Parkinson’s disease is a progressive neurodegenerative disorder primarily affecting movement, but with wide ranging non motor symptoms. It is marked by the loss of dopamine producing neurons in the substantia nigra and by abnormal protein aggregates rich in alpha synuclein. These changes disrupt communication in brain circuits that control movement, emotion and cognition.

Most cases are sporadic and arise from a complex interaction of aging, genetic susceptibility and environmental factors. Several genes are linked to familial forms, including SNCA, LRRK2, PARK2, PINK1 and GBA. Mutations in these genes affect protein handling, mitochondrial function, lysosomal activity and neuronal resilience. Environmental contributors under study include pesticides, solvents, air pollution and head trauma, while smoking and caffeine consumption appear inversely associated with risk.

Diagnosis remains clinical, based on motor features such as tremor, rigidity, slowness and postural instability, supported by response to dopaminergic therapy. Research aims to identify biomarkers in blood, cerebrospinal fluid and imaging that can detect disease earlier or track progression. Experimental assays for misfolded alpha synuclein and advanced MRI and nuclear imaging are central to this effort.

Current treatments are symptomatic. Levodopa and dopamine agonists improve motor function but do not stop neurodegeneration and may cause complications over time. Deep brain stimulation provides relief in selected patients. Intensive research is targeting disease modification through approaches that reduce alpha synuclein accumulation, enhance cellular clearance, protect mitochondria, modulate inflammation and correct specific genetic defects. Cell replacement strategies using stem cell derived dopamine neurons are also being tested, raising hope for more effective and personalized therapies.