Genetic association of dopamine beta-hydroxylase (DBH) rs72393728 and D-amino acid oxidase activator (DAOA) rs3918342 polymorphisms with bipolar disorder in northeastern Algeria

Association between DAOA gene polymorphisms and the risk of schizophrenia, bipolar disorder and depressive disorder

Specific anxiety disorders and subsequent risk for bipolar disorder: a nationwide study.

of a G72 susceptibility haplotype on fiber tract integrity in young healthy probands. They found clusters of increased fractional anisotropy in homozygous risk haplotype carriers in the right periinsular and inferior parietal region. Both regions have been hypothesized to be involved in the pathophysiology of bipolar disorder and schizophrenia, and alterations in fractional anisotropy may reflect changes in neuropil such as morphology of dendrites. In a functional magnetic resonance imaging (fMRI) study using a working memory task, Stegmayer et al. [4] found reduced functional interactions of the right amygdala with cortical regions supporting verbal working memory in 18 bipolar patients compared with 18 healthy controls. The results point to a disturbed right-hemispheric cognitive–emotional interaction between the amygdala and cortical regions, leading to deficits in working memory. In bipolar disorder, poorer prognosis is related to weight gain and obesity. Lackner et al. [5] investigated body mass index, obesity measures, lipometry, metabolic parameters and monoamines in a large sample of bipolar patients compared with healthy controls. In the patient group, they found increased abdominal fat accumulation and measures of the metabolic syndrome along with correlation with epinephrine levels. The glutamate system has been reported to be involved in the pathophysiology of both bipolar disorder and major depression. Quinolinic acid is produced by activated microglia and is an agonist at the glutamatergic N-methyl-d-aspartate (NMDA) receptor. In a postmortem study, Busse et al. [6] investigated immunohistochemistry of quinolinic acid in hippocampal subregions of 12 patients with depression, among them 6 unipolar and 6 bipolar, and 10 healthy controls. Quinolinic-positive microglia was reduced in unipolar and bipolar patients in the right CA1 subregion. A degradation of quinolinic acid may be involved in the In the new DSM-5 and ICD-11 classification systems, pure mania and mania with mild depression are subsumed under bipolar disorder. In a comprehensive review, Angst and Grobler [1] vote for improved differential diagnoses of unipolar mania. This is clinically relevant since the disorder has a prevalence of approximately 1.8 %, and clinical follow-up studies demonstrated good diagnostic stability. Moreover, mania is associated with a hyperthymic temperament, more psychotic symptoms and higher heritability compared with depression. In contrast, the concept of bipolar disorder has been widely investigated in neurogenetic studies. For example, the dopaminergic system has been suggested to be affected in bipolar disorder, but the impact of the genetic variants of the human dopamine transporter DAT1 (SLC6A3) is inconsistent. Huang et al. [2] investigated the association of 18 polymorphisms of the DAT1 gene with bipolar disorder and explored its influence on specific personality traits such as novelty seeking and harm avoidance. Several polymorphisms had a weak association with bipolar disorder, and the promotor G-A-C-G haplotype was overrepresented in their sample of 492 patients compared with 436 healthy controls. Bipolar II patients had the highest harm avoidance score and a significant association between rs40184 of DAT1 and this personality trait in patients with bipolar disorder. G72 (D-amino acid oxidase activator, DAOA) is a susceptibility gene for bipolar disorder and schizophrenia. In a diffusion tensor imaging (DTI) study, Nickl-Jockschat et al. [3] investigated the influence

Increased brain d-amino acid oxidase (DAAO) activity in schizophrenia

The Loudness Dependence of Auditory Evoked Potentials (LDAEP) in individuals at risk for developing bipolar disorders and schizophrenia

The risk of Bipolar Disorders in Multiple Sclerosis

Frontal brain activity in individuals at risk for schizophrenic psychosis and bipolar disorder during the emotional Stroop task - an fNIRS study.

