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1.
  • Joas, Erik, et al. (författare)
  • Effect of CYP2C19 polymorphisms on antidepressant prescription patterns and treatment emergent mania in bipolar disorder.
  • 2023
  • Ingår i: The pharmacogenomics journal. - : Springer Science and Business Media LLC. - 1473-1150 .- 1470-269X. ; 23:1, s. 28-35
  • Tidskriftsartikel (refereegranskat)abstract
    • Antidepressant medication is used extensively to treat bipolar depression despite uncertain efficacy. The cytochrome P450 (CYP) 2C19 enzyme metabolize several antidepressants, and polymorphisms in the corresponding gene CYP2C19 influence plasma concentration and hence treatment outcomes in major depressive disorder. Here, we investigate if CYP2C19 polymorphisms are associated with antidepressant treatment patterns and the risk of mania when antidepressants are used in bipolar disorder. Two single nucleotide polymorphisms (rs4244285 and rs12248560) were used to classify 5019 bipolar disorder patients into CYP2C19 metabolic phenotypes ranging from poor to ultra-rapid metabolizers. We used Swedish national registry data 2005-2017 on dispensed medications and inpatient care to estimate risks for early-treatment persistence, treatment discontinuation, switching to a new antidepressant medication, and mania within 3 months of treatment initiation in patients treated with citalopram, escitalopram, sertraline, amitriptyline, and clomipramine. Metabolic phenotypes of CYP2C19 were not robustly associated with the investigated treatment outcomes based on dispense patterns. Slower metabolism was associated with an increased risk of treatment emergent mania for sertraline (hazard ratio [HR]=1.3, 95% CI=1.04-1.62, p=0.02) and the tricyclic antidepressants amitriptyline and clomipramine (HR=1.46, 95% CI=1.05-2.02, p=0.024). In a large study of the impact of CYP2C19 metabolic phenotypes on antidepressant treatment of bipolar depression, we found an association between slower CYP2C19 metabolism and higher risk of treatment emergent mania, which is a step towards personalized risk assessments. There were, however, no clear associations with early treatment persistence, treatment discontinuation, and switching to a new antidepressant.
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2.
  • Folkersen, Lasse, et al. (författare)
  • Genomic and drug target evaluation of 90 cardiovascular proteins in 30,931 individuals.
  • 2020
  • Ingår i: Nature metabolism. - : Springer Science and Business Media LLC. - 2522-5812. ; 2:10, s. 1135-1148
  • Tidskriftsartikel (refereegranskat)abstract
    • Circulating proteins are vital in human health and disease and are frequently used as biomarkers for clinical decision-making or as targets for pharmacological intervention. Here, we map and replicate protein quantitative trait loci (pQTL) for 90 cardiovascular proteins in over 30,000 individuals, resulting in 451 pQTLs for 85 proteins. For each protein, we further perform pathway mapping to obtain trans-pQTL gene and regulatory designations. We substantiate these regulatory findings with orthogonal evidence for trans-pQTLs using mouse knockdown experiments (ABCA1 and TRIB1) and clinical trial results (chemokine receptors CCR2 and CCR5), with consistent regulation. Finally, we evaluate known drug targets, and suggest new target candidates or repositioning opportunities using Mendelian randomization. This identifies 11 proteins with causal evidence of involvement in human disease that have not previously been targeted, including EGF, IL-16, PAPPA, SPON1, F3, ADM, CASP-8, CHI3L1, CXCL16, GDF15 and MMP-12. Taken together, these findings demonstrate the utility of large-scale mapping of the genetics of the proteome and provide a resource for future precision studies of circulating proteins in human health.
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3.
  • Göteson, Andreas, 1991, et al. (författare)
  • Alterations in the Serum Proteome Following Electroconvulsive Therapy for a Major Depressive Episode: A Longitudinal Multicenter Study
  • 2023
  • Ingår i: Biological Psychiatry: Global Open Science. - : Elsevier BV. - 2667-1743. ; 3:4, s. 884-892
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Electroconvulsive therapy (ECT) is the most effective treatment for severe depression, but the biological changes induced by ECT remain poorly understood.METHODS: This study investigated alterations in blood serum proteins in 309 patients receiving ECT for a major depressive episode. We analyzed 201 proteins in samples collected at 3 time points (T): just before the first ECT treatment session (T0), within 30 minutes after the first ECT session (T1), and just before the sixth ECT session (T2).RESULTS: Using statistical models to account for repeated sampling, we identified 152 and 70 significantly (,5% false discovery rate) altered proteins at T1 and T2, respectively. The most pronounced alterations at T1 were tran-siently increased levels of prolactin, myoglobin, and kallikrein-6. However, most proteins had decreased levels at T1, with the largest effects observed for pro-epidermal growth factor, proto-oncogene tyrosine-protein kinase Src, tumor necrosis factor ligand superfamily member 14, sulfotransferase 1A1, early activation antigen CD69, and CD40 ligand. The change of several acutely altered proteins correlated with electric current and pulse frequency in a dose-response-like manner. Over a 5-session course of ECT, some acutely altered levels were sustained while others increased, e.g., serine protease 8 and chitinase-3-like protein 1. None of the studied protein biomarkers were associated with clinical response to ECT.CONCLUSIONS: We report experimental data on alterations in the circulating proteome triggered by ECT in a clinical setting. The findings implicate hormonal signaling, immune response, apoptotic processes, and more. None of the findings were associated with clinical response to ECT.
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4.
  • Göteson, Andreas, 1991, et al. (författare)
  • Cerebrospinal fluid proteomics targeted for central nervous system processes in bipolar disorder
  • 2021
  • Ingår i: Molecular Psychiatry. - : Springer Science and Business Media LLC. - 1359-4184 .- 1476-5578. ; 26, s. 7446-53
  • Tidskriftsartikel (refereegranskat)abstract
    • The etiopathology of bipolar disorder is largely unknown. We collected cerebrospinal fluid (CSF) samples from two independent case-control cohorts (total n = 351) to identify proteins associated with bipolar disorder. A panel of 92 proteins targeted towards central nervous system processes identified two proteins that replicated across the cohorts: the CSF concentrations of testican-1 were lower, and the CSF concentrations of C-type lectin domain family 1 member B (CLEC1B) were higher, in cases than controls. In a restricted subgroup analysis, we compared only bipolar type 1 with controls and identified two additional proteins that replicated in both cohorts: draxin and tumor necrosis factor receptor superfamily member 21 (TNFRSF21), both lower in cases than controls. This analysis additionally revealed several proteins significantly associated with bipolar type 1 in one cohort, falling just short of replicated statistical significance in the other (tenascin-R, disintegrin and metalloproteinase domain-containing protein 23, cell adhesion molecule 3, RGM domain family member B, plexin-B1, and brorin). Next, we conducted genome-wide association analyses of the case-control-associated proteins. In these analyses, we found associations with the voltage-gated calcium channel subunit CACNG4, and the lipid-droplet-associated gene PLIN5 with CSF concentrations of TNFRSF21 and CLEC1B, respectively. The reported proteins are involved in neuronal cell-cell and cell-matrix interactions, particularly in the developing brain, and in pathways of importance for lithium's mechanism of action. In summary, we report four novel CSF protein associations with bipolar disorder that replicated in two independent case-control cohorts, shedding new light on the central nervous system processes implicated in bipolar disorder.
