ArticleCommunications biology2024
Human α-synuclein aggregation activates ferroptosis leading to parvalbumin interneuron degeneration and motor learning impairment.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Microglia in Alzheimer's Disease: From Homeostatic Guardians to Multifaceted Drivers of Neuropathology.Cells · 2026Review
- Cell-Type-Selective Cortical Pathology and Functional Deficits in Synucleinopathy.bioRxiv : the preprint server for biology · 2026Article
- Braking Parkinson's progression: the hypothetical druggable role of striatal parvalbumin interneurons.NPJ Parkinson's disease · 2026Review
- When Pathways Converge: Iron, Lipid Peroxidation, and α-Synuclein in Ferroptosis-Driven Dopaminergic Neurodegeneration.Journal of neurochemistry · 2026Review
- The Multilayered Landscape of Ferroptosis: Plasticity, Propagation, and Evolutionary Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Ferroptosis-immune crosstalk in CNS diseases: mechanisms and translational insights.Frontiers in immunology · 2026Review
- Ferroptosis in Parkinson's disease: a review of molecular mechanisms and emerging therapeutic strategies.Frontiers in neuroscience · 2026Review
- Endothelial ferroptosis in blood-brain barrier dysfunction and neuroinflammation: mechanisms and immune-vascular crosstalk.Frontiers in immunology · 2026Review
- Ferroptosis and Iron Homeostasis: Molecular Mechanisms and Neurodegenerative Disease Implications.Antioxidants (Basel, Switzerland) · 2025Review
- NFE2L1 as a central regulator of proteostasis in neurodegenerative diseases: interplay with autophagy, ferroptosis, and the proteasome.Frontiers in molecular neuroscience · 2025Review
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9 authors.
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Abstract
The accumulation of α-synuclein induces neuronal loss in midbrain nuclei and leads to the disruption of motor circuits, while the pathology of α-synuclein in cortical regions remains elusive. To better characterize cortical synucleinopathy, here we generate a mouse model with the overexpression of human α-synuclein in the primary motor cortex (M1) of mice. A combination of molecular, in vivo recording, and behavioral approaches reveal that cortical expression of human α-synuclein results in the overexcitation of cortical pyramidal neurons (PNs), which are regulated by the decreased inhibitory inputs from parvalbumin-interneurons (PV-INs) to impair complex motor skill learning. Further mechanistic dissections reveal that human α-synuclein aggregation activates ferroptosis, contributing to PV-IN degeneration and motor circuit dysfunction. Taken together, the current study adds more knowledge to the emerging role and pathogenic mechanism of ferroptosis in neurodegenerative diseases.
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