Factors In Bipolar Disorder Research Articles

An e-Health Psychoeducation Program for Managing the Mental Health of People with Bipolar Disorder during the COVID-19 Pandemic: A Randomized Controlled Study.

Background: Social rhythm dysregulation has been identified as a determining factor in bipolar disorder (BD) relapses. It directly impacts individuals' quality of life (QoL). This study aims to present preliminary data on the efficacy of an e-health psychoeducational intervention for BD for improving clinical outcomes. Methods: This study used an open-label, crossover, randomized controlled trial design. The inclusion criteria consisted of a BD diagnosis, affiliation with the Consultation Psychiatry and Psychosomatic Center at the University Hospital in Cagliari, Italy, age over 18, and the obtaining of informed consent. Anxiety and depressive symptoms, QoL, and social and biological rhythms were measured using standardized instruments validated in Italian. Results: A total of 36 individuals were included in the experimental group (EG) and 18 in the control group (CG). The final sample consisted of 25 in the EG and 14 in the CG. A statistically significant improvement in QoL was found in the EG post-treatment (p = 0.011). Significant correlations were found between QoL and the dysregulation of biorhythms in the EG at T0 (p = 0.0048) and T1 (p = 0.0014). Conclusions: This study shows that, during extreme distress, an e-health group psychoeducation intervention for people with BD could significantly improve the perception of QoL. The results must be confirmed by studies conducted with larger-sized samples.

The Role of Genetical Factors in Bipolar Disorder and the Underlying Mechanisms

The Role of Genetical Factors in Bipolar Disorder and the Underlying Mechanisms

Prevention of Suicidal Behavior in Bipolar Disorder.

Excess mortality is a critical hallmark of bipolar disorder (BD) due to co-occurring general medical disorders and especially from suicide. It is timely to review of the status of suicide in BD and to consider the possibility of limiting suicidal risk. We carried out a semi-systematic review of recent research reports pertaining to suicide in BD. Suicide risk in BD is greater than with most other psychiatric disorders. Suicide rates (per 100,000/year) are approximately 11 and 4 in the adult and juvenile general populations, but over 200 in adults, and 100 among juveniles diagnosed with BD. Suicide attempt rates with BD are at least 20 times higher than in the adult general population, and over 50 times higher among juveniles. Notable suicidal risk factors in BD include: previous suicidal acts, depression, mixed-agitated-dysphoric moods, rapid mood-shifts, impulsivity, and co-occurring substance abuse. Suicide-preventing therapeutics for BD remain severely underdeveloped. Evidence favoring lithium treatment is stronger than for other measures, although encouraging findings are emerging for other treatments. Suicide is a leading clinical challenge for those caring for BD patients. Improved understanding of risk and protective factors combined with knowledge and close follow-up of BD patients should limit suicidal risk. Ethically appropriate and scientifically sound studies of plausible medicinal, physical, and psychosocial treatments aimed at suicide prevention specifically for BD patients are urgently needed.Reprinted from Bipolar Disord 2021; 23:14-23, with permission from John Wiley and Sons. Copyright © 2021.

Suicidal risk and protective factors in major affective disorders: A prospective cohort study of 4307 participants

BackgroundSuicidal behavior is strongly associated with major affective disorders, but there is a need to quantify and compare specific risk and protective factors in bipolar disorder (BD) and major depressive disorder (MDD). MethodsIn 4307 extensively evaluated major affective-disorder participants with BD (n = 1425) or MDD (n = 2882) diagnosed by current international criteria, we compared characteristics among those with versus without suicidal acts from illness-onset through 8.24 years of follow-up. ResultsSuicidal acts were identified in 11.4 % of participants; 25.9 % were violent and 6.92 % (0.79 % of all participants) were fatal. Associated risk factors included: diagnosis (BD > MDD), manic/psychotic features in first-episodes, family history of suicide or BD, separation/divorce, early abuse, young at illness-onset, female sex with BD, substance abuse, higher irritable, cyclothymic or dysthymic temperament ratings, greater long-term morbidity, and lower intake functional ratings. Protective factors included marriage, co-occurring anxiety disorder, higher ratings of hyperthymic temperament and depressive first episodes. Based on multivariable logistic regression, five factors remained significantly and independently associated with suicidal acts: BD diagnosis, more time depressed during prospective follow-up, younger at onset, lower functional status at intake, and women > men with BD. LimitationsReported findings may or may not apply consistently in other cultures and locations. ConclusionsSuicidal acts including violent acts and suicides were more prevalent with BD than MDD. Of identified risk (n = 31) and protective factors (n = 4), several differed with diagnosis. Their clinical recognition should contribute to improved prediction and prevention of suicide in major affective disorders.