The nature of the genetic relationship between major depression and bipolar disorder remains unclear and might be clarified by considering disorders outside of the mood spectrum. To better understand the relationship between genetic liabilities for major depression (MD) and bipolar disorder (BD). A cohort study was conducted with data for individuals born in Sweden to Swedish parents from 1960 to 1990, with follow-up through December 31, 2018. The data included family genetic risk scores for MD and BD and International Classification of Diseases codes for a range of disorders as reported in primary care, specialist, and hospital registries. Data analysis was conducted from April 2022 to July 2022. High and low genetic liability were defined as being in the upper and lower 2 risk deciles. Risk was compared in individuals at high genetic liability to (1) MD only, (2) BD only, and (3) both MD and BD and those at (4) high genetic liability to BD and low genetic liability to MD and (5) high genetic liability to MD and low genetic liability to BD. Risk for nonpsychotic MD and BD, psychotic MD and BD, anxiety disorders, obsessive-compulsive disorder, schizoaffective disorder (SAD), schizophrenia, and other nonaffective psychosis. Data were included for 2 736 950 individuals with a mean (SD) age at follow-up of 43.9 (9.1) years. High genetic liability to only BD increased risk for nonpsychotic BD, psychotic BD, and SAD. High genetic liability to only MD augmented risk for nonpsychotic MD, anxiety disorders, and nonpsychotic BD. High genetic liability to both BD and MD had the strongest association with risk for nonpsychotic BD, anxiety disorders, and nonpsychotic MD. High genetic liability to BD and low genetic liability to MD increased risk for psychotic BD, nonpsychotic BD, and SAD with no increased risk for nonpsychotic MD or anxiety disorders. High genetic liability to MD and low genetic liability to BD increased risk for nonpsychotic MD, nonpsychotic BD, and anxiety disorders with no increased risk for psychotic BD. In this study, hypotheses that BD and MD are either genetically distinct or genetically closely interrelated were not supported. Both BD and MD were associated with a genetic vulnerability to mood disorders, but even that liability was partially selective. However, compared with individuals at high liability to MD, those at elevated genetic liability for BD had a substantially increased risk for psychosis. Compared with individuals at elevated genetic liability to BD, those at high genetic risk for MD had a considerably augmented risk for anxiety disorders. Clarifying genetic relationships between psychiatric syndromes can be substantially aided by the consideration of profiles of risk for a range of disorders.

Background: A recent study has shown the beneficial effects of interferon (IFN)-based antiviral therapy (AVT) in reducing the risk of newly diagnosed depression among patients with hepatitis C virus (HCV) infection. But whether IFN-based AVT reduces the risk of bipolar disorder remains unknown. Methods: This is a retrospective study based on the Taiwan National Health Insurance Research Database. From enrollment to the end of 2013, 24,240 patients with HCV infection (4473 treated with IFN-based AVT and 19,767 without such treatment) as well as 96,960 age- and sex-matched controls were included in this study. Time-dependent Cox regression models were used to study the differences in risk of newly-diagnosed bipolar disorder between patients being treated with and without IFN-based AVT and the control participants. Results: Patients with HCV infection who had not yet received IFN-based AVT (hazard ratio = 4.86, 95% confidence interval = 1.87–12.66, p = 0.001), but not those who were receiving IFN-based AVT (1.69, 0.94 - 30.50, nonsignificance) and those who completed the IFN-based AVT (1.77, 0.69 - 4.54, nonsignificance), were significantly more to be diagnosed with bipolar disorder compared with the control group. Conclusion: Our study supports the temporal association between HCV infection and subsequent bipolar disorder, further suggesting that the optimal AVT to eradicate HCV may be associated with a reduced risk of incident bipolar disorder later in life.

