C9orf72 expansion within astrocytes reduces metabolic flexibility in amyotrophic lateral sclerosis
Author:
Affiliation:
1. Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, 385 Glossop Road, Sheffield S10 2HQ, UK
2. The Living Systems Institute, University of Exeter, Stocker Road, Exeter, EX4 4QD, UK
Abstract
Funder
Motor Neurone Disease Association Senior Fellowship
Medical Research Council
MND Association
NIHR Senior Investigator
Academy of Medical Sciences
Sheffield NIHR Biomedical Research Centre
Parkinson’s UK
Publisher
Oxford University Press (OUP)
Subject
Clinical Neurology
Link
http://academic.oup.com/brain/article-pdf/142/12/3771/31499307/awz302.pdf
Reference99 articles.
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3. Astrocyte adenosine deaminase loss increases motor neuron toxicity in amyotrophic lateral sclerosis;Allen;Brain,2019
4. Analysis of the cytosolic proteome in a cell culture model of familial amyotrophic lateral sclerosis reveals alterations to the proteasome, antioxidant defenses, and nitric oxide synthetic pathways;Allen;J Biol Chem,2003
5. Superoxide dismutase 1 mutation in a cellular model of amyotrophic lateral sclerosis shifts energy generation from oxidative phosphorylation to glycolysis;Allen;Neurobiol Aging,2014
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