Abstract
This chapter presents studies that established a clear and intriguing genetic link between α-synuclein and cysteine-string protein-α (CSP α) which are presynaptic proteins that are independently linked to neurodegeneration. The discovery of dominant α-synuclein Parkinson mutations and α-synuclein's tendency to aggregate has lead to the hypothesis that α-synuclein causes PD by a toxic gain-of-function, that is, a pathological function. The finding suggests that the seven amino acid changes between human and mouse α-synuclein are important for the pathogenesis of this neurodegenerative phenotype. The finding also indicates that it is possible to tease apart the physiological and pathological functions of α-synuclein using transgenic approaches. It is suggested that the normal physiological function of α-synuclein is neuroprotective to CSP α deletion. It is found that preservation of synaptic connections is also critical for PD treatments as the efficacy of dopamine replacement therapy closely depends on the remaining striatal terminals.
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