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

Created on 14 Sep 2026

Authors

Xiaobo Wang, Zhaohui Liu, Wanli W Smith

Published in

Brain sciences. Volume 16. Issue 5. May 14, 2026. Epub May 14, 2026.

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.

PMID:
42192837
Bibliographic data and abstract were imported from PubMed on 14 Sep 2026.

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