Benefits for Parkinson’s Disease (PD)
Parkinson’s Disease (PD) is a disorder of the central nervous system that affects between one and one-and-a-half million Americans. Clinically, the disease is characterized by a decrease in spontaneous movements, gait difficulty, postural instability, rigidity and tremor. PD may appear at any age, but it is uncommon in people younger than 30, and the risk of developing it increases with age.
Oxidative stress appears to play an important role in neuronal degeneration associated with PD (Beal. 1992; Burke, 1998; Adams et al.. 2001; Sayreet al., 2001). The depletion of glutathione (GSH) in the brain is the earliest know indicator of oxidative stress in presymptomatic PD. (Jenner, 1993). Studies using both in vitro and in vivo models have suggested that pretreatment with R-Lipoic acid increases cellular levels of GSH, probably by preventing its depletion thereby protecting mitochondrial integrity (Suzuki et al., 1991; Scott et al., 1994; Hanet al., 1997; Xu and Wells, 1996; Lykkesfeldt et al., 1998; Kagen et al., 1992).
R-lipoic acid administration has been reported to result in increased ambulatory activity and improved memory in aged animals and to partially restore age-associated mitochondrial decay in both the liver and heart.
Results with previous studies suggest that R-Lipoic acid may be an effective neuroprotective agent in age-associated neurodegeneration. Utilizing the PC 12 cell model system, we propose that R-Lipoic acid administration could be an effective way of circumventing or delaying mitochondrial dysfunction associated with PD.
Treatment with R-Lipoic acid alone seems to significantly increase GSH levels only in whole cell preparations but not in mitochondrial extracts. However, pretreatment of cells with R-Lipoic acid appears to prevent BSO-mediated GSH depletion in both whole cells and mitochondria. Decreases in mitochondrial NADH dehydrogenase activity associated with GSH depletion also appear to be preserved via R-Lipoic acid pretreatment.