Golgi fragmentation in amyotrophic lateral sclerosis, an overview of possible triggers and consequences

Vinod Sundaramoorthy, Jessica M. Sultana, Julie D. Atkin*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

31 Citations (Scopus)
60 Downloads (Pure)

Abstract

Amyotrophic Lateral Sclerosis (ALS) is an invariably fatal neurodegenerative disorder, which specifically targets motor neurons in the brain, brain stem and spinal cord. Whilst the etiology of ALS remains unknown, fragmentation of the Golgi apparatus is detected in ALS patient motor neurons and in animal/cellular disease models. The Golgi is a highly dynamic organelle that acts as a dispatching station for the vesicular transport of secretory/transmembrane proteins. It also mediates autophagy and maintains endoplasmic reticulum (ER) and axonal homeostasis. Both the trigger for Golgi fragmentation and the functional consequences of a fragmented Golgi apparatus in ALS remain unclear. However, recent evidence has highlighted defects in vesicular trafficking as a pathogenic mechanism in ALS. This review summarizes the evidence describing Golgi fragmentation in ALS, with possible links to other disease processes including cellular trafficking, ER stress, defective autophagy, and axonal degeneration.

Original languageEnglish
Article number400
Pages (from-to)1-11
Number of pages11
JournalFrontiers in Neuroscience
Volume9
DOIs
Publication statusPublished - 2015

Bibliographical note

Copyright the Author(s) 2015. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

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