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Monocyte activation, brain‐derived neurotrophic factor ( BDNF ), and S100B in bipolar offspring: a follow‐up study from adolescence into adulthood
Author(s) -
Mesman Esther,
Hillegers Ma HJ,
Ambree Oliver,
Arolt Volker,
Nolen Willem A,
Drexhage Hemmo A
Publication year - 2015
Publication title -
bipolar disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.285
H-Index - 129
eISSN - 1399-5618
pISSN - 1398-5647
DOI - 10.1111/bdi.12231
Subject(s) - offspring , neurochemical , medicine , psychology , context (archaeology) , bipolar disorder , endocrinology , brain derived neurotrophic factor , proinflammatory cytokine , neurotrophic factors , inflammation , mood , psychiatry , receptor , biology , pregnancy , paleontology , genetics
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 ( PTX 3), chemokine ligand 2 ( CCL 2), and interleukin‐1β ( IL ‐1β), 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 PTX 3 levels, but normal CCL 2 levels. BDNF levels were decreased, while S100B levels were normal. During young adulthood, monocyte activation remained, although to a lesser degree. Serum PTX 3 levels remained high, and signs of monocyte migration became apparent through increased CCL 2 levels. BDNF and S100B levels were not measured. At adulthood, circulating monocytes had lost their activation state, but CCL 2 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.