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

Abstract 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 in...

Full description

Saved in:
Bibliographic Details
Published in:Journal of the neurological sciences 2015-10, Vol.357 (1), p.22-27
Main Authors: Ngo, S.T, Steyn, F.J, Huang, L, Mantovani, S, Pfluger, C.M.M, Woodruff, T.M, O'Sullivan, J.D, Henderson, R.D, McCombe, P.A
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Abstract 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 (TNFα) 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.
ISSN:0022-510X
1878-5883
DOI:10.1016/j.jns.2015.06.053