Abstract.
The cause of neuronal cell death in Parkinson's disease is still an enigma. However, recent results obtained by analyses of postmortem brain suggest that a mitochondria-dependent apoptotic signal was activated. The involvement of dopamine-derived endogenous neurotoxin in the pathogenesis of PD was also indicated. N-Methyl(R)salsolinol was proved to be selectively toxic to dopamine neurons and its level increased in parkinsonian CSF. The enzyme which determines the level of N-methyl(R)salsolinol, (R)salsolinol N-methyltransferase, was found increased in the lymphocytes prepared from PD patients. The mechanism of dopamine cell death by N-methyl(R)salsolinol was studied in vitro. N-Methyl(R)salsolinol induced apoptosis in human dopaminergic neuroblastoma cells. It was suggested that in the mitochondria there is a molecule which interacts with N-methyl(R)salsolinol and initiates an apoptotic signal.
Similar content being viewed by others
Author information
Authors and Affiliations
Additional information
Correspondence to: Dr. W. Maruyama
Rights and permissions
About this article
Cite this article
Maruyama, W., Naoi, M. Cell death in Parkinson's disease. J Neurol 249 (Suppl 2), ii06–ii10 (2002). https://doi.org/10.1007/s00415-002-1202-6
Issue Date:
DOI: https://doi.org/10.1007/s00415-002-1202-6