In Vitro Model Shows Copper Disruption of α-Synuclein Clearance in Parkinson's Disease, Highlighting Neurodegenerative Risk.
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).
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Musarò et al. (2026) studied this question.
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