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Abstract Loss-of-function mutations in PARK2 (parkin) cause early-onset familial Parkinson’s disease (PD) and may also contribute to sporadic PD. While Lewy bodies, enriched in aggregated phosphorylated α-synuclein (α-Syn), are typical in PD, their presence in PARK2-mediated PD remains debated. Using human isogenic PARK2−/− induced pluripotent stem cell-derived neurons, we investigated α-Syn pathology under parkin deficiency.
As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
