Parkinson’s disease is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra, and its prevalence is rising with global population aging. Current treatments are largely symptomatic, and as the disease advances, dopamine imbalance frequently causes motor complications that severely impair quality of life. Our research is based on the finding that synaptic dysfunction at dopaminergic terminals occurs before neuronal death. By investigating the molecular mechanisms that regulate synapse formation and maintenance, particularly the role of C1q family proteins, we aim to establish proof-of-concept for a novel disease-modifying therapy that targets synapses directly, moving beyond symptomatic relief.