{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T10:32:52Z","timestamp":1791196372077,"version":"4.1.0"},"reference-count":33,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2014,7,17]],"date-time":"2014-07-17T00:00:00Z","timestamp":1405555200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000780","name":"European Commission","doi-asserted-by":"publisher","award":["22963"],"award-info":[{"award-number":["22963"]}],"id":[{"id":"10.13039\/501100000780","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100003246","name":"Netherlands Organisation for Scientific Research","doi-asserted-by":"crossref","award":["9120818"],"award-info":[{"award-number":["9120818"]}],"id":[{"id":"10.13039\/501100003246","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Bipolar Disorders"],"published-print":{"date-parts":[[2015,2]]},"abstract":"<jats:sec><jats:title>Objectives<\/jats:title><jats:p>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\u2010immune changes in a prospective study on children of patients with bipolar disorder.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Bipolar offspring, from the prospective Dutch bipolar offspring study (n\u00a0=\u00a0140), were evaluated cross\u2010sectionally within a longitudinal context at adolescence, young adulthood, and adulthood. We examined the expression of 44 inflammation\u2010related genes in monocytes, the cytokines pentraxin 3 (<jats:styled-content style=\"fixed-case\">PTX<\/jats:styled-content>3), chemokine ligand 2 (<jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2), and interleukin\u20101\u03b2 (<jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20101\u03b2), and brain\u2010derived neurotrophic factor (<jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content>) and S100 calcium binding protein B (S100B) in the serum of bipolar offspring and healthy controls.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>During adolescence, bipolar offspring showed increased inflammatory gene expression in monocytes, high serum <jats:styled-content style=\"fixed-case\">PTX<\/jats:styled-content>3 levels, but normal <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2 levels. <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content> levels were decreased, while S100B levels were normal. During young adulthood, monocyte activation remained, although to a lesser degree. Serum <jats:styled-content style=\"fixed-case\">PTX<\/jats:styled-content>3 levels remained high, and signs of monocyte migration became apparent through increased <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2 levels. <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content> and S100B levels were not measured. At adulthood, circulating monocytes had lost their activation state, but <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>2 levels remained increased. Both <jats:styled-content style=\"fixed-case\">BDNF<\/jats:styled-content> and S100B were now increased. Abnormalities were independent of psychopathology state at all stages.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>This study suggests an aberrant neuro\u2010immune 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\u2010immune state reflects a general state of vulnerability for mood disorders rather than being of direct predictive value.<\/jats:p><\/jats:sec>","DOI":"10.1111\/bdi.12231","type":"journal-article","created":{"date-parts":[[2014,7,18]],"date-time":"2014-07-18T04:18:04Z","timestamp":1405657084000},"page":"39-49","source":"Crossref","is-referenced-by-count":47,"title":["Monocyte activation, brain\u2010derived neurotrophic factor (<scp>BDNF<\/scp>), and S100B in bipolar offspring: a follow\u2010up study from adolescence into adulthood"],"prefix":"10.1111","volume":"17","author":[{"given":"Esther","family":"Mesman","sequence":"first","affiliation":[{"name":"Brain Center Rudolf Magnus Department of Psychiatry University Medical Center Utrecht Utrecht The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manon HJ","family":"Hillegers","sequence":"additional","affiliation":[{"name":"Brain Center Rudolf Magnus Department 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