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5.
  • Hansson, Caroline, 1981, et al. (författare)
  • Risk factors for suicide in bipolar disorder: a cohort study of 12 850 patients
  • 2018
  • Ingår i: Acta Psychiatrica Scandinavica. - : Wiley. - 0001-690X .- 1600-0447. ; 138:5, s. 456-463
  • Tidskriftsartikel (refereegranskat)abstract
    • ObjectiveMethodBipolar disorder carries a high risk of suicide. Identification of risk factors is important. The aim of this study was to study risk factors for suicide in a large cohort of men and women with bipolar disorder. A prospective cohort study using clinical data from the Swedish National Quality Register for Bipolar Affective Disorder (BipolaR). The outcome variable was suicide captured in the Cause of Death Register between 2004 and 2014. Hazard ratios (HR) were calculated using Cox proportional hazards models. ResultsConclusionsOf 12 850 persons (4844 men and 8006 women) with bipolar disorder, 90 (55 men and 35 women) died by suicide during the follow-up period (between 1 and 10 years). Male sex (HR 2.56), living alone (HR 2.45), previous suicide attempts (HR 4.10), comorbid psychiatric disorder (HR 2.64), recent affective episodes (HR 2.39), criminal conviction (HR 4.43), psychiatric inpatient care (HR 2.79), and involuntary commitment (HR 3.50) were significant risk factors for suicide. Several of the statistically significant risk factors for suicide in bipolar disorder differed between men and women. Risk factors for suicide in bipolar disorder include factors associated with suicide in general, but also diagnosis-specific factors.
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6.
  • Joas, Erik, 1983, et al. (författare)
  • Psychoeducation for bipolar disorder and risk of recurrence and hospitalization - a within-individual analysis using registry data.
  • 2020
  • Ingår i: Psychological medicine. - 1469-8978. ; 50:6, s. 1043-1049
  • Tidskriftsartikel (refereegranskat)abstract
    • The efficacy of psychoeducation for bipolar disorder has been demonstrated in clinical trials, but it is not known if the results translate into effectiveness in routine clinical practice. The aim was to determine the effectiveness of psychoeducation for bipolar disorder in a routine clinical setting.We identified 2819 patients with at least three registrations in the Swedish Quality Assurance Register for Bipolar Disorder. Among those, 402 had not been exposed to psychoeducation at the first visit, but received psychoeducation during any of the following registrations. Using within-individual analyses, the risk of recurrence after having received psychoeducation was compared with the risk prior to psychoeducation.In adjusted within-individuals comparisons, periods after psychoeducation was associated with decreased risks of any recurrence [odds ratio (OR) 0.57, 95% CI 0.42-0.78], (hypo-)manic or mixed episodes (OR 0.54, 95% CI 0.39-0.76), depressive episodes (OR 0.63, 95% CI 0.47-0.86), and inpatient care (OR 0.54, 95% CI 0.33-0.86) relative to periods prior to psychoeducation. There was no association with rates of involuntary sectioning or suicide attempts.The results suggest that psychoeducation for bipolar disorder reduces the risk of mood episodes and inpatient care also when implemented in routine clinical practice.
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7.
  • Jonsson, Lina, 1982, et al. (författare)
  • Association of Occupational Dysfunction and Hospital Admissions With Different Polygenic Profiles in Bipolar Disorder.
  • 2024
  • Ingår i: The American journal of psychiatry. - 1535-7228. ; 181:7, s. 620-629
  • Tidskriftsartikel (refereegranskat)abstract
    • Many but not all persons with bipolar disorder require hospital care because of severe mood episodes. Likewise, some but not all patients experience long-term occupational dysfunction that extends beyond acute mood episodes. It is not known whether these dissimilar outcomes of bipolar disorder are driven by different polygenic profiles. Here, polygenic scores (PGSs) for major psychiatric disorders and educational attainment were assessed for associations with occupational functioning and psychiatric hospital admissions in bipolar disorder.A total of 4,782 patients with bipolar disorder and 2,963 control subjects were genotyped and linked to Swedish national registers. Longitudinal measures from at least 10 years of registry data were used to derive percentage of years without employment, percentage of years with long-term sick leave, and mean number of psychiatric hospital admissions per year. Ordinal regression was used to test associations between outcomes and PGSs for bipolar disorder, schizophrenia, major depressive disorder, attention deficit hyperactivity disorder (ADHD), and educational attainment. Replication analyses of hospital admissions were conducted with data from the Bipolar Disorder Research Network cohort (N=4,219).Long-term sick leave and unemployment in bipolar disorder were significantly associated with PGSs for schizophrenia, ADHD, major depressive disorder, and educational attainment, but not with the PGS for bipolar disorder. By contrast, the number of hospital admissions per year was associated with higher PGSs for bipolar disorder and schizophrenia, but not with the other PGSs.Bipolar disorder severity (indexed by hospital admissions) was associated with a different polygenic profile than long-term occupational dysfunction. These findings have clinical implications, suggesting that mitigating occupational dysfunction requires interventions other than those deployed to prevent mood episodes.
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8.
  • Karanti, Alina (Aikaterini), et al. (författare)
  • Characteristics of bipolar I and II disorder: A study of 8766 individuals.
  • 2020
  • Ingår i: Bipolar disorders. - : Wiley. - 1399-5618 .- 1398-5647. ; 22:4, s. 392-400
  • Tidskriftsartikel (refereegranskat)abstract
    • Large-scale studies on phenotypic differences between bipolar disorder type I (BDI) and type II (BDII) are scarce.Individuals with BDI (N=4806) and BDII (N=3960) were compared with respect to clinical features, illness course, comorbid conditions, suicidality, and socioeconomic factors using data from the Swedish national quality assurance register for bipolar disorders (BipoläR).BDII had higher rate of depressive episodes and more frequent suicide attempts than BDI. Furthermore, the BDII group were younger at first sign of mental illness and showed higher prevalence of psychiatric comorbidity but were more likely to have completed higher education and to be self-sustaining than the BDI group. BDII more frequently received psychotherapy, antidepressants, and lamotrigine. BDI patients had higher rate of hospitalizations and elated episodes, higher BMI, and higher rate of endocrine, nutritional, and metabolic diseases. BDI were more likely to receive mood stabilizers, antipsychotic drugs, electroconvulsive therapy, and psychoeducation.These results demonstrate clear differences between BDI and II and counter the notion that BDII is a milder form of BDI, but rather a more complex condition with regard to clinical course and comorbidity.
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9.
  • Najar, Hemen, et al. (författare)
  • Recent Secular Trends of Body Mass Index in Individuals With Bipolar Disorders and in the General Population.
