GDF-15, a mitochondrial disease biomarker, is associated with the severity of multiple sclerosis.


Journal

Journal of the neurological sciences
ISSN: 1878-5883
Titre abrégé: J Neurol Sci
Pays: Netherlands
ID NLM: 0375403

Informations de publication

Date de publication:
15 Oct 2019
Historique:
received: 02 02 2019
revised: 14 08 2019
accepted: 14 08 2019
pubmed: 3 9 2019
medline: 15 9 2020
entrez: 3 9 2019
Statut: ppublish

Résumé

GDF-15, a member of the transforming growth factor beta superfamily, regulates inflammatory and apoptotic pathways in various diseases, such as heart failure, kidney dysfunction, and cancer. We aimed to clarify potentially confounding variables affecting GDF-15 and demonstrate its utility as a mitochondrial biomarker using serum samples from 15 patients with mitochondrial diseases (MD), 15 patients with limbic encephalitis (LE), 10 patients with multiple sclerosis/neuromyelitis optica spectrum disorders (MS/NMOSD), and 19 patients with amyotrophic lateral sclerosis (ALS). GDF-15 and FGF-21 were significantly elevated in MD. GDF-15 and FGF-21 showed a good correlation in MD but not in LE, MS, and ALS. GDF-15 was potentially influenced by age in LE, MS/NMOSD, and ALS but not in MD. FGF-21 was not correlated with age in MS/NMOSD, ALS, LE, and MD. GDF-15 was not correlated with clinical features in LE or BMI or body weight in ALS. GDF-15 positively correlated with the Expanded Disability Status Scale (EDSS) in MS/NMOSD, while EDSS showed no correlation with age. In conclusion, the results revealed that GDF-15 may be influenced by EDSS in MS/NMOPSD and by age in LE, MS/NMOSD, and ALS but not in MD. Mitochondrial damage in MS/NMOSD is a potentially confounding variable affecting GDF-15.

Identifiants

pubmed: 31476622
pii: S0022-510X(19)30361-2
doi: 10.1016/j.jns.2019.116429
pii:
doi:

Substances chimiques

Biomarkers 0
GDF15 protein, human 0
Growth Differentiation Factor 15 0
fibroblast growth factor 21 0
Fibroblast Growth Factors 62031-54-3

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

116429

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Seitaro Nohara (S)

Department of Neurology, University of Tsukuba, Japan.

Akiko Ishii (A)

Department of Neurology, University of Tsukuba, Japan. Electronic address: a_ishii@md.tsukuba.ac.jp.

Fumiko Yamamoto (F)

Department of Neurology, University of Tsukuba, Japan.

Kumi Yanagiha (K)

Department of Neurology, University of Tsukuba, Japan.

Tetsuya Moriyama (T)

Department of Neurology, University of Tsukuba, Japan.

Naoki Tozaka (N)

Department of Neurology, University of Tsukuba, Japan.

Zenshi Miyake (Z)

Department of Neurology, University of Tsukuba, Japan.

Shuichi Yatsuga (S)

Department of Pediatrics and Child Health, Kurume University School of Medicine, Japan.

Yasutoshi Koga (Y)

Department of Pediatrics and Child Health, Kurume University School of Medicine, Japan.

Takashi Hosaka (T)

Department of Neurology, University of Tsukuba, Japan.

Makoto Terada (M)

Department of Neurology, University of Tsukuba, Japan.

Tetsuto Yamaguchi (T)

Department of Neurology, University of Tsukuba, Japan.

Satoshi Aizawa (S)

Department of Neurology, University of Tsukuba, Japan.

Naomi Mamada (N)

Department of Neurology, University of Tsukuba, Japan.

Hiroshi Tsuji (H)

Department of Neurology, University of Tsukuba, Japan.

Yasushi Tomidokoro (Y)

Department of Neurology, University of Tsukuba, Japan.

Kiyotaka Nakamagoe (K)

Department of Neurology, University of Tsukuba, Japan.

Kazuhiro Ishii (K)

Department of Neurology, University of Tsukuba, Japan.

Masahiko Watanabe (M)

Department of Neurology, University of Tsukuba, Japan.

Akira Tamaoka (A)

Department of Neurology, University of Tsukuba, Japan.

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Classifications MeSH