Parkinson's disease is a chronic progressive neurodegenerative disorder primarily affecting dopamine-producing neurons in the central nervous system. It typically manifests after the age of 50, although early-onset cases have been reported. Core symptoms include bradykinesia, resting tremor, and muscular rigidity, which gradually worsen and significantly impair daily life. Currently, there is no cure, but symptoms can be effectively managed and disease progression delayed through medication, surgery, and rehabilitation therapies.
Globally, approximately 100-160 per 100,000 people are affected by this disease, with a slightly higher prevalence in males. Although the exact cause remains unclear, research indicates a link to genetic factors, environmental exposures, and decreased dopamine neurotransmission in the brain. Recent clinical studies have found that non-motor symptoms such as olfactory loss and sleep disturbances may exist years before motor symptoms appear, providing new avenues for early diagnosis.
The precise cause of Parkinson's disease requires further investigation, but current evidence suggests it results from an interplay of genetic and environmental factors. The progressive death of dopamine neurons in the substantia nigra is the main pathological feature, leading to an imbalance in neural transmission within the basal ganglia. Mutations in genes such as SNCA and LRRK2 increase the risk of developing the disease, with about 10-15% of patients having a family history.
Mutations such as PARK7 and PINK1 are associated with mitochondrial dysfunction, impairing neuronal autophagy. Recent genome-wide studies have identified that multiple gene polymorphisms increase susceptibility, although single-gene mutations account for only about 5% of cases. Familial cases often present with early non-motor symptoms.
Symptoms are divided into motor and non-motor categories, often initially affecting one side of the body. The development of motor impairments typically follows the