  • 2024
  • Ingår i: The American journal of psychiatry. - 1535-7228. ; 181:1, s. 39-46
  • Tidskriftsartikel (refereegranskat)abstract
    • The aims of this study were to investigate secular trends and distribution of body mass index (BMI) among individuals with bipolar disorders and the general population between 2008 and 2019.Data were from the Swedish National Quality Register for Bipolar Disorder, where 24,423 adults with bipolar disorders were identified, and from the national Swedish Living Conditions Surveys, where 77,485 adults from the general population were identified. Quantile regression was used to compare the 15th, 50th, and 85th percentiles of BMI across age and study years.The study sample included 22,127 individuals with bipolar disorders (mean age, 48 years; 63% women) and 71,894 individuals from the general population (mean age, 52 years; 51% women). BMI percentiles were higher among individuals with bipolar disorders. At the 50th percentile, the BMI group differences were 1.1 (95% CI=0.8-1.14) for men and 1.8 (95% CI=1.5-2.1) for women. The gap was widest at the 85th BMI percentile: men, 2.3 (95% CI=1.8-2.8); women, 4.1 (95% CI=3.7-4.6). BMI increased over time in both study groups, but more in the group with bipolar disorders. The changes per decade in mean BMI were 0.4 (95% CI=0.3-0.5) among men in the general population, 1.1 (95% CI=0.7-1.4) among men with bipolar disorders, 0.6 (95% CI=0.5-0.7) among women in the general population, and 1.4 (95% CI=1.1-1.7) among women with bipolar disorders. Women with bipolar disorders had the highest prevalence and the greatest rate of increase of obesity. In 2019, the obesity prevalence was 33% among women and 29% among men with bipolar disorders, compared with 13% and 15%, respectively, among women and men in the general population.Adults with bipolar disorders had a higher BMI and a higher prevalence of obesity than the general population, indicating a higher cardiometabolic risk. Annually, BMI increased more in the group with bipolar disorders than in the general population, particularly among women and among those with high BMI.
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10.
  • Najar, Hemen, 1979, et al. (författare)
  • Time effect on cardiometabolic risk indicators in patients with bipolar disorder: a longitudinal case-control study
  • 2023
  • Ingår i: European Archives of Psychiatry and Clinical Neuroscience. - : Springer Science and Business Media LLC. - 0940-1334 .- 1433-8491. ; 273:5, s. 1191-1200
  • Tidskriftsartikel (refereegranskat)abstract
    • Individuals with bipolar disorder are at increased risk for cardiovascular diseases. Most studies have described increases in cardiometabolic risk indicators (CMRIs) using clinical cut-off values. Further, there are no longitudinal studies on CMRIs. We aimed to investigate continuous measures of CMRIs in individuals with bipolar disorder and controls using both cross-sectional and longitudinal data. We used data from the Swedish St. Goran Bipolar project. Study individuals were examined at baseline and after a median of 6 and 7 years for the control and patient group, respectively. Data were collected December 2005-December 2020. The cohort included 281 individuals with bipolar disorder (mean age 39 years, 59% women) and 114 controls (mean age 38 years, 55% women). Of those, 155 patients and 74 controls also provided follow-up data. At baseline, individuals with bipolar disorder had significantly higher mean values of waist-to-hip ratio (WHR) (beta = 0.142, p = 0.001), body mass index (beta = 0.150, p = 0.006), plasma triacylglycerol (TAG) (beta = 0.218, p < 0.001), total/plasma high-density lipoprotein-cholesterol (TChol/HDL-C) ratio (beta = 0.103, p = 0.03), TAG/HDL-C ratio (beta = 0.151, p = 0.006), and non-HDL-C (beta = 0.168, p = 0.001) than controls. Most CMRIs remained higher in the patient group at follow-up. The difference between patients and controls increased over time for WHR (0.005 unit/year, p < 0.001), and systolic (1.1 mm Hg/year, p = 0.002) and diastolic (0.8 mm Hg/year, p < 0.001) blood pressure. Individuals with bipolar disorder displayed persistently higher levels of nearly all included CMRIs. Over time, a subset of CMRIs worsened in patients relative to controls. This suggests that active measures to counter cardiovascular risk in persons with bipolar disorder should be considered.
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11.
  • Najar, Hemen, 1979, et al. (författare)
  • Weight gain with add-on second-generation antipsychotics in bipolar disorder: a naturalistic study
  • 2017
  • Ingår i: Acta Psychiatrica Scandinavica. - : Wiley. - 0001-690X .- 1600-0447. ; 135:6, s. 606-611
  • Tidskriftsartikel (refereegranskat)abstract
    • ObjectiveOur aim was to investigate the prevalence and magnitude of weight gain in-patients with bipolar disorder when treated with a second-generation antipsychotic as an add-on treatment to a mood stabilizer in routine clinical practice. MethodsData were derived from the quality register for bipolar disorder in Sweden (BipolaR). Patients with bipolar disorder who started add-on treatment with a SGA (n=575) were compared at next yearly follow-up with age and sex matched patients who were only treated with a mood stabilizer (n=566). The primary outcome measure was change in body weight and body mass index (BMI). We also assessed the prevalence of clinically significant weight gain defined as 7% gain in body weight. ResultsThe group that received add-on treatment with antipsychotics neither gained more weight nor were at higher risk for a clinically significant weight gain than the reference group. Instead, factors associated with clinically significant weight gain were female sex, young age, low-baseline BMI, and occurrence of manic/hypomanic episodes. ConclusionWe found no evidence of an overall increased risk of weight gain for patients with bipolar disorder after receiving add-on SGA to a mood stabilizer in a routine clinical setting.
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12.
  • Pålsson, Erik, 1975, et al. (författare)
  • Cohort profile: the Swedish National Quality Register for bipolar disorder(BipolaR)
  • 2022
  • Ingår i: Bmj Open. - : BMJ. - 2044-6055. ; 12:12
  • Tidskriftsartikel (refereegranskat)abstract
    • PurposeThe Swedish National Quality Register for bipolar affective disorder, BipolaR, was established in 2004 to provide nationwide indicators for quality assessment and development in the clinical care of individuals with bipolar spectrum disorder. An ancillary aim was to provide data for bipolar disorder research.ParticipantsInclusion criteria for registration in BipolaR is a diagnosis of bipolar spectrum disorder (ICD codes: F25.0, F30.1-F30.2, F30.8-F31.9, F34.0) and treatment at an outpatient clinic in Sweden. BipolaR collects data from baseline and annual follow-up visits throughout Sweden. Data is collected using questionnaires administered by healthcare staff. The questions cover sociodemographic, diagnostic, treatment, outcomes and patient reported outcome variables. The register currently includes 39 583 individual patients with a total of 75 423 baseline and follow-up records.Findings to dateData from BipolaR has been used in several peer-reviewed publications. Studies have provided knowledge on effectiveness, side effects and use of pharmacological and psychological treatment in bipolar disorder. In addition, findings on the diagnosis of bipolar disorder, risk factors for attempted and completed suicide and health economics have been reported. The Swedish Bipolar Collection project has contributed to a large number of published studies and provides important information on the genetic architecture of bipolar disorder, the impact of genetic variation on disease characteristics and treatment outcome.Future plansData collection is ongoing with no fixed end date. Currently, approximately 5000 new registrations are added each year. Cohort data are available via a formalised request procedure from Centre of Registers Vastra Gotaland (e-mail: registercentrum@vgregion.se). Data requests for research purposes require an entity responsible for the research and an ethical approval.
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13.
