Copper Overload Affects α‐Synuclein Clearance Mechanisms in a Parkinson's Disease In Vitro Model (Advanced Biology 5/2026)
Parkinson's Disease This cover depicts copper-induced disruption of proteostasis in a Parkinson's disease cellular model. Copper overload impairs autophagic flux and ubiquitin–proteasome system activity, promoting neuritic accumulation of phosphorylated α-synuclein. The image emphasizes metal dyshomeostasis as a driving factor in α-synuclein pathology and neurodegenerative mechanisms. More details can be found in the Research Article by Debora Musarò, Michele Maffia, and co-workers (DOI: 10.1002/adbi.202500274).
Authors
- Debora Musarò
- Michele Maffia (ORCID: https://orcid.org/0000-0003-0665-4534)
- Chiara Coppola (ORCID: https://orcid.org/0000-0003-1836-7997)
- Marco Greco (ORCID: https://orcid.org/0000-0002-9228-1158)
- Marina Damato (ORCID: https://orcid.org/0000-0003-0104-4323)
Institutions
- University of Salento (IT)
- Ospedale Vito Fazzi (IT)
Publication Details
- Journal
- Advanced Biology
- Published
- 2026-05-01
- DOI
- https://doi.org/10.1002/adbi.70107
- Primary Topic
- Parkinson's Disease Mechanisms and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00