Unveiling the significance of synaptic proteins in parkinson's pathogenesis: A review

Parkinson's disease (PD) is a progressive neurodegenerative disorder that leads to death of dopaminergic neurons and deficiency of dopamine. It is the second most common neurodegenerative disorder worldwide after Alzheimer's disease (AD). It is mostly prevalent in elderly people above age 60. Clinical manifestations of PD include motor symptoms like tremor, akinesia, rigidity and gait imbalance; whereas non-motor symptoms include impaired olfaction and GI dysfunction. Α-synuclein is the major pathological hallmark of PD pathology. It aggregates and leads to formation of fibrils and Lewy bodies. It is a pre-synaptic protein that normally governs synaptic vesicle recycling. However, its aberration leads to its aggregation. There are several other synaptic proteins besides α-synuclein, and they might also have a pathological role. These synaptic proteins include synucleins (beta-synuclein, gamma-synuclein), synaptophysin, synaptobrevin, synaptogyrin, synaptotagmin and synaptojanin. In this review, we aim to explore underlying pathological role of these proteins. Clearer insights into the role of these synaptic proteins might aid in identifying newer targets which subsequently leads to development of novel therapeutics that target progression of the disease.