Parkinson’s disease (PD) is the most prevalent movement disorder among people over 65 years old. Denervation of dopaminergic neurons in the substantia nigra (SN) results in severely debilitating motor symptoms such as bradykinesia, resting tremor and rigidity (Farrer, 2006; Fearnley and Lees, 1991). Although the etiologies of most common forms of PD remain poorly understood, the disease is generally associated with an inflammatory component that is manifested in part by the presence of activated microglia (central nervous system-resident macrophages) and elevated serum or cerebrospinal fluid levels of pro-inflammatory factors (Block et al., 2007; McGeer and McGeer, 2008; Nagatsu and Sawada, 2005). Several lines of evidence suggest that inflammatory mediators such as tumor necrosis factor (TNF)α, nitric oxide (NO) and Interleukin (IL)-1β derived from non-neuronal cells, including microglia, modulate the progression of PD (Brown, 2007; Hartmann et al., 2003; Whitton, 2007). Whether inflammation is an initiating factor of PD in humans is unclear, but intracranial infusion of bacterial lipopolysaccharide (LPS), a ligand for Toll-like receptor (TLR)4 and a potent activator of microglia, is sufficient to induce the loss of TH+ neurons
