{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T12:43:12Z","timestamp":1785328992610,"version":"3.55.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2024,7,8]],"date-time":"2024-07-08T00:00:00Z","timestamp":1720396800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100012264","name":"NIH","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100012264","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"NINDS","doi-asserted-by":"publisher","award":["NS107404"],"award-info":[{"award-number":["NS107404"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"NINDS","doi-asserted-by":"publisher","award":["DoD W81XWH2110908"],"award-info":[{"award-number":["DoD W81XWH2110908"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003725","name":"National Research Foundation of Korea","doi-asserted-by":"publisher","award":["2022R1C1C1009937"],"award-info":[{"award-number":["2022R1C1C1009937"]}],"id":[{"id":"10.13039\/501100003725","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000864","name":"The Michael J. Fox Foundation for Parkinson\u2019s Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000864","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Aligning Science Across Parkinson\u2019s","award":["MJFF-ASAP-020608"],"award-info":[{"award-number":["MJFF-ASAP-020608"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,12,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Mutations in the GBA1 gene are common genetic risk factors for Parkinson\u2019s disease, disrupting enzymatic activity and causing lysosomal dysfunction, leading to elevated \u03b1-synuclein levels. Although the role of GBA1 in synucleinopathy is well established, recent research underscores neuroinflammation as a significant pathogenic mechanism in GBA1 deficiency.<\/jats:p>\n               <jats:p>This study investigates neuroinflammation in Gba1 E326K knock-in mice, a model associated with increased risk of Parkinson\u2019s disease and dementia. At 9 and 24 months, we assessed GBA1 protein and activity, \u03b1-synuclein pathology, neurodegeneration, motor deficits and gliosis in the ventral midbrain and hippocampus using immunohistochemistry, western blot and glucocerebrosidase assays. Additionally, primary microglia from wild-type and Gba1E326K\/E326K mice were treated with \u03b1-synuclein preformed fibrils to study microglia activation, pro-inflammatory cytokines, reactive astrocyte formation and neuronal death through quantitative PCR, western blot and immunocytochemistry analyses. We also evaluated the effects of gut inoculation of \u03b1-synuclein preformed fibrils in Gba1 E326K mice at 7 months and striatal inoculation at 10 months after injection, assessing motor\/non-motor symptoms, \u03b1-synuclein pathology, neuroinflammation, gliosis and neurodegeneration via behavioural tests, immunohistochemistry and western blot assays.<\/jats:p>\n               <jats:p>At 24 months, Gba1 E326K knock-in mice showed reduced glucocerebrosidase enzymatic activity and glucosylceramide build-up in the ventral midbrain and hippocampus. Increased pro-inflammatory cytokines and reactive astrocytes were observed in microglia and astrocytes from Gba1 E326K mice treated with pathological \u03b1-synuclein preformed fibrils. Gut inoculation of \u03b1-synuclein preformed fibrils increased Lewy body accumulation in the hippocampal dentate gyrus, with heightened microglia and astrocyte activation and worsened non-motor symptoms. Intrastriatal injection of \u03b1-synuclein preformed fibrils induced motor deficits, reactive glial protein accumulation and tauopathy in the prefrontal cortex and hippocampus of Gba1 E326K mice.<\/jats:p>\n               <jats:p>GBA1 deficiency attributable to the Gba1 E326K mutation exacerbates neuroinflammation and promotes pathogenic \u03b1-synuclein transmission, intensifying disease pathology in Parkinson\u2019s disease models. This study enhances our understanding of how the Gba1 E326K mutation contributes to neuroinflammation and the spread of pathogenic \u03b1-synuclein in the brain, suggesting new therapeutic strategies for Parkinson\u2019s disease and related synucleinopathies.<\/jats:p>","DOI":"10.1093\/brain\/awae222","type":"journal-article","created":{"date-parts":[[2024,7,8]],"date-time":"2024-07-08T18:24:22Z","timestamp":1720463062000},"page":"4072-4083","source":"Crossref","is-referenced-by-count":18,"title":["<i>Gba1<\/i> E326K renders motor and non-motor symptoms with pathological \u03b1-synuclein, tau and glial activation"],"prefix":"10.1093","volume":"147","author":[{"given":"Sin Ho","family":"Kweon","sequence":"first","affiliation":[{"name":"Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine , Baltimore, MD 21205 ,","place":["USA"]},{"name":"Department of Neurology, Johns Hopkins University School of Medicine , Baltimore, MD 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,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shi-Xun","family":"Ma","sequence":"additional","affiliation":[{"name":"Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine , Baltimore, MD 21205 ,","place":["USA"]},{"name":"Department of Neurology, Johns Hopkins University School of Medicine , Baltimore, MD 21205 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hee-Jung","family":"Jee","sequence":"additional","affiliation":[{"name":"Department of Information and Statistics, Chungbuk National University , Cheongju, Chungbuk 28644 ,","place":["Republic of Korea"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sangjune","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences and Biotechnology, Chungbuk National University , Cheongju, Chungbuk 28644 ,","place":["Republic of 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