ABSTRACT
Parkinson’s disease (PD) is one of the most common neurological disorders, afflicting millions of individuals worldwide. Idiopathic PD, the prevailing form of disease, has a late age onset, and results from a slow, progressive, and complex degeneration of the nigrostriatal dopaminergic neurons. Accordingly, PD patients experience a gradual deterioration of motor performance and show signs of dyskinesia, rigidity, gait imbalance, and/or uncontrollable resting tremors. When the disease reaches an advanced stage, without medical support, PD patients can virtually be debilitated and may also suffer cognitive and behavioral dysfunctions such as dementia, anxiety, and depression. These clinical manifestations are caused by the marked loss of dopamine containing neurons in the substantia nigra pars compacta and by the vast depletion of the key neurotransmitter, dopamine (DA). Although current therapeutic paradigms largely target the replenishing of the lost DA in the brain or temporarily correcting the declined motor functions by improving mobility and reducing tremors and stiffness, no protective strategies have yet been developed to clinically guard the remaining intact neurons from undergoing degeneration or to restore and remodel the degenerated neurons back to function.
