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Elevated C-reactive Protein as a Predictive Marker of Clinical Depression and Anxiety
Get PDFPrevious research has documented an association between elevated peripheral blood inflammation and depression diagnosis and symptom severity1. We investigated the association between inflammation and depression as well as anxiety symptom severity and response to treatment by assessing patients reporting depressive and anxiety symptoms for a period of three to six weeks, with quantified anxiety and depressive symptoms being documented weekly. The depressive and anxiety symptom severities were quantified using the Montgomery-Asberg Depression Rating Scale (MADRS) and Hamilton Anxiety Rating Scale (HAM-A), respectively. The sample included 472 patients (55% male, mean age = 27.5 years, mean duration of stay = 69.4 days, mean baseline MADRS score = 26.1, mean baseline HAM-A score = 19.6), of which 195 individuals reported depressive symptoms, while 198 individuals reported anxiety symptoms. Three blood samples per individual were collected and assessed to detect any elevated inflammatory responses as measured with blood serum levels of C-Reactive protein (CRP). The samples from each group of interest underwent a high-sensitivity assay for CRP levels during the pre-treatment and post-treatment periods. The relationship between patients’ baseline CRP levels/inflammatory responses collected at admission was cross-referenced with their response to treatment during the course stay at a psychiatric rehabilitation clinic as measured with reported symptom severity over time to determine if inflammation was a predictive marker of depression and anxiety treatment responses. We found that elevated CRP levels were positively associated with depressive treatment response as measured with ratings of reduction in depression symptom severity levels over time using the MADRS (p=0.004). In contrast, elevated CRP levels were not significantly associated with anxiety treatment response as measured with ratings of anxiety symptom severity levels over time using the HAM-A (p=0.109). Specifically, high CRP levels at admission correlated with less reduction in depressive symptoms over time, as if the effects of mental health rehabilitation treatment for depression were dampened by increased levels of inflammation as measured with CRP levels at the start of treatment. These findings suggest that baseline CRP levels at admission are a predictive marker for lingering depressive symptom severity over time even in people receiving treatment, but less so for anxiety symptom severity. Numerous limitations regarding the sample pool and the type of treatment administered were present in this study, including the lack of inclusion of healthy controls to account for the effects of low to no inflammation. Race and gender, factors that influence baseline inflammatory levels, were not controlled for when measuring CRP levels in the reported findings. Limitations regarding the structure and sensitivity of the outcome measure scales may have also skewed the reported MADRS and HAM-A scores. Future studies need to control for these limitations in order to better understand the association between inflammation and mental disorder treatment response as measured with symptom severity.Dell Medical Schoo
Integrating the homeostatic imbalance: Genetics and physiology of stress and the emotions
Get PDFMenselijke emoties worden beïnvloed door een complexe samenwerking tussen hersenactivaties en hormoonhuishouding. Deze worden op hun beurt beïnvloed door genetische kenmerken. Uit onderzoek van UMCG-promovendus Mbemba Jabbi blijkt dat de invloed van het COMT-gen op de hormoonhuishouding mede afhankelijk is van de aanwezigheid van de actieve variant van het MAOA-gen. Het serotonine transporter-gen lijkt invloed te hebben op hormonale stress respons bij proefpersonen die groot risico lopen om depressieve klachten te ontwikkelen. Deze bevindingen tonen aan dat de invloed van verschillende genen op emotionele kwetsbaarheid hierarchisch gestructureerd is. Met behulp van fMRI-metingen onderzocht Jabbi de activiteit in de insula en de cingulaat-kwabben bij de verwerking van emoties. Uit dit onderzoek blijkt dat er samenhang bestaat tussen het empathisch vermogen dat proefpersonen zichzelf toedichten en de activiteit in genoemde hersendelen. De verworven inzichten kunnen van belang zijn bij de ontwikkeling van betere medicijnen tegen emotionele stoornissen, bijvoorbeeld anti-depressiva.
