Unraveling the mystery: How autophagy deficiency in dopaminergic neurons drives human Parkinson’s disease
Abstract Alpha-synuclein (α-synuclein), a key component of Lewy body pathology, is a classical hallmark of Parkinson’s disease. In previous studies, our group has examined dopaminergic neuron-specific Atg7 autophagy-deficient mice, observing α-synuclein aggregation in vivo. This pathological process...
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| Main Authors: | , |
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| Format: | Article |
| Language: | English |
| Published: |
BMC
2025-07-01
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| Series: | Molecular Brain |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s13041-025-01235-5 |
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| Summary: | Abstract Alpha-synuclein (α-synuclein), a key component of Lewy body pathology, is a classical hallmark of Parkinson’s disease. In previous studies, our group has examined dopaminergic neuron-specific Atg7 autophagy-deficient mice, observing α-synuclein aggregation in vivo. This pathological process led to dopamine neuron loss and age-related motor impairments. Further, in a recent study, we developed a new mouse model by crossing human α-synuclein bacterial artificial chromosome transgenic mice with dopaminergic neuron-specific Atg7 conditional knockout mice to further investigate these mechanisms. These model mice exhibited accelerated Lewy body-like pathology and motor dysfunction, providing additional evidence that autophagy deficiency exacerbates synuclein toxicity in vivo. This nano-review provides essential clues that autophagy deficiency in dopamine neurons may contribute to the onset of human synuclein diseases. |
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| ISSN: | 1756-6606 |