Parkinson's disease (PD) is a progressive, debilitating movement disorder resulting from the death of the dopamine-synthesizing neurons and, consequently, dopamine deficiency in the basal ganglia, i.e. the brain structures concerned with control of movement. Current therapeutic approaches based on dopamine replacement provide temporary relief of the symptoms but do not cure or slow the disease process. Recent discoveries indicate an important role of neuroinflammation in progressive degeneration of the dopamine neurons and provide an exciting possibility that prevention of chronic neuroinflammatory response in the affected brain structures could be an effective therapeutic strategy to slowing, or perhaps even interrupting the progression of PD. The brain neuroinflammation is mediated by activated macrophage-like cells called microglia, which release proinflammatory chemicals that are injurious to neurons. Based on the recent observations that macrophage-mediated, peripheral tissue inflammation is suppressed by nicotine, we will evaluate a hypothesis that nicotine similarly can suppress the pro-inflammatory activity of microglia in the brain. Suppression of the microglial-mediated neuroinflammation by nicotine could be a mechanism through which nicotine exerts its reported, long-term neuroprotective effects in animal models of PD and may explain the reduced incidence or delayed onset of PD in cigarette smokers. A confirmation of anti-inflammatory effects of nicotine in the brain, might provide the basis for development of new drug treatments designed to mitigate chronic neuroinflammation and thereby slow the progression of Parkinson's disease.