  • Rolstad, Sindre, 1976, et al. (författare)
  • Polymorphisms of BDNF and CACNA1C are not associated with cognitive functioning in bipolar disorder or healthy controls.
  • 2016
  • Ingår i: Cognitive neuropsychiatry. - : Informa UK Limited. - 1464-0619 .- 1354-6805. ; 21:3, s. 271-8
  • Tidskriftsartikel (refereegranskat)abstract
    • The cause of cognitive dysfunction in bipolar disorder (BD) is not well understood. BDNF and CACNA1C are two susceptibility genes for the disorder that have also been reported to be associated with cognitive deficits in the disorder, but the studies have been small and with conflicting results. We therefore attempted to replicate an association between cognitive dysfunction with the most commonly studied single nucleotide polymorphisms rs6265 and rs1006737.
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14.
  • Sandberg, Johan V, et al. (författare)
  • Proteins associated with future suicide attempts in bipolar disorder: A large-scale biomarker discovery study
  • 2022
  • Ingår i: Molecular Psychiatry. - : Springer Science and Business Media LLC. - 1359-4184 .- 1476-5578.
  • Tidskriftsartikel (refereegranskat)abstract
    • Suicide is a major cause of death worldwide. Several biological systems have been implicated in suicidal behavior but studies of candidate biomarkers have failed to produce clinically relevant biomarkers for suicide prediction. The objective of the present study was to identify novel candidate biomarkers for suicidal behavior. We used a nested case-control study design where a large cohort of patients with bipolar disorder (N = 5 110) were followed up to 8 years after blood sampling. We included patients that attempted suicide during follow-up (N = 348) and matched bipolar disorder patients from the same cohort who did not attempt suicide during the study period (N = 348) and analyzed a total of 92 proteins with a neuro exploratory multiplex panel. Using a multivariate classification algorithm devised to minimize bias in variable selection, we identified a parsimonious set of proteins that best discriminated bipolar disorder patients with and without prospective suicide attempts. The algorithm selected 16 proteins for the minimal-optimal classification model, which outperformed 500 models with permuted outcome (p = 0.0004) but had low sensitivity (53%) and specificity (64%). The candidate proteins were then entered in separate logistic regression models to calculate protein-specific associations with prospective suicide attempts. In individual analyses, three of these proteins were significantly associated with prospective suicide attempt (SCGB1A1, ANXA10, and CETN2). Most of the candidate proteins are novel to suicide research.
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15.
  • Sköld, Martin, et al. (författare)
  • Regional lithium prescription rates and recurrence in bipolar disorder
  • 2021
  • Ingår i: International Journal of Bipolar Disorders. - : Springer Science and Business Media LLC. - 2194-7511. ; 9
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Lithium is the best documented maintenance treatment in bipolar disorder, but its use varies considerably across and within countries. It is not known whether regional differences in lithium prescription rates translate to differing regional outcomes. Aims To estimate associations between county specific lithium prescription rates and county specific recurrence odds of bipolar disorder in Sweden. Method Data from 14,616 patients with bipolar I disorder, bipolar II disorder, or bipolar disorder not otherwise specified were extracted from the Swedish national quality assurance register for bipolar disorders (BipolaR). Lithium prescription frequencies were calculated for 21 counties. Logistic regression analyses were run adjusted for confounders, with any type of recurrence as primary outcome, and incident elated and depressive episodes as secondary outcomes. Subsets of patients with bipolar I, II and not otherwise specified disorder were also analysed separately. Results Lithium prescription rates for populations with all bipolar subtypes ranged across counties from 37.7 to 84.9% (mean 52.4%). Higher regional prescription rates were significantly associated with lower rate of any type of recurrence. The association was stronger when bipolar I disorder was analysed separately. Conclusions The advantages for lithium use long acknowledged for bipolar I disorder are also seen for the rest of the bipolar spectrum. Results suggest that population level outcomes of bipolar disorder could be improved by increasing the number of patients using lithium.
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16.
  • Smedler, Erik, et al. (författare)
  • Association of CACNA1C polymorphisms with serum BDNF levels in bipolar disorder.
  • 2021
  • Ingår i: The British journal of psychiatry : the journal of mental science. - : Royal College of Psychiatrists. - 1472-1465. ; 218:2, s. 77-79
  • Tidskriftsartikel (refereegranskat)abstract
    • Variation in the CACNA1C gene has been associated with bipolar disorder in several genome-wide association studies. This gene encodes the alpha 1C subunit of L-type voltage-gated calcium channels, which play an essential role in neurons. We analysed 39 biomarkers in either cerebrospinal fluid or serum in relation to six different CACNA1C variants in 282 patients with bipolar disorder and 90 controls. We report associations of CACNA1C risk alleles with serum levels of BDNF as well as tissue plasminogen activator, which converts pro-BDNF to mature BDNF. This sheds light on links between CACNA1C genetic variants and pathophysiological mechanisms in bipolar disorder.Declaration of interestNone.
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17.
  • Smedler, Erik, et al. (författare)
  • CACNA1C polymorphism and brain cortical structure in bipolar disorder
  • 2019
  • Ingår i: Journal of psychiatry & neuroscience : JPN. - : CMA Joule Inc.. - 1488-2434 .- 1180-4882. ; 45:1
  • Tidskriftsartikel (refereegranskat)abstract
    • The CACNA1C gene encodes the 1C subunit of L-type voltage-gated calcium channels and has been associated with several psychiatric syndromes — including bipolar disorder — in several genome-wide association studies. Experimental and clinical studies have reported changes with respect to behaviour and biomarkers in risk allele carriers, corroborating the essential role of the CACNA1C gene in neurons, during development and in the mature brain. However, the association of this gene with regional cortical thickness has not been evaluated in patients with bipolar disorder.Using magnetic resonance imaging, we measured the average cortical thickness of 68 brain regions in 87 patients genotyped for the single-nucleotide polymorphism rs1006737 in CACNA1C.We found associations with the mean thickness of several cortical areas: the left lateral orbitofrontal and rostral anterior cingulate cortices, as well as other parts of the frontal and parietal cortices.This cross-sectional cohort study could not fully differentiate correlation from causation.The CACNA1C polymorphism rs1006737 is associated with the mean thickness of cortical brain areas that have been shown to be altered in bipolar disorder.
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18.
  • Smedler, Erik, et al. (författare)
  • Metabolomics analysis of cerebrospinal fluid suggests citric acid cycle aberrations in bipolar disorder
  • 2022
  • Ingår i: Neuroscience Applied. - : Elsevier BV. - 2772-4085. ; 1
  • Tidskriftsartikel (refereegranskat)abstract
    • Mounting evidence indicates mitochondrial dysfunction in bipolar disorder pathophysiology. Here, we employed Proton Nuclear Magnetic Resonance Spectroscopy (1H NMR) of cerebrospinal fluid (CSF) samples from well-characterized bipolar disorder patients (n ​= ​67) and healthy controls (n ​= ​55) in order to measure absolute concentrations of multiple metabolites. Focusing on four citric acid cycle metabolites — citrate, glucose, lactate, and pyruvate — we found higher concentrations of both citrate and glucose in patients compared with controls after correcting for age, sex and body mass index, but only the difference in CSF citrate survived correction for multiple comparisons. Within the patient group, CSF citrate concentrations were higher among lithium users than non-users. In conclusion, this report adds further evidence for a mitochondrial dysfunction in bipolar disorder.