Demographic, clinical and biochemical correlates of the length of stay for different polarities in Chinese inpatients with bipolar disorder: A real-world study.

Introduction: Many patients with bipolar disorder (BD) need hospitalization, while the number of hospital beds for these patients is limited. Managing the length of stay (LOS) is an effective solution to this issue. Research on LOS and its influencing factors in BD is limited in China. This study aimed to identify the factors relevant to LOS in different polarities in Chinese patients with BD. Method: This was a real-world, cross-sectional study. Data were obtained from the electronic medical record system. Patients admitted to Beijing Anding Hospital between Jan 2014 and Dec 2017 and diagnosed with BD were included. Demographic information, clinical characteristics, and biochemical variables were collected. Patients were classified into short and long LOS groups based on a cutoff value. A univariate study and a multivariate logistic regression analysis were performed to identify variables related to LOS in various BD polarities. The receiver operating characteristic (ROC) analysis was utilized to evaluate the discrimination accuracy of the regression model. Result: Four thousand six hundred and seventy-five visits from 4,451 individuals were included in the analysis. For the whole sample, unmarried status, psychotic features, and family history of mental disorders were positively associated with long LOS (all p < 0.05). There was an additive interaction between a family history of mental disorders and polarities (p < 0.05). For manic episodes, unmarried status, psychotic features, and family history of mental disorders were positively associated with long LOS (all p < 0.05). For depressive episodes, psychotic features and high-density lipoprotein cholesterol (HDLC) levels were positively associated with long LOS (all p < 0.05). For mixed states, unmarried status was positively associated with long LOS, while low-density lipoprotein cholesterol (LDLC) levels were negatively associated with LOS (all p < 0.05). The area under the curve (AUC) values for depressive episodes, manic episodes, and mixed states in the combined model were 0.587, 0.553, and 0.619, respectively (all p < 0.05). Discussion: The findings suggested that LOS correlates differed by polarity, with marital status, psychotic features, a family history of mental disorders, and lipid levels strongly linked with LOS in patients with BD.

Gender-related association among childhood maltreatment, brain structure and clinical features in bipolar disorder

Bipolar disorder (BD) and exposure to childhood maltreatment (CM), which is present at high rates in BD, are both associated with hippocampus and prefrontal cortex structural alterations thought to contribute to clinical features. Gender-related differences are implicated in BD for CM exposure, brain structure and clinical features. However, relationships among these factors in BD are understudied. This study aimed to investigate associations among gender, CM, hippocampus and prefrontal gray matter structure and clinical features in BD. Childhood trauma questionnaire, structured clinical assessments and 3 Tesla structural magnetic resonance imaging were obtained for 236 adults (18–63 years, 32.0 ± 12.6): 119 with BD (58.8% women) and 117 healthy controls (HCs, 50.4% women). Women with BD reported higher CM severity than men with BD and HCs (B=-14.34, 95% confidence intervals (CI)[-22.71,-5.97], p<.001). CM and gender showed a significant interaction for left hippocampus (B=-7.41, 95% CI[-14.10,-0.71], p<.05); CM severity was negatively associated with left hippocampus only in women with BD. In women with BD, CM was associated with post-traumatic stress disorder comorbidity (B = 25.68, 95% CI[15.11,36.25], p<.001). In men with BD, CM severity was associated with lower left frontal pole (B=-0.71, 95% CI[-1.14,-0.28], p<.05) and right superior frontal (B=-17.78, 95% CI[-30.66,-4.90], p<.05) surface area; the latter related to earlier age of first mood symptoms (B = 33.97, 95% CI[7.61, 60.33], p<.05). Findings support gender-related effects of CM on frontotemporal structure and clinical features of BD. The findings bring novel perspectives for gendered pathophysiological models of effects of CM in BD.

