The Parkinson's disease is a degenerative disease of the central nervous system which is characterised by a slow and progressive neuronal loss, the origin of which is still unknown. From a clinical point of view, this disease is defined by a lack of movement, rigidity and tremor. Neuropathological examination of the brain of the patients evidences a massive destruction of the neurons using dopamine as a chemical messenger. These neurons are located in a specific region of the brain called the substantia nigra. The major treatment of this pathology consist in giving to the patients the precursor of dopamine, L-Dopa, which leads to a dramatic alleviation of the clinical symptoms. Nevertheless, after a few years of treatment, the patients suffer from fluctuations in motor performances and display abnormal involuntary movements which are extremely painful. A neurosurgical approach of the disease has also been developed during the last years. This technique is based on the finding that the loss of dopaminergic neurons modifies the activity of others neurons located downstream to the lesions. Their activity is restored by delivering an electrical current using electrodes placed in the brain of the patients. Nevertheless, if all these therapeutical approaches are useful in alleviating the symptoms, they do not slow down the pathological process. Therefore, the etiology the disease should be better understood. Several hypothesis have been proposed to explain the etiology of the disease : 1) For some authors, Parkinson's disease is a consequence of an increased speed of aging. Nevertheless, juvenile forms of the disease have also been described. 2) The involvement of toxic compounds in some parkinsonian syndroms also suggests that environmental factors may play a role in the etiology of the disease. Nevertheless, several epidemiological studies have demonstrated an inverse relationship between cigarette smoking and the prevalence of Parkinson's disease. These data therefore suggest that compounds present in cigarette smoke may protect dopaminergic neurons against the still unknown agent causing the disease. 3) Familial forms of the disease have recently been described, but they represent less than 10 percent of all cases of Parkinson's disease. Therefore, in the absence of a definitive knowledge concerning the etiology of the disease, other approaches were developed with the aim to better understand the molecular mechanism involved in the neuronal degeneration in Parkinson's disease. We now know that the neurons which degenerate in Parkinson's disease are poorly protected against oxygen free radicals, which are species particularly unstable that can attack the cellular constituents. Recent studies even demonstrated that the neurons develop a suicide program called apoptosis in Parkinson's disease. Because in several in vitro models, nicotine blocks the development of apoptosis, the smaller prevalence of Parkinson's disease among the smokers may be explained by this phenomenon. Nevertheless, this hypothesis will required further analysis in vivo experimental models of the disease.