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Parkinson's disease (PD) is a degenerative disorder of the central nervous system characterized by the clinically asymmetric onset of resting tremor, bradykinesia, rigidity and postural instability. [1-3]
Non-motor complications, such as neuropsychiatric disturbances, can appear prior to the onset of motor complications or can result from complex interactions between the progressive and widespread pathological changes of the disease. Non-motor symptoms observed in PD patients include mood and anxiety disorders, fatigue and apathy, psychosis, cognitive impairments, restlessness, face flushing, sweating, increased salivation and sleep disorders.[4,5]
The primary pathology of PD is the death of dopaminergic neurons in the substantia nigra and the nigrostriatal pathway of the midbrain (Figure 1), with Lewy bodies (intracytoplasmic inclusion deposits of aggregated alpha-synuclein and ubiquitin protein, and damaged nerve cells[6]) present in proportions of surviving substantia nigra pars compacta neurons.
The reduction in dopamine concentrations resulting from this neuronal death causes neurons in the basal ganglia to adopt an abnormal pattern of burst firing, leading to involuntary movements.
Typically, degeneration of approximately 70-80% of dopaminergic neurons in the substantia nigra occurs before symptoms become clinically apparent.[7]
The exact aetiology of the death of dopaminergic neurons is not known, although there is growing evidence to suggest it is a combination of genetic and environmental factors.[8-11]