Understanding the Developmental Pathways and Onset of Bipolar Disorder and Borderline Personality Disorder in Young People: A Systematic Review of Reviews

AimsThere is still an ongoing debate on the nosological position of Bipolar Disorder (BD) and Borderline Personality Disorder (BPD). Identifying the unique and shared risks and developmental pathways in emerging BD and BPD could help the field refine aetiological hypotheses of these disorders. The study aims were to systematically synthesise the available evidence from systematic reviews and meta-analyses concerning environmental, psychosocial, biological, and clinical factors leading to the emergence of BD and BPD to identify the main differences and common characteristics between the two disorders to characterise their complex interplay whilst highlighting remaining evidence gaps.MethodsA literature search was conducted PubMed, PsychINFO, EMBASE, Cochrane, CINAHL, MEDLINE, and ISI Web of Science as the data sources. 19 systematic reviews and meta-analyses involving 217 prospective studies met eligibility criteria.ResultsResults demonstrated that family history of psychopathology, affective instability, attention deficit hyperactivity disorder, anxiety disorders, depression, sleep disturbances, substance abuse, psychotic symptoms, suicidality, childhood adversity and temperament dimensions were common predisposing factors across both disorders. There are also many distinct variables that could be found early in the course of both disorders. Most of the factors should be considered as a general, nonspecific precursor signs and symptoms of both BPD and BD, apart from subsyndromal depression, subsyndromal hypomania, cyclothymia disorder, psychotic symptoms, age at onset of major depression and frequency and loading of affective symptoms.ConclusionAlthough the findings of this review may lead to support the view of BD and BPD as two distinct disorders, there is not sufficient data to either indicate that BD and BPD are separate nosological entities or that BPD should be considered as an extension of BD disorders. Future research is required to increase our understanding of the aetiology of BD and BPD onset and their complex interplay by conducting prospective studies which concurrently examine multiple measures including biological, environmental, psychosocial and clinical factors in BD and BPD at-risk populations. Large, multilevel data sets will enable deep phenotyping and distinguish pathophysiological pathways.

Insecure attachment as a transdiagnostic risk factor for major psychiatric conditions: A meta-analysis in bipolar disorder, depression and schizophrenia spectrum disorder

Insecure attachment has been suggested as a major risk factor for mental health problems as well as a key element for the development and trajectory of psychiatric disorders. The aim of this meta-analysis was to assess whether insecure attachment constitutes a global transdiagnostic risk factor in bipolar disorder, depression, and schizophrenia spectrum disorders. We conducted a PRISMA-based systematic quantitative review to explore the prevalence of insecure attachment among patients of three representative psychiatric disorders - major depression, schizophrenia spectrum disorders and bipolar disorder - in comparison with healthy controls (HC) from a transdiagnostic point of view. Effect sizes on differences of anxious, avoidant and insecure prevalence were calculated based on 40 samples including a total of n = 2927 individuals. Overall, results indicated a large effect on prevalence of insecure attachment across all disorders compared to HC (k = 30, g = 0.88, I2 = 71.0%, p < 0.001). In a transdiagnostic comparison, the only difference was found in avoidant attachment, which was significantly lower (p = 0.04) compared to HC in the schizophrenia spectrum disorder subgroup (k = 10, g = 0.31, I2 = 76.60%, p < 0.0001) than the depression subgroup subgroup (k = 12, g = 0.83, I2 = 46.65%, p < 0.0001). The lack of further transdiagnostic differences between three distinct psychiatric disorders corroborates insecure attachment as a general vulnerability factor to psychopathology. Our findings warrant further investigations, which should explore the pathways from attachment insecurity towards psychopathology. Insecure attachment likely has implications on assessment, prediction and treatment of psychiatric patients.

