| dc.description.abstract | PD is the most common form of parkinsonism, a clinical syndrome characterized by akinesia/bradykinesia, muscle rigidity, and resting tremor. The pathological hallmarks of the disease are loss of dopaminergic neurons, intra-cytoplasmic protein inclusion called Lewy bodies, and neuroinflammation with reactive microglial cells in the PD brain. In most patients the disease is of unknown etiology, but familial PD accounts for approximately 10% of the cases. Several disease mechanisms have been implicated, including alpha-synuclein misfolding, oxidative stress, mitochondrial dysfunction, and defective cellular protein clearance. In addition to the cardinal motor symptoms of PD, the clinical picture also includes several non-motor symptoms (e.g., dementia, psychiatric disorders, sleep disorders, autonomic dysfunction, and pain) which is associated with functional impairment and poor health-related quality of life. No disease-modifying treatments are available for PD today. Dopaminergic therapy offers good control of initial motor symptoms, but non-motor symptoms often require non-dopaminergic approaches. As the disease progresses patients will experience motor complications such as “wearing off” and dyskinesias. While some of these symptoms might be alleviated by alterations in the pharmacologic regimen, some might benefit from advanced device-aided therapy, including levodopa-carbidopa intestinal gel, continuous infusion of apomorphine, and deep brain stimulation. | eng |