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Parkin reinvents itself to regulate fatty acid metabolism by tagging CD36

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Parkin reinvents itself to regulate fatty acid metabolism by tagging CD36

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Use of viral vectors to create animal models for Parkinson's disease

Use of viral vectors to create animal models for Parkinson's disease

Mimicking Phosphorylation at Serine 87 Inhibits the Aggregation of Human α-Synuclein and Protects against Its Toxicity in a Rat Model of Parkinson's Disease

Mitochondrial Dysfunction in Genetic Animal Models of Parkinson's Disease

Neurodegenerative phenotypes in an A53T-synuclein transgenic mouse model are independent of LRRK2

Alpha-Synuclein Effects at the ER-to-Golgi Level and Potential Biomarkers in Rat Models of the Early Phase of Parkinson's Disease

Dopaminergic Neuronal Loss, Reduced Neurite Complexity and Autophagic Abnormalities in Transgenic Mice Expressing G2019S Mutant LRRK2

Parkin promotes the ubiquitination and degradation of the mitochondrial fusion factor mitofusin 1

Motor Deficits upon Alpha-Synuclein Expression in the Nigrostriatal System Are Due to a Loss of Dopaminergic Vesicles and Reduced Dopamine Release at an early Stage of Neurodegeneration

The anti-Parkinsonian drug selegiline delays the nucleation phase of α-synuclein aggregation leading to the formation of nontoxic species

Neurodegenerative phenotypes in an A53T-synuclein transgenic mouse model are independent of LRRK2

Use of viral vectors to create animal models for Parkinson's disease

Dopaminergic Neuronal Loss, Reduced Neurite Complexity and Autophagic Abnormalities in Transgenic Mice Expressing G2019S Mutant LRRK2

The anti-Parkinsonian drug selegiline delays the nucleation phase of α-synuclein aggregation leading to the formation of nontoxic species

Alpha-Synuclein Effects at the ER-to-Golgi Level and Potential Biomarkers in Rat Models of the Early Phase of Parkinson's Disease

Mimicking Phosphorylation at Serine 87 Inhibits the Aggregation of Human α-Synuclein and Protects against Its Toxicity in a Rat Model of Parkinson's Disease

Use of viral vectors to create animal models for Parkinson's disease

Mitochondrial Dysfunction in Genetic Animal Models of Parkinson's Disease

Parkin promotes the ubiquitination and degradation of the mitochondrial fusion factor mitofusin 1

Motor Deficits upon Alpha-Synuclein Expression in the Nigrostriatal System Are Due to a Loss of Dopaminergic Vesicles and Reduced Dopamine Release at an early Stage of Neurodegeneration