Environmental Risk Factors for Schizophrenia and Bipolar Disorder and Their Relationship to Genetic Risk: Current Knowledge and Future Directions.

Schizophrenia (SZ) and bipolar disorder (BD) are severe psychiatric disorders which result from complex interplay between genetic and environmental factors. It is well-established that they are highly heritable disorders, and considerable progress has been made identifying their shared and distinct genetic risk factors. However, the 15–40% of risk that is derived from environmental sources is less definitively known. Environmental factors that have been repeatedly investigated and often associated with SZ include: obstetric complications, infections, winter or spring birth, migration, urban living, childhood adversity, and cannabis use. There is evidence that childhood adversity and some types of infections are also associated with BD. Evidence for other risk factors in BD is weaker due to fewer studies and often smaller sample sizes. Relatively few environmental exposures have ever been examined for SZ or BD, and additional ones likely remain to be discovered. A complete picture of how genetic and environmental risk factors confer risk for these disorders requires an understanding of how they interact. Early gene-by-environment interaction studies for both SZ and BD often involved candidate genes and were underpowered. Larger samples with genome-wide data and polygenic risk scores now offer enhanced prospects to reveal genetic interactions with environmental exposures that contribute to risk for these disorders. Overall, although some environmental risk factors have been identified for SZ, few have been for BD, and the extent to which these account for the total risk from environmental sources remains unknown. For both disorders, interactions between genetic and environmental risk factors are also not well understood and merit further investigation. Questions remain regarding the mechanisms by which risk factors exert their effects, and the ways in which environmental factors differ by sex. Concurrent investigations of environmental and genetic risk factors in SZ and BD are needed as we work toward a more comprehensive understanding of the ways in which these disorders arise.

For whom the circadian clock ticks? Investigation of PERIOD and CLOCK gene variants in bipolar disorder

ABSTRACT Clock genes play significant roles in the regulation of circadian rhythms, which are thought to be involved in the pathophysiology of neurodegenerative and psychiatric diseases. We aimed to investigate the association of five gene polymorphisms (PER3 VNTR (rs57875989), PER2 rs2304672, CLOCK rs1801260, CLOCK rs10462028, CLOCK rs11932595) with PCR-based methods as potential risk factors in bipolar disorder (BD). We used a multiple testing methodology in BD patients (n = 121) and healthy control individuals (n = 121) of Turkish descent to analyze the effects of these gene variants both as risk factors for the disorder and for the evaluation of these variants in the patient group with multiple subscales. We evaluated the circadian rhythm disturbances and seasonal variations in mood and behavior in BD patients using the Biological Rhythms Interview of Assessment in Neuropsychiatry (BRIAN) and Seasonal Pattern Assessment Questionnaire (SPAQ) to enlighten the possible links between these scores and the studied circadian gene variants. The results of our study revealed significant associations: PER3 VNTR (rs57875989) 5/5 repeat genotype displayed a protective effect against BD when compared with 4/4 repeat genotype. Moreover, patients with PER3 VNTR 5/5 repeat genotype displayed a higher ratio of hypomania. PER2 rs2304672 G allele frequency increased the risk for BD. There was no association in terms of genotype/allele frequency comparisons between patients and controls for CLOCK gene variants. However, significant associations were found in patients in terms of clinical and behavioral patterns such as mean age at disease onset and BRIAN total scores enabling some risk stratifications for patients. Our results indicate the significance of circadian gene variants in BD, which need to be confirmed in different studies with larger samples. Thus, the possible endophenotypes of BD can be enlightened and advanced chronotherapeutics approaches can be manipulated in the future for clinical benefit.

