The majority of patients with Parkinson’s disease (PD) are described as having idiopathic PD, i.e. the cause is unknown. Between 5% and 10% of patients have been shown to have hereditary PD, and some genes involved in PD have been identified but their role in sporadic disease is unclear. The disease has also been linked to toxin exposure, increased oxidative stress, heavy metals and head trauma. However, the condition most likely arises from a convergence of several factors including age-related changes in the brain, genetic predisposition and environmental factors.

The presence of motor symptoms in patients correlates well with the loss of dopaminergic neurons within the substantia nigra pars compacta, and the subsequent loss of dopamine throughout the brain. The mechanisms underlying the neurodegeneration of this specific population of neurons are unknown, but may involve abnormal protein aggregates called Lewy bodies. However, the presence of Lewy bodies is not solely restricted to dopaminergic neurons. Complications arising from dopaminergic therapies, and their general ineffectiveness at treating non-motor symptoms, indicate that other non-dopaminergic systems in the brain are also involved, particularly in advanced stages of the disease.