Golgi fragmentation in amyotrophic lateral sclerosis, an overview of possible triggers and consequences Sundaramoorthy, Vinod, Sultana, Jessica M. and Atkin, Julie D. 2015, Golgi fragmentation in amyotrophic lateral sclerosis, an overview of possible triggers and consequences, Frontiers in Neuroscience, vol. 9, pp. 1-11, doi: 10.3389/fnins.2015.00400. Attached Files Name Description MIMEType Size Downloads sundaramoorthy-golgifragmentation-2015.pdf Published version application/pdf 1.01MB 4 Title Golgi fragmentation in amyotrophic lateral sclerosis, an overview of possible triggers and consequences Author(s) Sundaramoorthy, Vinod orcid.org/0000-0001-6309-8031 Sultana, Jessica M. Atkin, Julie D. Journal name Frontiers in Neuroscience Volume number 9 Article ID 400 Start page 1 End page 11 Total pages 11 Publisher Frontiers Media Place of publication Lausanne, Switzerland Publication date 2015-10-27 ISSN 1662-453X Keyword(s) Science & Technology Life Sciences & Biomedicine Neurosciences Neurosciences & Neurology amyotrophic lateral sclerosis Golgi fragmentation ER stress axonal degeneration secretory trafficking inhibition autophagy dysfunction ENDOPLASMIC-RETICULUM STRESS PROTEIN-DISULFIDE-ISOMERASE ANTERIOR HORN CELLS CU,ZN SUPEROXIDE-DISMUTASE NUCLEOTIDE EXCHANGE FACTOR MOTOR-NEURON DEGENERATION SECRETORY PATHWAY HIPPOCAMPAL-NEURONS AXONAL-TRANSPORT Summary 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. Language eng DOI 10.3389/fnins.2015.00400 Indigenous content off Field of Research 1109 Neurosciences 1701 Psychology 1702 Cognitive Sciences HERDC Research category C1 Refereed article in a scholarly journal Copyright notice ©2015, Sundaramoorthy, Sultana and Atkin Free to Read? Yes Use Rights Persistent URL http://hdl.handle.net/10536/DRO/DU:30136634 Document type: Journal Article Collections: Faculty of Health School of Medicine Open Access Collection Related Links Link Description Link to full-text (open access)     Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved. Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au. Versions Version Filter Type Mon, 11 May 2020, 12:30:05 EST Tue, 12 May 2020, 05:01:42 EST Tue, 12 May 2020, 08:05:31 EST Wed, 13 Jan 2021, 13:20:22 EST Wed, 17 Feb 2021, 09:15:15 EST Wed, 17 Feb 2021, 09:42:38 EST Filtered Full Citation counts:   Cited 0 times in TR Web of Science Cited 0 times in Scopus Search Google Scholar Access Statistics: 6 Abstract Views, 4 File Downloads  -  Detailed Statistics Created: Mon, 11 May 2020, 12:30:05 EST

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