Pathological α-synuclein elicits granulovacuolar degeneration independent of tau
Our findings support that α-synuclein pathology can independently elicit granulovacuolar degeneration. The frequent co-accumulation of tau and GVBs suggests a parallel mechanism of cellular dysfunction. The ability of α-synuclein pathology to drive GVB formation in the absence of tau highlights the broader relevance of this process to neurodegeneration with relevance to the pathobiology of LBD.
Authors
- Dylan J. Dues
- An Phu Tran Nguyen
- Alysa Kasen (ORCID: https://orcid.org/0000-0002-8535-016X)
- Naman Vatsa (ORCID: https://orcid.org/0000-0003-4683-3086)
- Michael X. Henderson (ORCID: https://orcid.org/0000-0001-9710-0726)
- Darren J. Moore (ORCID: https://orcid.org/0000-0003-2359-5679)
- Madalynn Erb (ORCID: https://orcid.org/0000-0002-7651-6826)
- Erin T. Williams (ORCID: https://orcid.org/0000-0003-0491-0901)
Institutions
- Van Andel Institute (US)
- University of Wisconsin–Milwaukee (US)
Publication Details
- Journal
- Translational Neurodegeneration
- Published
- 2025-06-19
- DOI
- https://doi.org/10.1186/s40035-025-00494-5
- Citations
- 1
- Primary Topic
- Parkinson's Disease Mechanisms and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 1.39
Funders
- National Institute on Aging