Parkinson's disease (PD) is a progressive, disabling neurodegenerative disorder characterized by an insidious onset with variable expression of predominant motor, vegetative and psychopathological symptoms (1). Ongoing loss of nigral dopaminergic presynaptic neurons mainly leads to clinical diagnosis due to occurrence of motor symptoms, which results from a reduction of about 70-80% striatal dopamine. But neuronal cell loss of other neu-rotransmitter systems also takes place, for instance, in the predominant norepinephrinergic locus ceruleus, the serotonergic Raphe nuclei or the cholinergic nucleus basalis Meynert. These changes induce disturbances of cortical and limbic projections or dysfunction of vegetative innervation in the region of the dorsal nucleus of the nervus vagus or the ganglia of the sympathetic (1,2). Nowadays it is generally accepted, that glutamatergic, gamma aminobutyric acid-(GABA)ergic, cholinergic, tryptaminergic, noradrenergic, adrenergic, serotonergic and peptidergic neurons show serious cytoskeletal damage in addition to the altered nigrostriatal dopaminergic pathway accompanied by altered glial cell function with, for instance, increased synthesis and secretion of pro-inflammatory cytokines in PD (1,3). Increasing evidence suggests that the various hypotheses on the neurodegenerative processes, such as mitochondrial dysfunction, oxidative stress, increased excitotoxin and nitric oxide synthesis, etc. complement each other in PD (4,5). Thus finally, neuronal cell death occurs as a consequence of intracellular reduced energy metabolism accompanied by a slowly occurring neuronal loss of function. This leads to intracellular metabolic changes like increased apoptosis and necrosis, decreased synthesis of physiologic growth factor, altered function of cytoskeleton metabolizing proteases and induction of mediators of inflammation. As a result, neuronal cell death occurs in various extents in various neurotransmitter systems (6).

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