SNCA and Parkinson disease: In addition to overall decreases in mitochondrial respiration, α-synuclein has been reported to cause functional deficits, particularly at the level of Complex I. Cells expressing wild-type or mutant α-synuclein reportedly have deficits in Complex I (Chinta et al., 2010; Devi et al., 2008), which are also observed in post-mortem PD brain (Janetzky et al., 1994; Parker et al., 1989; Schapira et al., 1989).