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19.
  • Sparding, Timea, et al. (författare)
  • Classification of cognitive performance in bipolar disorder.
  • 2017
  • Ingår i: Cognitive neuropsychiatry. - : Informa UK Limited. - 1464-0619 .- 1354-6805. ; 22:5, s. 407-421
  • Tidskriftsartikel (refereegranskat)abstract
    • To understand the etiology of cognitive impairment associated with bipolar disorder, we need to clarify potential heterogeneity in cognitive functioning. To this end, we used multivariate techniques to study if the correlation structure of cognitive abilities differs between persons with bipolar disorder and controls.Clinically stable patients with bipolar disorder (type I: n=64; type II: n=44) and healthy controls (n=86) were assessed with a wide range of cognitive tests measuring executive function, speed, memory, and verbal skills. Data were analysed with multivariate techniques.A distinct subgroup (∼30%) could be identified that performed significantly poorer on tests concerning memory function. This cognitive phenotype subgroup did not differ from the majority of bipolar disorder patients with respect to other demographic or clinical characteristics.Whereas the majority of patients performed similar to controls, a subgroup of patients with bipolar disorder differed substantially from healthy controls in the correlation pattern of low-level cognitive abilities. This suggests that cognitive impairment is not a general trait in bipolar disorder but characteristic of a cognitive subgroup. This has important clinical implications for cognitive rehabilitation and remediation.
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20.
  • Sparding, Timea, et al. (författare)
  • Cognitive Functioning in Clinically Stable Patients with Bipolar Disorder I and II
  • 2015
  • Ingår i: Plos One. - : Public Library of Science (PLoS). - 1932-6203. ; 10:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives Bipolar disorder is accompanied by cognitive impairments, which persists during euthymic phases. The purpose of the present study was to identify those neuropsychological tests that most reliably tell euthymic bipolar patients and controls apart, and to clarify the extent to which these cognitive impairments are clinically significant as judged from neuropsychological norms. Patients with bipolar disorder (type I: n = 64; type II: n = 44) and controls (n = 86) were examined with a comprehensive neuropsychological test battery yielding 47 measures of executive functioning, speed, memory, and verbal skills. Multivariate analysis was used to build a model of cognitive performance with the ability to expose underlying trends in data and to reveal cognitive differences between patients and controls. Patients with bipolar disorder and controls were partially separated by one predictive component of cognitive performance. Additionally, the relative relevance of each cognitive measure for such separation was decided. Cognitive tests measuring set shifting, inhibition, fluency, and searching (e.g., Trail Making Test, Color-Word) had strongest discriminating ability and most reliably detected cognitive impairments in the patient group. Both bipolar disorder type I and type II were associated with cognitive impairment that for a sizeable minority is significant in a clinical neuropsychological sense. We demonstrate a combination of neuropsychological tests that reliably detect cognitive impairment in bipolar disorder.
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21.
  • Sparding, Timea, et al. (författare)
  • Long-term trajectory of cognitive performance in people with bipolar disorder and controls: 6-year longitudinal study
  • 2021
  • Ingår i: Bjpsych Open. - : Royal College of Psychiatrists. - 2056-4724. ; 7:4
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Cross-sectional studies have found impaired cognitive functioning in patients with bipolar disorder, but long-term longitudinal studies are scarce. Aims The aims of this study were to examine the 6-year longitudinal course of cognitive functioning in patients with bipolar disorder and healthy controls. Subsets of patients were examined to investigate possible differences in cognitive trajectories. Method Patients with bipolar I disorder (n = 44) or bipolar II disorder (n = 28) and healthy controls (n = 59) were tested with a comprehensive cognitive test battery at baseline and retested after 6 years. We conducted repeated measures ANCOVAs with group as a between-subject factor and tested the significance of group and time interaction. Results By and large, the change in cognitive functioning between baseline and follow-up did not differ significantly between participants with bipolar disorder and healthy controls. Comparing subsets of patients, for example those with bipolar I and II disorder and those with and without manic episodes during follow-up, did not reveal subgroups more vulnerable to cognitive decline. Conclusions Cognitive performance remained stable in patients with bipolar disorder over a 6-year period and evolved similarly to healthy controls. These findings argue against the notion of a general progressive decline in cognitive functioning in bipolar disorder.
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22.
  • Sparding, Timea, et al. (författare)
  • Personality traits in bipolar disorder and influence on outcome.
  • 2017
  • Ingår i: BMC psychiatry. - : Springer Science and Business Media LLC. - 1471-244X. ; 17:1
  • Tidskriftsartikel (refereegranskat)abstract
    • The aim was to investigate the personality profile of bipolar disorder I and II, and healthy controls, and to study whether personality influences the course of bipolar disorder.One hundred ten patients with bipolar disorder I, 85 patients with bipolar disorder II, and 86 healthy individuals had their personality profile assessed using the Swedish universities Scales of Personality (SSP), an instrument developed to explore personality-related vulnerabilities and correlates of psychiatric disorders. Patients were followed prospectively for 2years. To assess the impact of Neuroticism, Aggressiveness, and Disinhibition on illness course, we performed logistic regressions with the outcome variables mood episodes (depressive, hypo/manic, mixed), suicide attempts, violence, and the number of sick leave days.Bipolar disorder I and II demonstrated higher global measures of Neuroticism, Aggressiveness, and Disinhibition as compared with healthy controls. A third of the patients scored ≥1 SD above the population-based normative mean on the global neuroticism measure. The two subtypes of bipolar disorder were, however, undistinguishable on all of the personality traits. In the unadjusted model, higher neuroticism at baseline predicted future depressive episodes and suicide attempts/violent behavior, but this association disappeared when adjusting for baseline depressive symptoms as assessed with MADRS.A significant minority of the patients scored ≥1 SD above the population mean on the global measures of Neuroticism, Aggressiveness and Disinhibition; scores this high are usually evident clinically. Yet, the personality profile does not seem to have prognostic value over a 2-year period.
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23.
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24.