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Suicide, machine learning, and the brain
Get PDFSuicide causes around 800,000 deaths worldwide each year, making premature deaths due to suicide a significant public health problem (WHO 2018). The expression of suicidal behaviors is a complex phenotype with underlying biological, psychological, clinical, and sociocultural risk factors (Turecki et al., 2019). From a neurobiological perspective, suicidal behaviors (ideation, attempt) are associated with the degree of anatomical, physiological, and neurotranscriptomic dysregulations of a network of brain regions. This network includes the anterior insula, anterior cingulate, and prefrontal cortical regions that mediate emotional-regulatory behaviors. From a clinical perspective, diagnostic measures of depressive symptoms in major depressive disorder and bipolar disorders (i.e., mood disorders) are associated with over sixty percent of suicide deaths (WHO 2018). Of interest, the brain anatomical and related depressive symptoms associated with suicidal behavior are characterized by regionally specific brain measures of aberrant gene expression profiles in the post-mortem brains of suicide completed donors (Jabbi et al., 2020). These convergent neurobiological correlates for depressive illness and suicidal phenotypes lead me to ask: 1) are regional brain gene expression dysregulations underlying depressive illness in mood disorders differentially associated with suicide mortality? 2) And crucially, how do the brain’s gene expression dysregulations measured in post-mortem studies relate to diagnostic and demographic variables to confer risk for suicide across the psychiatric continuum? Answering these questions using a deterministic post-mortem sample with well-characterized suicide outcomes could help identify the convergent molecular and clinical risk factors for suicide deaths across the lifespan. Furthermore, this line of research could resolve the specificity of how such clinically defined molecular risk factors for suicide mortality may differ across mood disorders and other mental illnesses, ultimately aiding in diagnostically informed suicide prevention. I reviewed the extant literature on studies of brain gene expression correlates of suicide by focusing on unique suicide-related gene expression dysregulations in mood disorders. Moving forward, I propose using machine learning tools to integrate brain-based gene expression measures in conjunction with clinical/demographic variables to identify molecular and phenotypic risk predictors for suicide mortality.Neuroscienc
Integrating the homeostatic imbalance:Genetics and physiology of stress and the emotions
No full textMenselijke emoties worden beïnvloed door een complexe samenwerking tussen hersenactivaties en hormoonhuishouding. Deze worden op hun beurt beïnvloed door genetische kenmerken. Uit onderzoek van UMCG-promovendus Mbemba Jabbi blijkt dat de invloed van het COMT-gen op de hormoonhuishouding mede afhankelijk is van de aanwezigheid van de actieve variant van het MAOA-gen. Het serotonine transporter-gen lijkt invloed te hebben op hormonale stress respons bij proefpersonen die groot risico lopen om depressieve klachten te ontwikkelen. Deze bevindingen tonen aan dat de invloed van verschillende genen op emotionele kwetsbaarheid hierarchisch gestructureerd is. Met behulp van fMRI-metingen onderzocht Jabbi de activiteit in de insula en de cingulaat-kwabben bij de verwerking van emoties. Uit dit onderzoek blijkt dat er samenhang bestaat tussen het empathisch vermogen dat proefpersonen zichzelf toedichten en de activiteit in genoemde hersendelen. De verworven inzichten kunnen van belang zijn bij de ontwikkeling van betere medicijnen tegen emotionele stoornissen, bijvoorbeeld anti-depressiva
Integrating the homeostatic imbalance:Genetics and physiology of stress and the emotions
Get PDFMenselijke emoties worden beïnvloed door een complexe samenwerking tussen hersenactivaties en hormoonhuishouding. Deze worden op hun beurt beïnvloed door genetische kenmerken. Uit onderzoek van UMCG-promovendus Mbemba Jabbi blijkt dat de invloed van het COMT-gen op de hormoonhuishouding mede afhankelijk is van de aanwezigheid van de actieve variant van het MAOA-gen. Het serotonine transporter-gen lijkt invloed te hebben op hormonale stress respons bij proefpersonen die groot risico lopen om depressieve klachten te ontwikkelen. Deze bevindingen tonen aan dat de invloed van verschillende genen op emotionele kwetsbaarheid hierarchisch gestructureerd is. Met behulp van fMRI-metingen onderzocht Jabbi de activiteit in de insula en de cingulaat-kwabben bij de verwerking van emoties. Uit dit onderzoek blijkt dat er samenhang bestaat tussen het empathisch vermogen dat proefpersonen zichzelf toedichten en de activiteit in genoemde hersendelen. De verworven inzichten kunnen van belang zijn bij de ontwikkeling van betere medicijnen tegen emotionele stoornissen, bijvoorbeeld anti-depressiva
