4.5 Article

Altered expression of metabolic proteins and adipokines in patients with amyotrophic lateral sclerosis

Journal

JOURNAL OF THE NEUROLOGICAL SCIENCES
Volume 357, Issue 1-2, Pages 22-27

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.jns.2015.06.053

Keywords

Amyotrophic lateral sclerosis; Metabolism; Body mass index; Adipose; Adipokines; Neurodegeneration

Funding

  1. Motor Neurone Disease Research Institute of Australia (MNDRIA)
  2. Royal Brisbane & Women's Hospital Foundation
  3. MND and Me Foundation funds
  4. MNDRIA Bill Gole Fellowship
  5. University of Queensland
  6. Scott Sullivan MND Research Fellowship - Queensland Brain Institute
  7. Royal Brisbane & Womens Hospital Foundation
  8. MND and Me Foundation
  9. School of Biomedical Sciences, University of Queensland

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Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease characterized by the loss of upper cortical and lower motor neurons. ALS causes death within 2-5 years of diagnosis. Diet and body mass index influence the clinical course of disease, however there is limited information about the expression of metabolic proteins and fat-derived cytokines (adipokines) in ALS. In healthy controls and subjects with ALS, we have measured levels of proteins and adipokines that influence metabolism. We find altered levels of active ghrelin, gastric inhibitory peptide (GIP), pancreatic polypeptide (PP), lipocalin-2, plasminogen activator inhibitor-1 (PAI-1), interleukin-6 (IL-6) and 8 (IL-8), and tumor necrosis factor alpha (TNF alpha) in the plasma of ALS patients relative to controls. We also observe a positive correlation between the expression of plasma nerve growth factor (NGF) relative to disease duration, and an inverse correlation between plasma glucagon and the ALS functional rating scale-revised (ALSFRS-R). Further studies are required to determine whether altered expression of metabolic proteins and adipokines contribute to motor neuron vulnerability and how these factors act to modify the course of disease. Crown Copyright (C) 2015 Published by Elsevier B.V.

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