Mitochondria are considered a target in neurodegenerative disorder since reactive oxygen species generated during ATP generation tip the balance toward neuronal damage and apoptosis (Figure 1). Elevated levels of mitochondrial ROS particularly in the neurons may target the lipid bilayers and cause neurochemical alterations. Further, compromised membrane potential could be associated with enhanced apoptosis due to activation of intrinsic apoptotic pathway. Amelioration of oxidative damage either through chelating ROS or promoting the expression of anti-oxidant enzymes is considered a potential mechanism through which L-NBP exerts its anti-oxidant effect (Peng et al., 2008, 2010).