Parkinson's disease (PD) is the most frequent neurodegenerative disorder after Alzheimer's disease. It is characterized by motor symptoms (rigidity, tremor, slowness of movements), and non-motor symptoms (neuropsychological, psychiatric, pain ...). Neuronal death initiates in the brainstem and extends progressively through the entire cortex. The processes leading to cell death are poorly understood. Pathological cells exhibit abnormal deposits, called Lewy bodies, which contain numerous proteins. A major constituent of these protein deposits is alpha-synuclein. It has recently been demonstrated, in the Laboratory of Molecular Biophysics of the CNRS (Scientific Research National Center) in Orleans, that α-synuclein interacts with Cytogaligin, a protein produced by the proapoptotic GALIG gene. Cytogaligin could thus be a factor regulating α-synuclein activity or aggregation. It is postulated that the level of expression of the GALIG gene is different in Parkinson's disease patients compared with control subjects.