Disease Basis

Although the neuropathology of PD is well established, the molecular mechanisms underlying neurodegeneration have not been elucidated. Biochemical abnormalities in PD patients include: dysfunction in complex I of the mitochondrial respiratory chain with consequent energy (ATP) depletion, increased free radical damage, and oxidative stress. Environmental factors, e.g., exposure to pesticides and herbicides like rotenone and paraquat, inhibitors of complex I, may be causal in PD. Reduction of ATP reduces proteasomal protein degradation. Defects in protein handling occur in PD and appear to underlie the formation of Lewy bodies, an intracytoplasmic aggregate of several proteins, including a-synuclein and ubiquitin that is a hallmark feature of the disease.

Genetic linkage studies of familial PD have revealed abnormal expression or mutation in at least eight proteins (Table 1), some of which are associated with mitochondrial function (e.g., DJ-1, PINK-1).66

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