{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T01:00:47Z","timestamp":1787878847036,"version":"build-2784847793"},"reference-count":66,"publisher":"Oxford University Press (OUP)","issue":"3-4","license":[{"start":{"date-parts":[[2021,2,1]],"date-time":"2021-02-01T00:00:00Z","timestamp":1612137600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"German Research Council"},{"name":"Center for Nanoscale Microscopy and Physiology"},{"DOI":"10.13039\/501100001655","name":"German Academic Exchange Service","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001655","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,4,26]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Beta (\u00df)-synuclein (\u00df-Syn) has long been considered to be an attenuator for the neuropathological effects caused by the Parkinson\u2019s disease-related alpha (\u03b1)-synuclein (\u03b1-Syn) protein. However, recent studies demonstrated that overabundant \u00df-Syn can form aggregates and induce neurodegeneration in central nervous system (CNS) neurons in vitro and in vivo, albeit at a slower pace as compared with \u03b1-Syn. Here, we demonstrate that \u00df-Syn mutants V70M, detected in a sporadic case of dementia with Lewy bodies (DLB), and P123H, detected in a familial case of DLB, robustly aggravate the neurotoxic potential of \u00df-Syn. Intriguingly, the two mutations trigger mutually exclusive pathways. \u00df-Syn V70M enhances morphological mitochondrial deterioration and degeneration of dopaminergic and non-dopaminergic neurons, but it has no influence on neuronal network activity. Conversely, \u00df-Syn P123H silences neuronal network activity, but it does not aggravate neurodegeneration. \u00df-Syn wild type (WT), V70M and P123H formed proteinase K-resistant intracellular fibrils within neurons, albeit with less stable C-termini as compared with \u03b1-Syn. Under cell-free conditions, \u00df-Syn V70M demonstrated a much slower pace of fibril formation as compared with WT \u00df-Syn, and P123H fibrils present with a unique phenotype characterized by large numbers of short, truncated fibrils. Thus, it is possible that V70M and P123H cause structural alterations in \u00df-Syn, which are linked to their distinct neuropathological profiles. The extent of the lesions caused by these neuropathological profiles is almost identical to that of overabundant \u03b1-Syn and is thus likely to be directly involved into the etiology of DLB. Overall, this study provides insights into distinct disease mechanisms caused by mutations of \u00df-Syn.<\/jats:p>","DOI":"10.1093\/hmg\/ddab036","type":"journal-article","created":{"date-parts":[[2021,2,5]],"date-time":"2021-02-05T13:30:17Z","timestamp":1612531817000},"page":"247-264","source":"Crossref","is-referenced-by-count":16,"title":["Dementia with Lewy bodies\u2014associated \u00df-synuclein mutations V70M and P123H cause mutation-specific neuropathological lesions"],"prefix":"10.1093","volume":"30","author":[{"given":"Maryna","family":"Psol","sequence":"first","affiliation":[{"name":"Department of Neurology, University Medicine G\u00f6ttingen, G\u00f6ttingen 37073, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sofia Guerin","family":"Darvas","sequence":"additional","affiliation":[{"name":"Department of Neurology, University Medicine G\u00f6ttingen, G\u00f6ttingen 37073, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kristian","family":"Leite","sequence":"additional","affiliation":[{"name":"Department of Neurology, University Medicine G\u00f6ttingen, G\u00f6ttingen 37073, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sameehan U","family":"Mahajani","sequence":"additional","affiliation":[{"name":"Department of Neurology, University Medicine G\u00f6ttingen, G\u00f6ttingen 37073, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mathias","family":"B\u00e4hr","sequence":"additional","affiliation":[{"name":"Department of Neurology, University Medicine G\u00f6ttingen, G\u00f6ttingen 37075, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5130-2012","authenticated-orcid":false,"given":"Sebastian","family":"K\u00fcgler","sequence":"additional","affiliation":[{"name":"Department of Neurology, University Medicine G\u00f6ttingen, G\u00f6ttingen 37073, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2021,2,10]]},"reference":[{"key":"2021050309131633200_ref1","doi-asserted-by":"crossref","first-page":"161","DOI":"10.1002\/jnr.23149","article-title":"Synucleins: are they two-edged swords?","volume":"91","author":"Surguchov","year":"2013","journal-title":"J. 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