Targeting transcellular transport of α-synuclein for developing disease-modifying therapies for synucleinopathy

Parkinson's disease (PD) is the second most common neurodegenerative disorder and it is characterized by progressive physical disability along with a variety of non-motor symptoms. Drugs that replenish dopamine can partly alleviate the motor symptoms; however, they do not cure the disease itself. Therefore, there is an urgent need for disease modifying therapies that would delay or prevent neurodegeneration. Increasing evidence suggests that α-synudein, a key molecule in PD, is secreted into the extracellular environment and can be transported from cell-to-cell, thereby affecting the physiological state of the neighboring cells in a prion-like manner. Given the potential role of extracellular α-synudein as the cause of disease progression, its prion-like propagation is a promising target for developing disease-modifying therapies for PD and other synudeinopathies.