  • Brundin, L., et al. (författare)
  • An enzyme in the kynurenine pathway that governs vulnerability to suicidal behavior by regulating excitotoxicity and neuroinflammation
  • 2016
  • Ingår i: Translational Psychiatry. - : Springer Science and Business Media LLC. - 2158-3188. ; 6
  • Tidskriftsartikel (refereegranskat)abstract
    • Emerging evidence suggests that inflammation has a key role in depression and suicidal behavior. The kynurenine pathway is involved in neuroinflammation and regulates glutamate neurotransmission. In the cerebrospinal fluid (CSF) of suicidal patients, levels of inflammatory cytokines and the kynurenine metabolite quinolinic acid (QUIN), an N-methyl-D-aspartate receptor agonist, are increased. The enzyme amino-beta-carboxymuconate-semialdehyde-decarboxylase (ACMSD) limits QUIN formation by competitive production of the neuroprotective metabolite picolinic acid (PIC). Therefore, decreased ACMSD activity can lead to excess QUIN. We tested the hypothesis that deficient ACMSD activity underlies suicidal behavior. We measured PIC and QUIN in CSF and plasma samples from 137 patients exhibiting suicidal behavior and 71 healthy controls. We used DSM-IV and the Montgomery-Asberg Depression Rating Scale and Suicide Assessment Scale to assess behavioral changes. Finally, we genotyped ACMSD tag single nucleotide polymorphisms (SNPs) in 77 of the patients and 150 population-based controls. Suicide attempters had reduced PIC and a decreased PIC/QUIN ratio in both CSF (P<0.001) and blood (P=0.001 and P<0.01, respectively). The reductions of PIC in CSF were sustained over 2 years after the suicide attempt based on repeated measures. The minor C allele of the ACMSD SNP rs2121337 was more prevalent in suicide attempters and associated with increased CSF QUIN. Taken together, our data suggest that increased QUIN levels may result from reduced activity of ACMSD in suicidal subjects. We conclude that measures of kynurenine metabolites can be explored as biomarkers of suicide risk, and that ACMSD is a potential therapeutic target in suicidal behavior.
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25.
  • Clements, C. C., et al. (författare)
  • Genome-wide association study of patients with a severe major depressive episode treated with electroconvulsive therapy
  • 2021
  • Ingår i: Molecular Psychiatry. - : Springer Science and Business Media LLC. - 1359-4184 .- 1476-5578. ; 26:10
  • Tidskriftsartikel (refereegranskat)abstract
    • Although large genome-wide association studies (GWAS) of major depressive disorder (MDD) have identified many significant loci, the SNP-based heritability remains notably low, which might be due to etiological heterogeneity in existing samples. Here, we test the utility of targeting the severe end of the MDD spectrum through genome-wide SNP genotyping of 2725 cases who received electroconvulsive therapy (ECT) for a major depressive episode (MDE) and 4035 controls. A subset of cases (n = 1796) met a narrow case definition (MDE occurring in the context of MDD). Standard GWAS quality control procedures and imputation were conducted. SNP heritability and genetic correlations with other traits were estimated using linkage disequilibrium score regression. Results were compared with MDD cases of mild-moderate severity receiving internet-based cognitive behavioral therapy (iCBT) and summary results from the Psychiatric Genomics Consortium (PGC). The SNP-based heritability was estimated at 29-34% (SE: 6%) for the narrow case definition, considerably higher than the 6.5-8.0% estimate in the most recent PGC MDD study. Our severe MDE cases had smaller genetic correlations with neurodevelopmental disorders and neuroticism than PGC MDD cases but higher genetic risk scores for bipolar disorder than iCBT MDD cases. One genome-wide significant locus was identified (rs114583506, P = 5e-8) in an intron of HLA-B in the major histocompatibility locus on chr6. These results indicate that individuals receiving ECT for an MDE have higher burden of common variant risk loci than individuals with mild-moderate MDD. Furthermore, severe MDE shows stronger relations with other severe adult-onset psychiatric disorders but weaker relations with personality and stress-related traits than mild-moderate MDD. These findings suggest a different genetic architecture at the severest end of the spectrum, and support further study of the severest MDD cases as an extreme phenotype approach to understand the etiology of MDD.
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26.
  • Drakopoulos, Julia, et al. (författare)
  • Executive functioning but not IQ or illness severity predicts occupational status in bipolar disorder
  • 2020
  • Ingår i: International Journal of Bipolar Disorders. - : Springer Science and Business Media LLC. - 2194-7511. ; 8:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Bipolar disorder is associated with significant functional deficits including occupational functioning. Despite the high rates of unemployment and sick leave in the patient population, only a limited number of studies have examined factors associated with occupational functioning in bipolar disorder. The aim of the study was to investigate the relative importance of demographic, clinical, and neuropsychological factors on occupational dysfunction in bipolar disorder. Methods A sample of 120 partially or fully remitted bipolar disorder I and II patients were included in the study. Patients were stratified into an active and an inactive group based on the number of hours per week working or studying. Active (n = 86) and inactive (n = 34) patients were compared with respect to demographic factors, clinical characteristics, medication, measures of psychosocial functioning, and cognitive functioning (i.e., IQ and executive functions). No other cognitive domains were examined. Results Univariate analyses revealed better overall cognitive function in active patients in terms of IQ and executive functioning. However, only executive functioning accounted for a significant amount of the variance in occupational status when other significant predictors were taken into account. Conclusions Executive functioning was a more powerful predictor of occupational status in bipolar disorder patients than IQ and other clinical factors, including illness severity.
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27.
  • Engel, Jörgen, 1942, et al. (författare)
  • Ghrelin activates the mesolimbic dopamine system via nitric oxide associated mechanisms in the ventral tegmental area
  • 2023
  • Ingår i: Nitric Oxide-Biology and Chemistry. - : Elsevier BV. - 1089-8603. ; 131, s. 1-7
  • Tidskriftsartikel (refereegranskat)abstract
    • Besides enhanced feeding, the orexigenic peptide ghrelin activates the mesolimbic dopamine system to cause reward as measured by locomotor stimulation, dopamine release in nucleus accumbens shell (NAcS), and conditioned place preference.Although the ventral tegmental area (VTA) appears to be a central brain region for this ghrelin-reward, the underlying mechanisms within this area are unknown. The findings that the gaseous neurotransmitter nitric oxide (NO) modulate the ghrelin enhanced feeding, led us to hypothesize that ghrelin increases NO levels in the VTA, and thereby stimulates reward-related behaviors. We initially demonstrated that inhibition of NO synthesis blocked the ghrelin-induced activation of the mesolimbic dopamine system. We then established that antagonism of downstream signaling of NO in the VTA, namely sGC, prevents the ability of ghrelin to stimulate the meso-limbic dopamine system. The association of ghrelin to NO was further strengthened by in vivo electrochemical recordings showing that ghrelin enhances the NO release in the VTA. Besides a GABAB-receptor agonist, known to reduce NO and cGMP, blocks the stimulatory properties of ghrelin. The present series of experiments reveal that ablated NO signaling, through pharmacologically inhibiting the production of NO and/or cGMP, prevents the ability of ghrelin to induced reward-related behaviors.
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28.
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29.
  • Fejgin, Kim, 1978, et al. (författare)
  • Nitric oxide signaling in the medial prefrontal cortex is involved in the biochemical and behavioral effects of phencyclidine.
