Rong Chen

This paper maps α-synuclein pathology and dopaminergic degeneration in mice using multimodal imaging and microscopy, showing spread along the nigrostriatal pathway and microstructural changes.

This study shows that gut-to-brain propagation of alpha-synuclein fibrils induces REM sleep behavior disorder and other non-motor and motor Parkinson's disease phenotypes.

This study identifies microglial Lag3 as a key receptor linking extracellular α-synuclein PFF recognition to neurotoxic astrocyte conversion and dopaminergic neurodegeneration.

The paper shows a copper-containing nanozyme worsens alpha-synucleinopathy by increasing nitrosative stress, while a copper-free version reduces pathology in neurodegenerative models.

This study shows neuronal LAG3 is essential for α-synuclein propagation and neurodegeneration in Parkinson's disease, suggesting LAG3 as a therapeutic target.

The paper identifies distinct α-synuclein strains associated with cognitive decline in Parkinson's disease and shows AI-based analysis of these strains improves clinical stratification.

This study identifies Lag3 as a neuronal receptor for Tau preformed fibrils, essential for their uptake, propagation, and transmission in Tauopathies.

This study shows that defects in mitochondrial biogenesis, not mitophagy, are the primary cause of mitochondrial alterations in PINK1-deficient human dopamine neurons.

This study identifies that pathological α-synuclein destabilizes the TSC1-TSC2 complex, activates mTORC1, and enhances protein translation, contributing to neurodegeneration in Parkinson's disease.