A
Andrew J. Grierson
Researcher at University of Sheffield
Publications - 67
Citations - 5473
Andrew J. Grierson is an academic researcher from University of Sheffield. The author has contributed to research in topics: Amyotrophic lateral sclerosis & Neurofilament. The author has an hindex of 33, co-authored 63 publications receiving 4988 citations. Previous affiliations of Andrew J. Grierson include University of Amsterdam & King's College London.
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Journal ArticleDOI
Role of Axonal Transport in Neurodegenerative Diseases
TL;DR: The role of axonal transport in neurodegenerative disease is reviewed and disruption of axon transport is an early and perhaps causative event in many of these diseases.
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Molecular pathways of motor neuron injury in amyotrophic lateral sclerosis
TL;DR: Ongoing research on the cellular pathways highlighted in this Review is predicted to open the door to new therapeutic interventions to slow disease progression in ALS.
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Familial amyotrophic lateral sclerosis-linked SOD1 mutants perturb fast axonal transport to reduce axonal mitochondria content
Kurt J. De Vos,Kurt J. De Vos,Anna L. Chapman,Maria E. Tennant,Catherine Manser,Elizabeth L. Tudor,Kwok-Fai Lau,Janet Brownlees,Steven Ackerley,Pamela J. Shaw,Declan M. McLoughlin,Christopher Shaw,P. Nigel Leigh,Christopher C.J. Miller,Andrew J. Grierson +14 more
TL;DR: Time-lapse microscopy is used to monitor for the first time the effect of mutant S OD1 on fast axonal transport (FAT) of bona fide cargoes in living neurons and finds that mutant SOD1 damages transport of both mitochondria and MBOs, and that the precise details of this damage are cargo-specific.
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Mitochondrial Function and Actin Regulate Dynamin-Related Protein 1-Dependent Mitochondrial Fission
TL;DR: It is shown that inhibitors of electron transport, ATP synthase, or the permeability transition pore (mtPTP) induced reversible mitochondrial fission and the results suggest that the actin cytoskeleton is involved in mitochondrial fissions by facilitating mitochondrial recruitment of DRP1.
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The C9orf72 protein interacts with Rab1a and the ULK1 complex to regulate initiation of autophagy.
Christopher P. Webster,Emma F. Smith,Claudia S. Bauer,Annekathrin Moller,Guillaume M. Hautbergue,Laura Ferraiuolo,Monika A Myszczynska,Adrian Higginbottom,Matthew J. Walsh,Alexander J. Whitworth,Brian K. Kaspar,Kathrin Meyer,Pamela J. Shaw,Andrew J. Grierson,Kurt J. De Vos +14 more
TL;DR: The data identify C9orf72 as a novel Rab1a effector in the regulation of autophagy and indicate that C 9orf72 haploinsufficiency and associated reductions in Autophagy might be the underlying cause of C9ALS/FTD‐associated p62 pathology.