{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T06:51:34Z","timestamp":1782283894914,"version":"3.54.5"},"reference-count":49,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T00:00:00Z","timestamp":1782172800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,6,23]],"date-time":"2026-06-23T00:00:00Z","timestamp":1782172800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100002283","name":"Alzheimer\u2019s Research UK","doi-asserted-by":"publisher","award":["ARUK\u2010SRF2022A\u2010006"],"award-info":[{"award-number":["ARUK\u2010SRF2022A\u2010006"]}],"id":[{"id":"10.13039\/501100002283","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000272","name":"National Institute for Health and Care Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000272","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Brain Pathology"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Lewy bodies (LBs), composed primarily of aggregated \u03b1\u2010synuclein (\u03b1\u2010syn), are the pathological hallmark of Lewy body diseases, including Parkinson's disease, Parkinson's disease dementia and dementia with Lewy bodies (DLB). Despite their diagnostic significance, the mechanisms underlying LB formation and their contribution to neurodegeneration remain poorly understood. Previous studies have reported that structures labelled with ubiquitin phosphorylated at serine 65 (p\u2010Ub\n                    <jats:sup>S65<\/jats:sup>\n                    )\u2014a marker of mitophagy\u2014localise both at the periphery of and within LBs. This study aimed to further characterise these structures and clarify their relationship to \u03b1\u2010syn pathology in DLB. Immunofluorescence analysis of\n                    <jats:italic>post\u2010mortem<\/jats:italic>\n                    DLB brain tissue revealed intermittent co\u2010localisation of p\u2010Ub\n                    <jats:sup>S65+<\/jats:sup>\n                    puncta with conventional mitochondrial markers. Given previous findings that granulovacuolar degeneration bodies (GVBs)\u2014vesicular structures frequently associated with tau pathology, itself a concomitant feature of DLB\u2014are immunopositive for p\u2010Ub\n                    <jats:sup>S65<\/jats:sup>\n                    , we next examined whether peri\u2010LB p\u2010Ub\n                    <jats:sup>S65+<\/jats:sup>\n                    structures are actually GVBs. p\u2010Ub\n                    <jats:sup>S65<\/jats:sup>\n                    puncta co\u2010stained with established GVB markers including charged multivesicular body protein 2B (CHMP2B) and casein kinase 1 delta (CK1D), and, more variably with hyperphosphorylated tau (AT8), across multiple brain regions associated with LB pathology. Notably, GVB abundance within the anterior cingulate gyrus was found to positively correlate with p\u2010\u03b1\u2010syn\n                    <jats:sup>S129<\/jats:sup>\n                    burden. In summary, p\u2010Ub\n                    <jats:sup>S65+<\/jats:sup>\n                    GVBs, containing both auto\u2010 and endolysosomal material, cluster around LBs in DLB. Frequently immunoreactive for tau, these hybrid waste vesicles provide a tangible mechanistic link between \u03b1\u2010syn and tau pathology and may offer new insight into the processes underlying LB formation in DLB.\n                  <\/jats:p>","DOI":"10.1111\/bpa.70119","type":"journal-article","created":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T06:45:27Z","timestamp":1782283527000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Lewy bodies are surrounded by granulovacuolar degeneration bodies in dementia with Lewy bodies"],"prefix":"10.1111","author":[{"given":"Searlait","family":"Thom","sequence":"first","affiliation":[{"name":"Translational and Clinical Research Institute, Faculty of Medical Sciences Newcastle University  Newcastle Upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pawel","family":"Palmowski","sequence":"additional","affiliation":[{"name":"Newcastle University Protein and Proteome Analysis Unit Newcastle University  Newcastle Upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew","family":"Porter","sequence":"additional","affiliation":[{"name":"Newcastle University Protein and Proteome Analysis Unit Newcastle University  Newcastle Upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joe","family":"O'Neill","sequence":"additional","affiliation":[{"name":"Translational and Clinical Research Institute, Faculty of Medical Sciences Newcastle University  Newcastle Upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Attems","sequence":"additional","affiliation":[{"name":"Translational and Clinical Research Institute, Faculty of Medical Sciences Newcastle University  Newcastle Upon Tyne UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laura 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