Searching for the Causes of Bipolar Disorder: Mitochondrial Dysfunction Hypothesis and Beyond

Although the involvement of genomic factors in bipolar disorder is clear, its neural basis remains a question. We proposed the mitochondrial dysfunction hypothesis of bipolar disorder in 2000 and have since been testing it. Our results showed that mitochondrial DNA (mtDNA) polymorphisms affected mitochondrial Ca2+ concentration, and mitochondrial Ca2+ uptake and intracellular Ca2+ signaling were altered. Spontaneous repetitive depressive episodes were seen in mice in which mtDNA mutations accumulated in the brain (mutant Polg transgenic mice). We searched for the brain regions with the accumulation of mutant mtDNA in these mice, and found that it was most abundant in the paraventricular nucleus of the thalamus (PVT). Neural circuit manipulation of the PVT caused similar repetitive hypoactive episodes, suggesting that the PVT may be involved in causing bipolar disorder.

The effects of childhood emotional maltreatment and alexithymia on depressive and manic symptoms and suicidal ideation in females with bipolar disorder: emotion dysregulation as a mediator

Objectives The relations of childhood emotional maltreatment and alexithymia to the clinical course of bipolar disorder (BD) have been widely recognised. Difficulties in regulating emotions may explain these relationships. The current study evaluated the effects of childhood emotional maltreatment and alexithymia on depressive and manic symptoms as well as suicidal ideation in female patients with BD. Emotion dysregulation was evaluated as a mediating factor. Methods Three hundred hospitalised female patients with a diagnosis of BD provided information regarding their history of childhood emotional maltreatment, alexithymia, difficulties in emotion regulation, depressive and manic symptoms, and suicidal ideation. A series of structural equation models (SEMs) were calculated to assess the associations between these variables. Results Childhood emotional abuse and difficulty in identifying feelings were indirectly associated with depressive and manic symptoms as well as suicidal ideation. This association was mediated by emotion dysregulation. This association remained significant after depressive and manic symptoms were controlled in the model. Conclusions This study indicates that patients with BD who experienced emotional abuse during childhood and have difficulties identifying emotions report greater emotion dysregulation. These individuals, in turn, are more likely to experience more severe depressive and manic symptoms as well as suicidal ideation. Key points Childhood emotional maltreatment and emotional and clinical factors in bipolar disorder were assessed. Childhood emotional abuse indirectly affected clinical factors via emotion dysregulation. Difficulty in identifying feelings was linked to clinical factors via emotional dysregulation. Emotional dysregulation affected the links of childhood emotional maltreatment and difficulty in identifying feelings on suicidal ideation after controlling for clinical symptoms. Emotional dysregulation dimensions of impulse, strategies, and goals emerge in relation to suicidal ideation.

Evaluation of 45bp Ins/Del Genetic Variant in UCP-2 Gene as a Risk factor for Bipolar Disorder

Evaluation of 45bp Ins/Del Genetic Variant in UCP-2 Gene as a Risk factor for Bipolar Disorder

Environmental Risk Factors in Bipolar Disorder and Psychotic Depression: A Systematic Review and Meta-Analysis of Prospective Studies.

The aim of this systematic review and meta-analysis was to study the association between specific environmental risk factors (ERF) and later development of Bipolar disorder and Psychotic depression. A systematic search of prospective studies was conducted in MEDLINE, EMBASE and PsycINFO databases, and supplemented by hand searching, according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines (registration number: CRD42018092253). Selected ERF included: pre-/peri-natal factors-paternal age at birth, maternal infection, obstetric complications, perinatal stress; early childhood factors-urbanicity at birth, childhood infection, childhood adversity; later life factors-substance misuse, ethnic minority and migration, urbanicity later in life, stressful life events, and traumatic head injury. Pooled effect sizes of the association between these ERF and affective psychoses were calculated from systematically selected studies. When studies examining each ERF were insufficient for meta-analysis, results were presented narratively. Forty-six studies were included for quantitative analyses among selected ERF for affective psychosis, with significant association found for paternal age >40 years (OR 1.17, 95%CI 1.12-1.23), early (OR 1.52, 95%CI 1.07-2.17) and late (OR 1.32, 95%CI 1.05-1.67) gestational age, childhood adversity (OR 1.33, 95%CI 1.18-1.50), substance misuse (OR 2.87, 95%CI 1.63-5.50), and being from an ethnic minority (OR 1.99, 95%CI 1.39-2.84). These results suggest some shared environmental load between non-affective and affective psychosis, implying generalized risks for psychosis rather than for specific diagnostic categories. Nonetheless, published studies for some ERF in the affective psychoses are scarce, and further longitudinal studies are needed.

