Affiliations: Department of Neurology, University of Szeged, Szeged, Hungary | Neuroscience Research Group of the Hungarian Academy of Sciences and University of Szeged, Szeged, Hungary | Department of Physiology, Anatomy and Neuroscience, University of Szeged, Szeged, Hungary
Note:  Correspondence to: László Vécsei, Tel.: +36 62 545 348; Fax: +36 62 545 597; E-mail: firstname.lastname@example.org
Abstract: The pathomechanism behind the neurodegenerative process in Parkinson's disease involves damage to the dopaminergic and nondopaminergic systems with dysfunctioning of the dopaminergic-glutamatergic circuitry in the basal ganglional neural processing. Excitotoxicity may contribute markedly to neuronal damage and loss. Beside the cardinal motor signs of the disease, non-motor symptoms, including mental disturbances, are characteristic features of the clinical course. Affective or autonomic changes may precede motor symptoms. Neuroprotective drugs are not yet available. However, new modes of therapy targeting the defective dopaminergic-glutamatergic system might also be effective both for symptomatologic treatment and for neuroprotection. Alterations in the kynurenine pathway have been demonstrated in Parkinson's disease. Preclinical studies suggest that intervention in the kynurenine pathway may result in neuroprotection and additionally alleviate the symptoms through influencing the glutamatergic neurotransmission.