Parkinson disease
Core of basic research: Focus on Lewy bodies formed by α-synuclein (α-Syn) aggregation, explore Parkin/PINK1-mediated mitophagic defects, abnormal kinase activity of LRRK2 mutations, and the mechanism of selective degeneration of midbrain substantia nigra dopaminergic neurons.
Core key proteins: α-Syn (α-synuclein producing toxicity upon aggregation), Parkin/PINK1 (mediate mitophagy, deficiency causes mitochondrial damage), DJ-1 (antioxidant protein, mutation causes oxidative stress), LRRK2 (kinase, activation upon mutation promotes neuronal damage), UCH-L1 (ubiquitination-related enzyme, dysfunction affects protein degradation), TH (tyrosine hydroxylase, key enzyme for dopamine synthesis), Dopamine receptor (signal transduction).
Core key proteins: α-Syn (α-synuclein producing toxicity upon aggregation), Parkin/PINK1 (mediate mitophagy, deficiency causes mitochondrial damage), DJ-1 (antioxidant protein, mutation causes oxidative stress), LRRK2 (kinase, activation upon mutation promotes neuronal damage), UCH-L1 (ubiquitination-related enzyme, dysfunction affects protein degradation), TH (tyrosine hydroxylase, key enzyme for dopamine synthesis), Dopamine receptor (signal transduction).
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