GALIG Gene Expression in Parkinson's Disease
GALIG Gene Expression in Parkinson's Disease
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.
Inclusion Criteria:

 -  Patients with Parkinson's Disease according to the criteria of the UKPDBB (UK
 Parkinson's disease brain bank).

 Exclusion Criteria:

 -  Insane patient arriving without a third party.

 -  Patient with Parkinson's disease arising from another etiology.