Unveiling the mechanism of neurodegeneration in Parkinson's disease
In Parkinson's disease (PD), oxidised dopamine and alpha-synuclein serve as key mediators of mitochondrial and lysosomal dysfunction in midbrain dopaminergic neurons that preferentially degenerate in this progressive movement disorder. The working hypothesis of the EU-funded oxDOPAMINE project is that oxidation of dopamine aberrantly increases in PD. Scientists will investigate pathways of dopamine oxidation that predisposes human neurons to selective vulnerability and degeneration. Based on recent data implicating defective synaptic dopamine metabolism and iron dyshomeostasis in the oxidation of dopamine early in disease pathogenesis, they will study disorders associated with iron accumulation and progressive dopamine neuron degeneration to find common pathogenic mechanisms. Results may lead to novel strategies for restoring synaptic dysfunction and iron homeostasis as a means of preventing neurodegeneration.
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