Parkinson’s Disease (PD) is a progressive neurodegenerative disorder primarily affecting motor function but increasingly recognized for its extensive non-motor features. It is the second most common neurodegenerative disease after Alzheimer’s and typically manifests after the age of 60, although early-onset forms can occur. The core motor symptoms, bradykinesia, resting tremor, rigidity, and postural instability, arise from the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to dopamine depletion in the striatum and dysregulation of basal ganglia circuits. However, PD is a multisystem disorder with widespread neurodegeneration beyond the dopaminergic system, involving noradrenergic, serotonergic, and cholinergic pathways. Non-motor symptoms such as REM sleep behavior disorder, anosmia, depression, autonomic dysfunction, and cognitive decline often precede motor symptoms and worsen with disease progression.
The pathological hallmark of PD is the accumulation of α-synuclein into Lewy bodies and Lewy neurites in affected brain regions. Although most cases are sporadic, several genetic mutations, such as those in SNCA, LRRK2, PARK7, PINK1, and GBA, have been implicated in familial and risk-associated PD, illuminating mechanisms including protein aggregation, impaired lysosomal function, mitochondrial dysfunction, and oxidative stress.
Despite the symptomatic relief provided by dopaminergic therapies such as levodopa and dopamine agonists, disease progression remains unhalted, and long-term use is associated with complications like dyskinesia and motor fluctuations. Ongoing research aims to better define PD subtypes, identify disease-modifying treatments, and understand the interplay of genetic, environmental, and cellular pathways driving pathogenesis.
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