Brain-derived Neurotrophic Factor: a Key Gene Risk Factor and Potential Therapy Target in Bipolar Disorder

Bipolar Disorder (BD) is a worldwide, multifactorial mental disorder characterized by manic and depressive symptoms of varying degrees. Among all the genetic risk factors correlated with BD, brain-derived neurotrophic factor (BDNF) has emerged as a crucial neutropin that influences BD susceptibility with strong conservative across species and multiple downstream signaling pathways. However, the mechanisms of how BDNF polymorphism can contribute to BD are not yet lucid and systematically reviewed. BDNF Val66Met variant is capable of inducing neurodegenisis and Long-term Depression (LTD), both of which account for pathogenesis in BD. The Val66Met variant is associated with rapid cycling episodes in BD. Another variant, Arg125Met is a potential BD risk variant which elicits neuronal apoptosis by affecting the maturation of BDNF. In this paper, we briefly summarized BD epidemiology, symptoms, BDNF structure, and its action of function. We reviewed various mechanisms of BDNF Val66Met and Arg125Met variant for BD pathogenesis in detail and provided insights into possible BD clinical treatment targets. BDNF has been proven to be a noteworthy gene factor in BD and gene therapy targeted on BDNF is a promising therapeutic strategy that requires further research.

Towards a Comprehensive Understanding of Bipolar Disorder: In Vivo MRS Investigation of the Phosphatidylinositol Cycle

&#x0D; &#x0D; &#x0D; &#x0D; At present, both the neuropathophysiology of bipolar disorder as well as the mechanism(s) through which current mood-stabilizing agents provide symptom relief are unknown. Through the recent utilization of magnetic resonance spectroscopy (MRS), progress has been made; with optimistic interest being focused on the phosphatidylinositol (PI) cycle as a likely neuropathophysiological factor in bipolar disorder. The present manuscript reviews this interesting and promising area, placing emphasis on the magnetic resonance spectroscopy investigations of PI- cycle function in bipolar disorder reported to date. While relatively few well-designed MRS studies have investigated PI-cycle function in bipolar disorder, current evidence does lend support to PI-cycle involvement in bipolar neuropathophysiology as a means through which mood-stabilizing agents act; pointing to PI-cycle dysfunction as an important neuropathophysiological factor in bipolar disorder. However, there still remains a dearth of information about this interesting hypothesis. In addition to lithium, more data is needed regarding the effects on PI-cycle function of the other commonly prescribed mood-stabilizing agents. As well, studies investigating the temporal relationship between medication effect on PI-cycle functioning and symptom improvement are warranted. In tandem with clinical MRS investigation of bipolar disorder, further preclinical study of the neurochemical effects of mood-stabilizing agents is needed. Finally, greater methodological rigor needs to be implemented during the design phase of any future MRS investigation into bipolar disorder, with particular attention aimed at recruiting a large homogenous sample of bipolar patients.&#x0D; &#x0D; &#x0D; &#x0D;

Prevention of suicidal behavior in bipolar disorder.

Excess mortality is a critical hallmark of bipolar disorder (BD) due to co-occurring general medical disorders and especially from suicide. It is timely to review of the status of suicide in BD and to consider the possibility of limiting suicidal risk. We carried out a semi-systematic review of recent research reports pertaining to suicide in BD. Suicide risk in BD is greater than with most other psychiatric disorders. Suicide rates (per 100,000/year) are approximately 11 and 4 in the adult and juvenile general populations, but over 200 in adults, and 100 among juveniles diagnosed with BD. Suicide attempt rates with BD are at least 20 times higher than in the adult general population, and over 50 times higher among juveniles. Notable suicidal risk factors in BD include: previous suicidal acts, depression, mixed-agitated-dysphoric moods, rapid mood-shifts, impulsivity, and co-occurring substance abuse. Suicide-preventing therapeutics for BD remain severely underdeveloped. Evidence favoring lithium treatment is stronger than for other measures, although encouraging findings are emerging for other treatments. Suicide is a leading clinical challenge for those caring for BD patients. Improved understanding of risk and protective factors combined with knowledge and close follow-up of BD patients should limit suicidal risk. Ethically appropriate and scientifically sound studies of plausible medicinal, physical, and psychosocial treatments aimed at suicide prevention specifically for BD patients are urgently needed.

