Axonal Transport Deficits in Parkinson’s Disease: Insights from Neurotoxin, Genetic, and Sporadic Models
Open Access
- 14 May 2026
- journal article
- review article
- Published by MDPI AG in Brain Sciences
- Vol. 16 (5) , 525
Abstract
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.Keywords
Funding Information
- Hangzhou Normal University (4255C50223204043)
This publication has 93 references indexed in Scilit:
- Regulatory imbalance between LRRK2 kinase, PPM1H phosphatase, and ARF6 GTPase disrupts the axonal transport of autophagosomesCell Reports, 2023
- Increased LRRK2 kinase activity alters neuronal autophagy by disrupting the axonal transport of autophagosomesCurrent Biology, 2021
- Neuronal Soma-Derived Degradative Lysosomes Are Continuously Delivered to Distal Axons to Maintain Local Degradation CapacityCell Reports, 2019
- Mitochondrial dysfunction in fibroblasts of Multiple System AtrophyBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2018
- The rescue of microtubule-dependent traffic recovers mitochondrial function in Parkinson's diseaseBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 2014
- Axonal transport deficit in a KIF5A –/– mouse modelneurogenetics, 2012
- PINK1 and Parkin Target Miro for Phosphorylation and Degradation to Arrest Mitochondrial MotilityCell, 2011
- Mitochondrial Dysfunction as a Therapeutic Target in Progressive Supranuclear PalsyJournal of Molecular Neuroscience, 2011
- Dominant-Negative Myosin Va Impairs Retrograde but Not Anterograde Axonal Transport of Large Dense Core VesiclesCellular and Molecular Neurobiology, 2009
- Accelerated α-synuclein aggregation after differentiation of SH-SY5Y neuroblastoma cellsBrain Research, 2004