Molecules for Neuroprotection and Regeneration in Animal Models of Parkinson’s Disease

Parkinson’s disease (PD) is a progressive neurodegenerative disease characterized clinically by bradykinesia, rigidity, and resting tremor. The motor abnormalities are associated with a specific loss of dopamine (DA) neurons in the substantia nigra pars compacts (SNc) and the secondary depletion of striatal DA levels (1). While the loss of striatal DA correlates with the severity of clinical disability, clinical manifestations of PD are not apparent until 80–85% of SNc neurons have degenerated and striatal DA levels are depleted by 60–80% (2) Administration of L-Dopa, the precursor of DA, initially relieves Parkinsonian motor signs, but long-term use is associated with severe fluctuations in drug response. As pathologic changes precede the manifestation of clinical symptoms, it is reasonable to develop strategies to protect remaining DA neurons during the subclinical stage.