  • 2008
  • Ingår i: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. - : Springer Science and Business Media LLC. - 0893-133X. ; 33:8, s. 1874-83
  • Tidskriftsartikel (refereegranskat)abstract
    • The prefrontal cortex (PFC) is believed to play an important role in the cognitive impairments observed in schizophrenia and has also been shown to be involved in the modulation of prepulse inhibition (PPI), a measure of preattentive information processing that is impaired in schizophrenic individuals. Phencyclidine (PCP), a noncompetitive inhibitor of the NMDA receptor, exerts psychotomimetic effects in humans, disrupts PPI, and causes hypofrontality in rodents and monkeys. We have previously demonstrated that interfering with the production of nitric oxide (NO) can prevent a wide range of PCP-induced behavioral deficits, including PPI disruption. In the present study, the role of NO signaling for the behavioral and biochemical effects of PCP was further investigated. Dialysate from the medial PFC of mice receiving systemic treatment with PCP and/or the NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg), was analyzed for cGMP content. Furthermore, a specific inhibitor of NO-sensitive soluble guanylyl cyclase (sGC), 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one (ODQ, 0.01-1 mM), was administered into the medial PFC of mice in combination with systemic injections of PCP, followed by PPI and locomotor activity testing. PCP (5 mg/kg) caused an increase in prefrontal cGMP that could be attenuated by pretreatment with the NO synthase inhibitor, L-NAME. Moreover, bilateral microinjection of the sGC inhibitor, ODQ, into the medial PFC of mice attenuated the disruption of PPI, but not the hyperlocomotion, caused by PCP. The present study shows that NO/sGC/cGMP signaling pathway in the medial PFC is involved in specific behavioral effects of PCP that may have relevance for the disabling cognitive dysfunction found in patients with schizophrenia.
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30.
  • Fejgin, Kim, 1978, et al. (författare)
  • Prefrontal GABA(B) Receptor Activation Attenuates Phencyclidine-Induced Impairments of Prepulse Inhibition: Involvement of Nitric Oxide.
  • 2009
  • Ingår i: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. - : Springer Science and Business Media LLC. ; 34:7, s. 1673-84
  • Tidskriftsartikel (refereegranskat)abstract
    • Recent theories propose that both GABA and glutamate signaling are compromised in patients with schizophrenia. These deficits can be observed in several brain regions including the prefrontal cortex (PFC), an area extensively linked to the cognitive dysfunction in this disease and notably affected by NMDA receptor antagonists such as phencyclidine (PCP). We have previously demonstrated that inhibition of the nitric oxide (NO) pathways in the brain, particularly in the PFC, prevents a wide range of PCP-induced behavioral deficits including disruption of prepulse inhibition (PPI). This study investigated the role of GABA(B) receptor signaling and NO in the effects of PCP on PPI. Mice received systemic or prefrontal injections of the GABA(B) receptor agonist baclofen (2.5-5 mg/kg and 1 mM) before PCP treatment (5 mg/kg) and were thereafter tested for PPI. GABA/NO interactions were studied by combining baclofen and the NO synthase inhibitor L-NAME (20 mg/kg) in subthreshold doses. The role of GABA(B) receptors for NO production in vivo was assessed using NO-sensors implanted into the rat PFC. PCP-induced PPI deficits were attenuated in an additive manner by systemic baclofen treatment, whereas prefrontal microinjections of baclofen completely blocked the effects of PCP, without affecting PPI per se. The combination of baclofen and L-NAME was more effective in preventing the effects of PCP than any compound by itself. Additionally, baclofen decreased NO release in the PFC in a dose-related manner. This study proposes a role for GABA(B) receptor signaling in the effects of PCP, with altered NO levels as a downstream consequence. Thus, prefrontal NO signaling mirrors an altered level of cortical inhibition that may be of importance for information processing deficits in schizophrenia.Neuropsychopharmacology (2009) 34, 1673-1684; doi:10.1038/npp.2008.225; published online 14 January 2009.
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31.
  • Fejgin, Kim, 1978, et al. (författare)
  • The atypical antipsychotic, aripiprazole, blocks phencyclidine-induced disruption of prepulse inhibition in mice.
  • 2007
  • Ingår i: Psychopharmacology. - : Springer Science and Business Media LLC. - 0033-3158 .- 1432-2072. ; 191:2, s. 377-85
  • Tidskriftsartikel (refereegranskat)abstract
    • RATIONALE: The psychotomimetic drug, phencyclidine, induces schizophrenia-like behavioural changes in both humans and animals. Phencyclidine-induced disruption of sensory motor gating mechanisms, as assessed by prepulse inhibition of the acoustic startle, is widely used in research animals as a screening model for antipsychotic properties in general and may predict effects on negative and cognitive deficits in particular. Dopamine (DA) stabilizers comprise a new generation of antipsychotics characterized by a partial DA receptor agonist or antagonist action and have been suggested to have a more favourable clinical profile. OBJECTIVE: The aim of the present study was to investigate the ability of first, second and third generation antipsychotics to interfere with the disruptive effect of phencyclidine on prepulse inhibition in mice. RESULTS: Aripiprazole blocked the phencyclidine-induced disruption of prepulse inhibition. The atypical antipsychotic clozapine was less effective, whereas olanzapine, and the typical antipsychotic haloperidol, failed to alter the effects of phencyclidine on prepulse inhibition. CONCLUSIONS: The somewhat superior efficacy of clozapine compared to haloperidol may be explained by its lower affinity and faster dissociation rate for DA D2 receptors possibly combined with an interaction with other receptor systems. Aripiprazole was found to be more effective than clozapine or olanzapine, which may be explained by a partial agonist activity of aripiprazole at DA D2 receptors. In conclusion, the present findings suggest that partial DA agonism leading to DA stabilizing properties may have favourable effects on sensorimotor gating and thus tentatively on cognitive dysfunctions in schizophrenia.
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32.
  • Finnerty, N., et al. (författare)
  • Increased brain nitric oxide levels following ethanol administration
  • 2015
  • Ingår i: Nitric oxide. - : Elsevier BV. - 1089-8603 .- 1089-8611. ; 47, s. 52-57
  • Tidskriftsartikel (refereegranskat)abstract
    • Nitric oxide is a ubiquitous messenger molecule, which at elevated concentrations has been implicated in the pathogenesis of several neurological disorders. Its role in oxidative stress, attributed in particular to the formation of peroxynitrite, proceeds through its high affinity for the superoxide radical. Alcoholism has recently been associated with the induction of oxidative stress, which is generally defined as a shift in equilibrium between pro-oxidant and anti-oxidant species in the direction of the former. Furthermore, its primary metabolite acetaldehyde, has been extensively associated with oxidative damage related toxic effects following alcohol ingestion. The principal objective of this study was the application of long term in vivo electrochemistry (LIVE) to investigate the effect of ethanol (0.125, 0.5 and 2.0 g kg-1) and acetaldehyde (12.5, 50 and 200 mg kg-1) on NO levels in the nucleus accumbens of freely moving rats. Systemic administrations of ethanol and acetaldehyde resulted in a dose-dependent increases in NO levels, albeit with very differing time courses. Subsequent to this the effect on accumbal NO levels, of subjecting the animal to different drug combinations, was also elucidated. The nitric oxide synthase inhibitor L-NAME (20 mg kg-1) and acetaldehyde sequestering agent D-penicillamine (50 mg kg-1) both attenuated the increase in NO levels following ethanol (1 g kg-1) administration. Conversely, the alcohol dehydrogenase inhibitor 4-methylpyrazole (25 mg kg-1) and catalase inhibitor sodium azide (10 mg kg-1) potentiated the increase in NO levels following ethanol administration. Finally, dual inhibition of aldehyde dehydrogenase and catalase by cyanamide (25 mg kg-1) caused an attenuation of ethanol effects on NO levels. Taken together these data highlight a robust increase in brain NO levels following systemic alcohol administration which is dependent on NO synthase activity and may involve both alcohol- and acetaldehyde-dependent mechanisms. © 2015 Elsevier Inc. All rights reserved.