Integrating the homeostatic imbalance:Genetics and physiology of stress and the emotions
Get PDFMenselijke emoties worden beïnvloed door een complexe samenwerking tussen hersenactivaties en hormoonhuishouding. Deze worden op hun beurt beïnvloed door genetische kenmerken. Uit onderzoek van UMCG-promovendus Mbemba Jabbi blijkt dat de invloed van het COMT-gen op de hormoonhuishouding mede afhankelijk is van de aanwezigheid van de actieve variant van het MAOA-gen. Het serotonine transporter-gen lijkt invloed te hebben op hormonale stress respons bij proefpersonen die groot risico lopen om depressieve klachten te ontwikkelen. Deze bevindingen tonen aan dat de invloed van verschillende genen op emotionele kwetsbaarheid hierarchisch gestructureerd is. Met behulp van fMRI-metingen onderzocht Jabbi de activiteit in de insula en de cingulaat-kwabben bij de verwerking van emoties. Uit dit onderzoek blijkt dat er samenhang bestaat tussen het empathisch vermogen dat proefpersonen zichzelf toedichten en de activiteit in genoemde hersendelen. De verworven inzichten kunnen van belang zijn bij de ontwikkeling van betere medicijnen tegen emotionele stoornissen, bijvoorbeeld anti-depressiva
Integrating the homeostatic imbalance:Genetics and physiology of stress and the emotions
Get PDFMenselijke emoties worden beïnvloed door een complexe samenwerking tussen hersenactivaties en hormoonhuishouding. Deze worden op hun beurt beïnvloed door genetische kenmerken. Uit onderzoek van UMCG-promovendus Mbemba Jabbi blijkt dat de invloed van het COMT-gen op de hormoonhuishouding mede afhankelijk is van de aanwezigheid van de actieve variant van het MAOA-gen. Het serotonine transporter-gen lijkt invloed te hebben op hormonale stress respons bij proefpersonen die groot risico lopen om depressieve klachten te ontwikkelen. Deze bevindingen tonen aan dat de invloed van verschillende genen op emotionele kwetsbaarheid hierarchisch gestructureerd is. Met behulp van fMRI-metingen onderzocht Jabbi de activiteit in de insula en de cingulaat-kwabben bij de verwerking van emoties. Uit dit onderzoek blijkt dat er samenhang bestaat tussen het empathisch vermogen dat proefpersonen zichzelf toedichten en de activiteit in genoemde hersendelen. De verworven inzichten kunnen van belang zijn bij de ontwikkeling van betere medicijnen tegen emotionele stoornissen, bijvoorbeeld anti-depressiva
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Convergent neurobiological predictors of mood and anxiety symptoms and treatment response
No full textIntroduction: Mood and anxiety disorders are leading contributors to the global burden of diseases. Comorbid mood and anxiety disorders have a lifetime prevalence of ~20% globally and increases the risk for suicide, a leading cause of death.
Areas covered: In this review, authors highlight recent advances in the understanding of multilevel-neurobiological mechanisms for normal/pathological human affective-functioning. The authors then address the complex interplay between environmental-adversity and molecular-genetic mediators of brain correlates of affective-symptoms. The molecular focus is strategically limited to GTF2i, BDNF, and FKBP5 genes that are, respectively, involved in transcriptional-, neurodevelopmental- and neuroendocrine-pathway mediation of affective-functions. The importance of these genes is illustrated with studies of copy-number-variants, genome-wide association (GWAS), and candidate gene-sequence variant associations with disease etiology. Authors concluded by highlighting the predictive values of integrative neurobiological processing of gene-environment interactions for affective disorder symptom management.
Expert opinion: Given the transcriptional, neurodevelopmental and neuroimmune relevance of GTF2i, BDNF, and FKBP5 genes, respectively, authors reviewed the putative roles of these genes in neurobiological mediation of adaptive affective-responses. Authors discussed the importance of studying gene-dosage effects in understanding affective disorder risk biology, and how such targeted neurogenetic studies could guide precision identification of novel pharmacotherapeutic targets and aid in prediction of treatment response
Going Beyond Counting First Authors in Author Co-citation Analysis
Get PDFThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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