S100B and brain derived neurotrophic factor in monozygotic twins with, at risk of and without affective disorders.


Journal

Journal of affective disorders
ISSN: 1573-2517
Titre abrégé: J Affect Disord
Pays: Netherlands
ID NLM: 7906073

Informations de publication

Date de publication:
01 09 2020
Historique:
received: 27 04 2019
revised: 15 04 2020
accepted: 10 05 2020
entrez: 16 7 2020
pubmed: 16 7 2020
medline: 16 2 2021
Statut: ppublish

Résumé

The calcium binding protein S100B and brain derived neurotrophic factor (BDNF) are both biomarkers implicated in neuronal processes in the central nervous system and seem to be associated with affective disorders. Here we investigated both markers in a sample of monozygotic (MZ) twins with, at risk of and without affective disorders, aiming to evaluate whether these markers have a role as causal factors- or trait markers for affective disorders. We measured serum S100B and plasma BDNF levels in 204 monozygotic twins (MZ) with unipolar or bipolar disorder in remission or partial remission (affected), their unaffected co-twins (high-risk) and twins with no personal or family history of affective disorder (low-risk). No significant group differences in S100B and BDNF levels were found between the three groups. Exploratory analysis revealed that higher S100B levels were correlated with lower cognitive performance. The cross-sectional design cannot elucidate the two neuronal biomarkers role as causal factors. We would have preferred a higher sample size in the high- and low-risk groups. The present result did not support a role for S100B and BDNF as neither causal factors nor trait markers for affective disorders. Elevated S100B levels may associate with impaired cognition, but further studies are warranted.

Sections du résumé

BACKGROUND
The calcium binding protein S100B and brain derived neurotrophic factor (BDNF) are both biomarkers implicated in neuronal processes in the central nervous system and seem to be associated with affective disorders. Here we investigated both markers in a sample of monozygotic (MZ) twins with, at risk of and without affective disorders, aiming to evaluate whether these markers have a role as causal factors- or trait markers for affective disorders.
METHOD
We measured serum S100B and plasma BDNF levels in 204 monozygotic twins (MZ) with unipolar or bipolar disorder in remission or partial remission (affected), their unaffected co-twins (high-risk) and twins with no personal or family history of affective disorder (low-risk).
RESULTS
No significant group differences in S100B and BDNF levels were found between the three groups. Exploratory analysis revealed that higher S100B levels were correlated with lower cognitive performance.
LIMITATIONS
The cross-sectional design cannot elucidate the two neuronal biomarkers role as causal factors. We would have preferred a higher sample size in the high- and low-risk groups.
CONCLUSION
The present result did not support a role for S100B and BDNF as neither causal factors nor trait markers for affective disorders. Elevated S100B levels may associate with impaired cognition, but further studies are warranted.

Identifiants

pubmed: 32664008
pii: S0165-0327(19)31101-2
doi: 10.1016/j.jad.2020.05.015
pii:
doi:

Substances chimiques

Brain-Derived Neurotrophic Factor 0
S100 Calcium Binding Protein beta Subunit 0
S100B protein, human 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

726-732

Informations de copyright

Copyright © 2020. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of Competing interest MV has received consultancy fees from Lundbeck, Sunovion and Janssen in the past three years. LVK has within the preceding three years been a consultant for Sunovion and Lundbeck. KWM has received consultancy fees from Lundbeck, Allergan and Janssen in the past three years. The remaining authors declare no conflicts of interest.

Auteurs

Ninja Meinhard Ottesen (NM)

Copenhagen Affective Disorders Research Centre (CADIC), Psychiatric Centre Copenhagen, Rigshospitalet; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen.

Iselin Meluken (I)

Copenhagen Affective Disorders Research Centre (CADIC), Psychiatric Centre Copenhagen, Rigshospitalet; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen.

Ruth Frikke-Schmidt (R)

Department of Clinical Biochemistry Rigshospitalet, Copenhagen University Hospital; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen.

Peter Plomgaard (P)

Department of Clinical Biochemistry Rigshospitalet, Copenhagen University Hospital; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen.

Thomas Scheike (T)

Section of Biostatistics, Department of Public Health, University of Copenhagen, Denmark.

Lars Vedel Kessing (LV)

Copenhagen Affective Disorders Research Centre (CADIC), Psychiatric Centre Copenhagen, Rigshospitalet; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen.

Kamilla Miskowiak (K)

Copenhagen Affective Disorders Research Centre (CADIC), Psychiatric Centre Copenhagen, Rigshospitalet; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen; Department of Psychology, University of Copenhagen, Denmark.

Maj Vinberg (M)

Copenhagen Affective Disorders Research Centre (CADIC), Psychiatric Centre Copenhagen, Rigshospitalet; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen; Psychiatric Research Unit, Psychiatric Centre North Zealand, Hillerød. Electronic address: maj.vinberg@regionh.dk.

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Classifications MeSH