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Ultimately, these are scientifically supported and highly bioavailable

Mitochondrial dysfunction associated with increased oxidative stress and -synuclein accumulation in PARK2 iPSC-derived neurons and postmortem brain tissue

10.1016/j.biolcel.2004.03.010 Biol

Acknowledgements The authors would like to thank members of the Hubrecht Institute Flow Cytometry and Animal facilities for essential support
