PMID- 25039314
OWN - NLM
STAT- MEDLINE
DCOM- 20160418
LR  - 20181202
IS  - 1399-5618 (Electronic)
IS  - 1398-5647 (Linking)
VI  - 17
IP  - 1
DP  - 2015 Feb
TI  - Monocyte activation, brain-derived neurotrophic factor (BDNF), and S100B in 
      bipolar offspring: a follow-up study from adolescence into adulthood.
PG  - 39-49
LID - 10.1111/bdi.12231 [doi]
AB  - OBJECTIVES: There is increasing evidence that both immune and neurochemical 
      alterations are involved in the pathogenesis of bipolar disorder; however, their 
      precise role remains unclear. In this study, we aimed to evaluate neuro-immune 
      changes in a prospective study on children of patients with bipolar disorder. 
      METHODS: Bipolar offspring, from the prospective Dutch bipolar offspring study 
      (n = 140), were evaluated cross-sectionally within a longitudinal context at 
      adolescence, young adulthood, and adulthood. We examined the expression of 44 
      inflammation-related genes in monocytes, the cytokines pentraxin 3 (PTX3), 
      chemokine ligand 2 (CCL2), and interleukin-1beta (IL-1beta), and brain-derived 
      neurotrophic factor (BDNF) and S100 calcium binding protein B (S100B) in the 
      serum of bipolar offspring and healthy controls. RESULTS: During adolescence, 
      bipolar offspring showed increased inflammatory gene expression in monocytes, 
      high serum PTX3 levels, but normal CCL2 levels. BDNF levels were decreased, while 
      S100B levels were normal. During young adulthood, monocyte activation remained, 
      although to a lesser degree. Serum PTX3 levels remained high, and signs of 
      monocyte migration became apparent through increased CCL2 levels. BDNF and S100B 
      levels were not measured. At adulthood, circulating monocytes had lost their 
      activation state, but CCL2 levels remained increased. Both BDNF and S100B were 
      now increased. Abnormalities were independent of psychopathology state at all 
      stages. CONCLUSIONS: This study suggests an aberrant neuro-immune state in 
      bipolar offspring, which followed a dynamic course from adolescence into 
      adulthood and was present irrespective of lifetime or future mood disorders. We 
      therefore assumed that the aberrant neuro-immune state reflects a general state 
      of vulnerability for mood disorders rather than being of direct predictive value.
CI  - (c) 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
FAU - Mesman, Esther
AU  - Mesman E
AD  - Brain Center Rudolf Magnus, Department of Psychiatry, University Medical Center 
      Utrecht, Utrecht, The Netherlands.
FAU - Hillegers, Manon Hj
AU  - Hillegers MH
FAU - Ambree, Oliver
AU  - Ambree O
FAU - Arolt, Volker
AU  - Arolt V
FAU - Nolen, Willem A
AU  - Nolen WA
FAU - Drexhage, Hemmo A
AU  - Drexhage HA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140717
PL  - Denmark
TA  - Bipolar Disord
JT  - Bipolar disorders
JID - 100883596
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Interleukin-1beta)
RN  - 0 (S100 Calcium Binding Protein beta Subunit)
RN  - 0 (S100B protein, human)
RN  - 0 (Serum Amyloid P-Component)
RN  - 148591-49-5 (PTX3 protein)
RN  - 7171WSG8A2 (BDNF protein, human)
RN  - 9007-41-4 (C-Reactive Protein)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - *Bipolar Disorder/diagnosis/immunology/psychology
MH  - Brain-Derived Neurotrophic Factor/*blood
MH  - C-Reactive Protein/analysis
MH  - Child of Impaired Parents/*psychology
MH  - Female
MH  - Follow-Up Studies
MH  - Gene Expression Profiling
MH  - Humans
MH  - Inflammation/immunology
MH  - Interleukin-1beta/blood
MH  - Male
MH  - Monocytes/*metabolism
MH  - Prospective Studies
MH  - Psychiatric Status Rating Scales
MH  - S100 Calcium Binding Protein beta Subunit/*blood
MH  - Serum Amyloid P-Component/analysis
MH  - Statistics as Topic
OTO - NOTNLM
OT  - biomarker
OT  - bipolar disorder
OT  - brain-derived neurotrophic factor (BDNF)
OT  - cytokines
OT  - high risk
OT  - inflammation
EDAT- 2014/07/22 06:00
MHDA- 2016/04/19 06:00
CRDT- 2014/07/22 06:00
PHST- 2013/09/29 00:00 [received]
PHST- 2014/04/29 00:00 [accepted]
PHST- 2014/07/22 06:00 [entrez]
PHST- 2014/07/22 06:00 [pubmed]
PHST- 2016/04/19 06:00 [medline]
AID - 10.1111/bdi.12231 [doi]
PST - ppublish
SO  - Bipolar Disord. 2015 Feb;17(1):39-49. doi: 10.1111/bdi.12231. Epub 2014 Jul 17.