Interplay between childhood trauma and BDNF val66met variants on blood BDNF mRNA levels and on hippocampus subfields volumes in schizophrenia spectrum and bipolar disorders

Aas, Monica; Haukvik, Unn K.; Djurovic, Srdjan; Tesli, Martin; Athanasiu, Lavinia; Bjella, Thomas; Hansson, Lars Johan; Cattaneo, Annamaria; Agartz, Ingrid; Andreassen, Ole A.; Melle, Ingrid

doi:10.1016/j.jpsychires.2014.08.011

Cited by 97 publications

(76 citation statements)

References 55 publications

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“…We can hypothesize that physical abuse impacts on several biological pathways (related to inflammatory processes, neuroplasticity, circadian systems or premature ageing among others) , maybe such effect(s) not being fully counteracted by lithium salts, thus explaining why some bipolar patients who received lithium remained at high risk for mood recurrences. For example, some studies have shown that childhood trauma reduces BDNF mRNA blood levels among exposed schizophrenia spectrum disorders and BD and also modifies levels of numerous inflammatory markers in clinical and non‐clinical populations , such as C‐reactive protein, interleukin‐6 or tumour necrosis factor‐alpha . This has been proposed to create an imbalance between neuroplasticity and proinflammatory cytokines levels with some increase in BDNF levels being a possible attempt to neutralize the negative effects of childhood trauma on the brain.…”

Section: Discussionmentioning

confidence: 99%

Childhood trauma and mixed episodes are associated with poor response to lithium in bipolar disorders

Étain

Lajnef

Brichant‐Petitjean

et al. 2016

Acta Psychiatr Scand

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Objectives: Reliable predictors of response to lithium are still lacking in bipolar disorders (BD).However, childhood trauma has been hypothesized to be associated with poor response to lithium. Methods:We included 148 patients with BD, euthymic when retrospectively and clinically assessed for response to lithium and childhood trauma using reliable scales.Results: According to the "Alda scale", the sample consisted in 20.3% of excellent responders, 49.3% of partial responders and 30.4% of non-responders to lithium. A higher level of physical abuse significantly correlated with a lower level of response to lithium (p=0.009). As compared to patients not exposed to any abuse, patients with at least two trauma abuses (emotional, physical or sexual) were more at risk of belonging to the non-responders group (OR=4.91 95CI(1.01-27.02)). Among investigated clinical variables, lifetime presence of mixed episodes and alcohol misuse were associated to non-response to lithium. Multivariate analyses demonstrated that physical abuse and mixed episodes were independently associated with poor response to lithium (p=0.005 and p=0.013 respectively). Conclusions:Childhood physical abuse might be involved in a poor future response to lithium prophylaxis, this effect being independent of the association between clinical expression of BD and poor response to lithium.

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Section: Discussionmentioning

confidence: 99%

Childhood trauma and mixed episodes are associated with poor response to lithium in bipolar disorders

Étain

Lajnef

Brichant‐Petitjean

et al. 2016

Acta Psychiatr Scand

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“…The reliability and validity of the CTQ have been demonstrated previously . In this study, the short version (28‐itemversion) of the CTQ validated in French and Norwegian was used …”

Section: Methodsmentioning

confidence: 99%

“…23 In this study, the short version (28-itemversion) of the CTQ validated in French and Norwegian was used. 24,25…”

Section: Childhood Trauma Questionnaire (Ctq)mentioning

confidence: 99%

Childhood maltreatment and polygenic risk in bipolar disorders

et al. 2019

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Background Childhood maltreatment is a well‐known risk factor for developing a more severe and complex form of bipolar disorders (BD). However, knowledge is scarce about the interactions between childhood maltreatment and underlying genetic vulnerability on the clinical expression of BD. Method We assigned a BD‐polygenic risk score (BD‐PRS), calculated from the Psychiatric Genomics Consortium, to each individual in a sample of 402 cases with BD. The lifetime clinical expression of BD was characterized using structured interviews and patients completed the Childhood Trauma Questionnaire (CTQ) to assess the severity of childhood maltreatment. Results Cases who reported more severe childhood maltreatment had a lower BD‐PRS (rho = −0.12, P = .01), especially when considering emotional abuse (rho = −0.16, P = .001). An interaction between BD‐PRS and childhood maltreatment was observed for the risk of rapid cycling (P = .01). No further interactions between BD‐PRS and childhood maltreatment were observed for other clinical characteristics (age at onset, suicide attempts, number of mood episodes, mixed features, substance use disorders and psychotic symptoms). Conclusion Our study is the first to show that less genetic risk may be needed to develop a more unstable form of BD when exposed to childhood maltreatment. Our study supports childhood trauma as an independent risk factor for BD.

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“…In concert, the emerging genetic and genomic findings in PTSD implicate molecular pathways that might alter hippocampal-prefrontal-thalamic circuitry – perhaps impacting hippocampal volume or context-relevant hippocampal function like neurogenesis and LTP. For example, polymorphisms in BDNF (Gatt et al, 2009; Aas et al, 2014), ADBR2 and FKBP5 (Fani et al, 2013), or methylation of SLC6A4 (Dannlowski et al, 2014) or FKBP5 (Fani et al, 2013) , all have hippocampal effects, and each has evidence for association with PTSD. These findings resonate with reports of hippocampal size differences seen in PTSD, which may constitute a risk factor for PTSD development (Gilbertson et al, 2002; Bremner et al, 2003; Kitayama et al, 2005).…”

Section: A New Model: Deficient Context Processingmentioning

confidence: 99%

Context Processing and the Neurobiology of Post-Traumatic Stress Disorder

Liberzon

Abelson

2016

Neuron

338

335

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Summary Progress in clinical and affective neuroscience is redefining psychiatric illness as symptomatic expression of cellular/molecular dysfunctions in specific brain circuits. Post-traumatic stress disorder (PTSD) has been an exemplar of this progress, with improved understanding of neurobiological systems subserving fear learning, salience detection, and emotion regulation explaining much of its phenomenology and neurobiology. However, many features remain unexplained and a parsimonious model that more fully accounts for symptoms and the core neurobiology remains elusive. Contextual processing is a key modulatory function of hippocampal-prefrontal-thalamic circuitry, allowing organisms to disambiguate cues and derive situation-specific meaning from the world. We propose that dysregulation within this context-processing circuit is at the core of PTSD pathophysiology, accounting for much of its phenomenology and most of its biological findings. Understanding core mechanisms like this, and their underlying neural circuits, will sharpen diagnostic precision and understanding of risk factors, enhancing our ability to develop preventive and “personalized” interventions.

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Interplay between childhood trauma and BDNF val66met variants on blood BDNF mRNA levels and on hippocampus subfields volumes in schizophrenia spectrum and bipolar disorders

Cited by 97 publications

References 55 publications

Childhood trauma and mixed episodes are associated with poor response to lithium in bipolar disorders

Childhood trauma and mixed episodes are associated with poor response to lithium in bipolar disorders

Childhood maltreatment and polygenic risk in bipolar disorders

Context Processing and the Neurobiology of Post-Traumatic Stress Disorder

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