Abstracts for the IXth World Congress of Psychiatric Genetics, Saint Louis, Missouri

Attention-deficit hyperactivity disorder (ADHD) is associated with bipolar disorder and schizophrenia, and it has been suggested that combined bipolar disorder and ADHD is aetiologically distinct from the pure disorders. To clarify whether ADHD shares genetic and environmental factors with bipolar disorder and schizophrenia. By linking longitudinal Swedish national registers, we identified 61 187 persons with ADHD (the proband group) and their first- and second-degree relatives, and matched them with a control group of people without ADHD and their corresponding relatives. Conditional logistic regression was used to determine the risks of bipolar disorder and schizophrenia in the relatives of the two groups. First-degree relatives of the ADHD proband group were at increased risk of both bipolar disorder (odds ratio (OR) = 1.84-2.54 for parents, offspring and full siblings) and schizophrenia (OR = 1.71-2.22 for parents, offspring and full siblings). The risks of bipolar disorder and schizophrenia among second-degree relatives were substantially lower than among full siblings. These findings suggest that the co-occurrence of ADHD and bipolar disorder as well as ADHD and schizophrenia is due to shared genetic factors, rather than representing completely aetiologically distinct subsyndromes.

New serological evidence points toward an infectious route to bipolar disorder.

Influence of DAOA and RGS4 genes on the risk for psychotic disorders and their associated executive dysfunctions: A family-based study

Bipolar disorders (BD) are characterized by symptoms of grandiosity, decreased need for sleep, pressure to keep talking, flight of ideas, distractibility, increased goal-directed activities, psychomotor agitation, and excessive involvement in pleasurable activities. Those with a bipolar disorder have a high degree of psychiatric comorbidity including substance use disorders, and they also experience increased mortality. Despite the widespread recognition of BD as an important psychiatric condition, available population-based estimates for BD prevalence differs across data sources. Cannabis is one of the most widely-used illicit substances. Evidence supports it as a risk factor for psychotic symptoms and disorders. Because populations with psychotic disorders and populations with bipolar disorder share genetic characteristics, cannabis may increase risk for bipolar disorders through the same pathways as it does with psychotic disorders. Limited and conflicting evidence regarding the association of cannabis use and bipolar disorder is currently available. This dissertation investigates cannabis use as a risk factor for incident manic symptoms and bipolar disorders in a large nationally representative longitudinal cohort. The first aim of this dissertation is to evaluate the implications for manic, hypomanic and major depressive episode prevalence estimates arising from the different approaches to assessing DSM-IV criterion between two national surveys. Differences in the assessment of impairment strongly influence manic or hypomanic classification within the NESARC. Compared to multiple imputation estimates (19.7% [95% CI: 19.3-20.1]) which treat depressed mood and anhedonia as separate symptoms, symptom assessment in the NESARC substantially underestimates major depressive episode prevalence (16.9% [95% CI: 16.1-17.6]). The second research objective examined self-reported cannabis use as a risk factor for incident manic symptoms, bipolar spectrum disorders (including manic and hypomanic episodes) and SCID-based recalibrated BD I and II. Cannabis use risk was assessed in the population as a whole and in sub-populations defined by age, substance abuse/dependence status, and family history. Among those reporting no lifetime major depressive or manic symptoms at baseline, self-reported past-year cannabis use was associated with increased odds of an incident week of extremely elevated or irritable mood accompanied by at least two manic episode criterion B symptoms (adj. OR 1.69, 95% CI: 1.08-2.65, p=.02) over the three year follow-up period. Among adults (ages 26 to 45) >=1 reported use(s) of cannabis per week was associated with incident manic or hypomanic episodes (adjusted OR 2.52, 95% CI: 1.32-4.80, p=.006). Among those endorsing no major depressive symptoms, substance abuse/dependence, or anti-social traits in their first degree relatives, past year cannabis use is associated with increased risk for incident bipolar spectrum disorders (adjusted OR 2.27, 95% CI: 1.01-5.10, p=.05) and CIDI…

Characteristics of youth at high risk for bipolar disorder compared to youth with bipolar I or II disorder