Axonal Transport Deficits in Parkinson's Disease: Insights from Neurotoxin, Genetic, and Sporadic Models

Parkinson's disease (PD) is a prevalent neurodegenerative disorder, characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta and the accumulation of Lewy bodies. Over recent decades, various cellular mechanisms underlying PD have been elucidated, including autophagy, mitochondrial dysfunction, neuroinflammation, and axonal transport. Among them, axonal transport plays a critical role in maintaining the dynamic homeostasis of proteins, membrane-bound organelles, and cellular metabolism within neurons. Unfortunately, a comprehensive overview of axonal transport in PD remains absent. In this review, we synthesized the current literature on axonal transport in PD, leveraging neurotoxic and genetic models to explore the causes and consequences of axonal transport alterations in PD. Through this summary, we aim to deepen our understanding of PD pathogenesis and provide potential therapeutic targets for intervention.