Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra and the accumulation of alpha-synuclein aggregates (Lewy bodies). Clinically, PD presents with bradykinesia, rigidity, resting tremor, and postural instability, alongside a broad range of non-motor symptoms including cognitive impairment, mood disorders, sleep disturbances, autonomic dysfunction, and sensory changes.

Disease progression is highly variable and influenced by genetic, environmental, and age-related factors. While most cases are idiopathic, monogenic forms involving genes such as LRRK2, GBA, SNCA, and PARKIN have provided insight into disease mechanisms, including mitochondrial dysfunction, impaired proteostasis, and neuroinflammation.

Therapeutic strategies remain centered on dopaminergic replacement and modulation:

• Levodopa/carbidopa remains the gold standard for symptomatic control.
• Dopamine agonists and MAO-B inhibitors are used in early or adjunctive therapy.
• COMT inhibitors prolong levodopa activity in advanced disease.

Advanced interventions include deep-brain stimulation (DBS) targeting the subthalamic nucleus or globus pallidus interna, particularly for patients with motor fluctuations or dyskinesias. Emerging approaches under investigation include alpha-synuclein–targeted antibodies, gene therapies delivering dopamine-synthesizing enzymes, and neuroprotective strategies aimed at slowing disease progression.