Abstract: Parkinson’s disease (PD) has a complex and multifactorial pathophysiology. Various studies, conducted both in pre-clinical models and PD patients, have reported a link between the disruption of calcium (Ca2+) homeostasis and the subsequent development of PD. Ca2+ regulation is crucial for neuronal survival, differentiation, exocytosis at synapses, gene transcription, and proliferation. In PD, disturbances in calcium homeostasis have been correlated with the selective degeneration of dopaminergic neurons within the substantia nigra pars compacta (SNpc), compared to neurons within other regions of the brain. More recently, there has been growing evidence to support the contribution of transient receptor potential (TRP) channels in calcium-mediated excitotoxicity and oxidative stress-induced death of dopaminergic neurons in PD.