Inflammatory markers are associated with general cognitive abilities in schizophrenia and bipolar disorder patients and healthy controls

Hope, Sigrun; Hoseth, Eva; Dieset, Ingrid; Mørch, Ragni Helene; Aas, Monica; Aukrust, Pål; Djurovic, Srdjan; Melle, Ingrid; Ueland, Torill; Agartz, Ingrid; Ueland, Thor; Westlye, Lars T.; Andreassen, Ole A.

doi:10.1016/j.schres.2015.04.004

Cited by 91 publications

(61 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The second study, comparing children with Prader-Willi syndrome to healthy siblings, found no significant difference between the groups in plasma sCD40L, though the trend was for higher values in the syndromic children [63]. There are several studies documenting elevated levels of sCD40L in adult psychiatric and health conditions, where a negative relationship between sCD40L and cognitive function has been demonstrated [64, 65]. …”

Section: Discussionmentioning

confidence: 99%

Serum and cerebrospinal fluid immune mediators in children with autistic disorder: a longitudinal study

et al. 2017

View full text Add to dashboard Cite

BackgroundThe causes of autism likely involve genetic and environmental factors that influence neurobiological changes and the neurological and behavioral features of the disorder. Immune factors and inflammation are hypothesized pathogenic influences, but have not been examined longitudinally.MethodsIn a cohort of 104 participants with autism, we performed an assessment of immune mediators such as cytokines, chemokines, or growth factors in serum and cerebrospinal fluid (n = 67) to determine potential influences of such mediators in autism.ResultsAs compared with 54 typically developing controls, we found no evidence of differences in the blood profile of immune mediators supportive of active systemic inflammation mechanisms in participants with autism. Some modulators of immune function (e.g., EGF and soluble CD40 ligand) were increased in the autism group; however, no evidence of group differences in traditional markers of active inflammation (e.g., IL-6, TNFα, IL-1β) were observed in the serum. Further, within-subject stability (measured by estimated intraclass correlations) of most analytes was low, indicating that a single measurement is not a reliable prospective indicator of concentration for most analytes. Additionally, in participants with autism, there was little correspondence between the blood and CSF profiles of cytokines, chemokines, and growth factors, suggesting that peripheral markers may not optimally reflect the immune status of the central nervous system. Although the relatively high fraction of intrathecal production of selected chemokines involved in monocyte/microglia function may suggest a possible relationship with the homeostatic role of microglia, control data are needed for further interpretation of its relevance in autism.ConclusionsThese longitudinal observations fail to provide support for the hypothesized role of disturbances in the expression of circulating cytokines and chemokines as an indicator of systemic inflammation in autism. ClinicalTrials.gov, NCT00298246.Electronic supplementary materialThe online version of this article (doi:10.1186/s13229-016-0115-7) contains supplementary material, which is available to authorized users.

show abstract

Section: Discussionmentioning

confidence: 99%

Serum and cerebrospinal fluid immune mediators in children with autistic disorder: a longitudinal study

et al. 2017

View full text Add to dashboard Cite

show abstract

“…118 In addition, further findings in BD have also described significant negative associations between inflammatory markers and general cognitive abilities, as well as neuroanatomical alterations. [165][166][167][168][169] However, another systematic review claims that an absolute conclusion cannot be reached regarding the presence of neuroinflammation in BD, since the findings are not consistent. 170 Several different mechanisms have been proposed to explain the role of immune dysfunction in BD, 171 including changes in blood-brain barrier, cell deathinduced release of damage-associate molecular patterns with consequent immune activation, genetic mechanisms, dysfunction of the gut-brain axis, and a role of the kynurenine pathway.…”

Section: Immune-inflammatory Imbalance and Kynurenine Pathwaymentioning

confidence: 99%

Neurobiology of bipolar disorders: a review of genetic components, signaling pathways, biochemical changes, and neuroimaging findings

Scaini

Valvassori

Diaz

et al. 2020

Braz. J. Psychiatry

View full text Add to dashboard Cite

Bipolar disorder (BD) is a chronic mental illness characterized by changes in mood that alternate between mania and hypomania or between depression and mixed states, often associated with functional impairment. Although effective pharmacological and non-pharmacological treatments are available, several patients with BD remain symptomatic. The advance in the understanding of the neurobiology underlying BD could help in the identification of new therapeutic targets as well as biomarkers for early detection, prognosis, and response to treatment in BD. In this review, we discuss genetic, epigenetic, molecular, physiological and neuroimaging findings associated with the neurobiology of BD. Despite the advances in the pathophysiological knowledge of BD, the diagnosis and management of the disease are still essentially clinical. Given the complexity of the brain and the close relationship between environmental exposure and brain function, initiatives that incorporate genetic, epigenetic, molecular, physiological, clinical, environmental data, and brain imaging are necessary to produce information that can be translated into prevention and better outcomes for patients with BD.

show abstract

“…The plasma levels of sTNF-R1, OPG and IL1-Ra were measured at the laboratory at Research Institute of Internal Medicine (Oslo University Hospital, Rikshospitalet) using enzyme immunoassays (EIA) obtained from R&D systems (Minneapolis, MN, USA). The inflammatory markers were selected based on earlier findings in our research group considered to represent distinct inflammatory pathways with stable markers showing little diurnal fluctuations (Hope et al, 2015). IL-1Ra is a regulator of IL-1α activity; sTNF-R1 is a marker of activity in upstream inflammatory pathways and OPG is a soluble member of the tumor necrosis family (Dieset et al, 2012).…”

Section: Biochemical Variablesmentioning

confidence: 99%

Low vitamin D is associated with negative and depressive symptoms in psychotic disorders

Nerhus

Berg

Kvitland

et al. 2016

Schizophrenia Research

Self Cite

View full text Add to dashboard Cite

show abstract

Inflammatory markers are associated with general cognitive abilities in schizophrenia and bipolar disorder patients and healthy controls

Cited by 91 publications

References 53 publications

Serum and cerebrospinal fluid immune mediators in children with autistic disorder: a longitudinal study

Serum and cerebrospinal fluid immune mediators in children with autistic disorder: a longitudinal study

Neurobiology of bipolar disorders: a review of genetic components, signaling pathways, biochemical changes, and neuroimaging findings

Low vitamin D is associated with negative and depressive symptoms in psychotic disorders

Contact Info

Product

Resources

About