biomarkers for disease progression in trials of potential disease-modifying interventions.<\/jats:p>","DOI":"10.1093\/braincomms\/fcag035","type":"journal-article","created":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T12:36:50Z","timestamp":1770122210000},"source":"Crossref","is-referenced-by-count":1,"title":["Peripheral and CSF protein quantification in Parkinson\u2019s disease and multiple system atrophy\u2014the nucleic acid-linked immuno-sandwich assay"],"prefix":"10.1093","volume":"8","author":[{"given":"Nirosen","family":"Vijiaratnam","sequence":"first","affiliation":[{"name":"Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology , London WC1N 3BG 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WC1N 3BG ,","place":["UK"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jennifer","family":"Hay","sequence":"additional","affiliation":[{"name":"The Francis Crick Institute Neurodegenration Biology Laboratory, , London NW1 1AT ,","place":["UK"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Nicola","family":"O\u2019Reilly","sequence":"additional","affiliation":[{"name":"The Francis Crick Institute Neurodegenration Biology Laboratory, , London NW1 1AT ,","place":["UK"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5473-3774","authenticated-orcid":false,"given":"Huw","family":"Morris","sequence":"additional","affiliation":[{"name":"Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology , London WC1N 3BG ,","place":["UK"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Camille","family":"Carroll","sequence":"additional","affiliation":[{"name":"Translational and Clinical Research Institute Clinical Ageing Research Unit, Newcastle University , Newcastle ,","place":["UK"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6382-5841","authenticated-orcid":false,"given":"Michele T M","family":"Hu","sequence":"additional","affiliation":[{"name":"Oxford University and Oxford University Hospitals NHS Foundation Trust Nuffield Department of CLinical Neurosciences, , Oxford OX3 9DU ,","place":["UK"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Monty A","family":"Silverdale","sequence":"additional","affiliation":[{"name":"Manchester Centre for Clinical Neurosciences, Northern Care Alliance NHS Foundation Trust, Manchester Academic Health Science Centre, University of Manchester , Manchester M13 9NQ 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