Abstract
While mutation of α-synuclein is a cause of autosomal-dominant Parkinson’s disease (PD), it is still elusive as to how α-synuclein is involved in the pathogenesis of PD. Here, we show that dopamine-dependent accumulation of α-synuclein in cultured cells results in apoptosis. Furthermore, activation of insulin-like growth factor 1 (IGF-1) pathway can rescue α-synuclein toxicity and suppress α-synuclein aggregation through the activation of PI3K/Akt pathways. These results suggest the therapeutic potential of IGF-1 pathway in Parkinson disease.
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