Disruption of axonal transport in neurodegeneration

被引：47

作者：

Berth, Sarah H. ^{[1
,2
]}

Lloyd, Thomas E. ^{[1
,2
]}

机构：

[1] Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD USA

[2] Johns Hopkins Univ, Sch Med, Dept Neurol, 855 N Wolfe St,Suite 248, Baltimore, MD 21205 USA

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2023年 / 133卷 / 11期

关键词：

HEREDITARY SPASTIC PARAPLEGIA; MARIE-TOOTH-DISEASE; ONSET PARKINSONS-DISEASE; CYTOPLASMIC DYNEIN; MUTANT HUNTINGTIN; MOUSE MODEL; MITOCHONDRIAL DYNAMICS; TUBULIN ACETYLATION; ALZHEIMERS-DISEASE; MESSENGER-RNA;

D O I：

10.1172/JCI168554

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

Neurons are markedly compartmentalized, which makes them reliant on axonal transport to maintain their health. Axonal transport is important for anterograde delivery of newly synthesized macromolecules and organelles from the cell body to the synapse and for the retrograde delivery of signaling endosomes and autophagosomes for degradation. Dysregulation of axonal transport occurs early in neurodegenerative diseases and plays a key role in axonal degeneration. Here, we provide an overview of mechanisms for regulation of axonal transport; discuss how these mechanisms are disrupted in neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, hereditary spastic paraplegia, amyotrophic lateral sclerosis, and Charcot-Marie-Tooth disease; and discuss therapeutic approaches targeting axonal transport.

引用

页数：13

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