Brain-derived neurotrophic factor in bipolar disorder: Associations with age at onset and illness duration

Bipolar disorder (BD) is a heterogeneous disorder that contains neurodevelopmental differences. Defining homogeneous subgroups of BD patients by using age at onset (AAO) as a specifier may promote the classification of biomarkers. This study compares peripheral BDNF levels between pediatric and adult BD patients to investigate the associations between BDNF levels, AAO, and illness duration. We enrolled two groups of euthymic patients, those with pediatric BD (n = 39) and those with adult BD (n = 31), as well as a group of healthy controls (HCs) (n = 90). Participants were assessed using clinical measures and BDNF serum levels were obtained using ELISA. We observed that BDNF levels were comparable between adult BD and HCs, but were clearly lower in pediatric BD than in HCs. In adult BD with AAO ≥30 years, BDNF levels were significantly higher than in adult BD with AAO <30 years. In pediatric BD, patients with prepubertal-onset had higher BDNF levels than those with pubertal-onset. BDNF levels demonstrated the accuracy of being able to distinguish pediatric BD from healthy controls in a receiver operating characteristic (ROC) curve analysis (area under the curve [AUC] = 0.792). In adult BD, higher BDNF levels were associated with later disease onset, but this was not the case in pediatric BD. Finally, reduced BDNF levels were associated with illness duration in adult BD. The findings indicate that BDNF levels in BD patients are associated with AAO. BDNF may, therefore, potentially serve as a developmental marker in BD, when AAO is taken into account.

Genetics, not child‐rearing, main factor in bipolar disorder

The Brown University Child & Adolescent Psychopharmacology UpdateVolume 22, Issue 5 p. 8-8 Research Briefs Genetics, not child-rearing, main factor in bipolar disorder First published: 14 April 2020 https://doi.org/10.1002/cpu.30493Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume22, Issue5May 2020Pages 8-8 RelatedInformation

One Single Nucleotide Polymorphism of the TRPM2 Channel Gene Identified as a Risk Factor in Bipolar Disorder Associates With Autism Spectrum Disorder in a Japanese Population

The transient receptor potential melastatin 2 (TRPM2) is a non-specific cation channel, resulting in Ca2+ influx at warm temperatures from 34 °C to 47 °C, thus including the body temperature range in mammals. TRPM2 channels are activated by β-NAD+, ADP-ribose (ADPR), cyclic ADPR, and 2′-deoxyadenosine 5′-diphosphoribose. It has been shown that TRPM2 cation channels and CD38, a type II or type III transmembrane protein with ADP-ribosyl cyclase activity, simultaneously play a role in heat-sensitive and NAD+ metabolite-dependent intracellular free Ca2+ concentration increases in hypothalamic oxytocinergic neurons. Subsequently, oxytocin (OT) is released to the brain. Impairment of OT release may induce social amnesia, one of the core symptoms of autism spectrum disorder (ASD). The risk of single nucleotide polymorphisms (SNPs) and variants of TRPM2 have been reported in bipolar disorder, but not in ASD. Therefore, it is reasonable to examine whether SNPs or haplotypes in TRPM2 are associated with ASD. Here, we report a case-control study with 147 ASD patients and 150 unselected volunteers at Kanazawa University Hospital in Japan. The sequence-specific primer-polymerase chain reaction method together with fluorescence correlation spectroscopy was applied. Of 14 SNPs examined, one SNP (rs933151) displayed a significant p-value (OR = 0.1798, 95% CI = 0.039, 0.83; Fisher’s exact test; p = 0.0196). The present research data suggest that rs93315, identified as a risk factor for bipolar disorder, is a possible association factor for ASD.