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33.
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34.
  • Finnerty, N. J., et al. (författare)
  • Brain nitric oxide: Regional characterisation of a real-time microelectrochemical sensor
  • 2012
  • Ingår i: Journal of Neuroscience Methods. - : Elsevier BV. - 0165-0270. ; 209:1, s. 13-21
  • Tidskriftsartikel (refereegranskat)abstract
    • A reliable method of directly measuring endogenously generated nitric oxide (NO) in real-time and in various brain regions is presented. An extensive characterisation of a previously described amperometric sensor has been carried out in the prefrontal cortex and nucleus accumbens of freely moving rats. Systemic administration of saline caused a transient increase in signal from baseline levels in both the prefrontal cortex (13 +/- 3 pA, n = 17) and nucleus accumbens (12 +/- 3 pA, n = 8). NO levels in the prefrontal cortex were significantly increased by 43 +/- 9 pA (n = 9) following administration of L-arginine. A similar trend was observed in the nucleus accumbens, where an increase of 44 +/- 9 pA (n = 8) was observed when compared against baseline levels. Systemic injections of the non-selective NOS inhibitor L-NAME produced a significant decrease in current recorded in the prefrontal cortex (24 +/- 6 pA, n = 5) and nucleus accumbens (17 +/- 3 pA, n = 6). Finally it was necessary to validate the sensors functionality in vivo by investigating the effect of the interferent ascorbate on the oxidation current. The current showed no variation in both regions over the selected time interval of 60 min, indicating no deterioration of the polymer membrane. A detailed comparison identified significantly greater affects of administrations on NO sensors implanted in the striatum than those inserted in the prefrontal cortex and the nucleus accumbens. (c) 2012 Elsevier B.V. All rights reserved.
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35.
  • Göteson, Andreas, 1991, et al. (författare)
  • A serum proteomic study of two case-control cohorts identifies novel biomarkers for bipolar disorder
  • 2022
  • Ingår i: Translational Psychiatry. - : Springer Science and Business Media LLC. - 2158-3188. ; 12:1
  • Tidskriftsartikel (refereegranskat)abstract
    • We set out to identify novel protein associations with potential as clinically viable biomarkers for bipolar disorder. To this end, we used proximity extension assay to analyze 201 unique proteins in blood serum from two independent cohorts comprising patients with bipolar disorder and healthy controls (total n = 493). We identified 32 proteins significantly associated with bipolar disorder in both case-control cohorts after adjusting for relevant covariates. Twenty-two findings are novel to bipolar disorder, but 10 proteins have previously been associated with bipolar disorder: chitinase-3-like protein 1, C-C motif chemokine 3 (CCL3), CCL4, CCL20, CCL25, interleukin 10, growth/differentiation factor-15, matrilysin (MMP-7), pro-adrenomedullin, and TNF-R1. Next, we estimated the variance in serum protein concentrations explained by psychiatric drugs and found that some case-control associations may have been driven by psychiatric drugs. The highest variance explained was observed between lithium use and MMP-7, and in post-hoc analyses and found that the serum concentration of MMP-7 was positively associated with serum lithium concentration, duration of lithium therapy, and inversely associated with estimated glomerular filtration rate in an interaction with lithium. This is noteworthy given that MMP-7 has been suggested as a mediator of renal tubulointerstitial fibrosis, which is characteristic of lithium-induced nephropathy. Finally, we used machine learning to evaluate the classification performance of the studied biomarkers but the average performance in unseen data was fair to moderate (area under the receiver operating curve = 0.72). Taken together, our serum biomarker findings provide novel insight to the etiopathology of bipolar disorder, and we present a suggestive biomarker for lithium-induced nephropathy. © 2022, The Author(s).
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36.
  • Hörbeck, Elin, 1984, et al. (författare)
  • Dissecting the impact of complement component 4A in bipolar disorder.
  • 2023
  • Ingår i: Brain, behavior, and immunity. - 1090-2139. ; 116, s. 150-159
  • Tidskriftsartikel (refereegranskat)abstract
    • The genetic overlap between schizophrenia (SZ) and bipolar disorder (BD) is substantial. Polygenic risk scores have been shown to dissect different symptom dimensions within and across these two disorders. Here, we focused on the most strongly associated SZ risk locus located in the extended MHC region, which is largely explained by copy numbers of the gene coding for complement component 4A (C4A). First, we utilized existing brain tissue collections (N=1,202 samples) and observed no altered C4A expression in BD samples. The generated C4A seeded co-expression networks displayed no genetic enrichment for BD. To study if genetically predicted C4A expression discriminates between subphenotypes of BD, we applied C4A expression scores to symptom dimensions in a total of 4,739 BD cases with deep phenotypic data. We identified a significant association between C4A expression and psychotic mood episodes in BD type 1 (BDI). No significant association was observed between C4A expression and the occurrence of non-affective psychotic episodes in BDI, the psychosis dimensions in the total BD sample, or any other subphenotype of BD. Overall, these results points to a distinct role of C4A in BD that is restricted to vulnerability for developing psychotic symptoms during mood episodes in BDI.
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37.
  • Isgren, Anniella, et al. (författare)
  • Increased cerebrospinal fluid interleukin-8 in bipolar disorder patients associated with lithium and antipsychotic treatment.
  • 2015
  • Ingår i: Brain, behavior, and immunity. - : Elsevier BV. - 1090-2139 .- 0889-1591. ; 43, s. 198-204
  • Tidskriftsartikel (refereegranskat)abstract
    • Inflammation has been linked to the pathophysiology of bipolar disorder based on studies of inflammation markers, such as cytokine concentrations, in plasma and serum samples from cases and controls. However, peripheral measurements of cytokines do not readily translate to immunological activity in the brain. The aim of the present study was to study brain immune and inflammatory activity. To this end, we analyzed cytokines in cerebrospinal fluid from 121 euthymic bipolar disorder patients and 71 age and sex matched control subjects. Concentrations of 11 different cytokines were determined using immunoassays. Cerebrospinal fluid IL-8 concentrations were significantly higher in patients as compared to controls. The other cytokines measured were only detectable in part of the sample. IL-8 concentrations were positively associated to lithium- and antipsychotic treatment. The findings might reflect immune aberrations in bipolar disorder, or be due to the effects of medication.
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38.
  • Jakobsson, Joel, et al. (författare)
  • CACNA1C polymorphism and altered phosphorylation of tau in bipolar disorder.
  • 2016
  • Ingår i: The British journal of psychiatry : the journal of mental science. - : Royal College of Psychiatrists. - 1472-1465. ; 208:2, s. 195-196
  • Tidskriftsartikel (refereegranskat)abstract
    • Several genome-wide association studies and case-control studies have associated the single nucleotide polymorphism (SNP) rs1006737, situated in CACNA1C encoding the alpha 1C subunit of the L-type voltage-gated calcium channel, with bipolar disorder and other psychiatric disorders. However, the causal pathway linking genetic variants in CACNA1C with increased risk for developing brain disorders remains unclear. Here, we explored the association between the rs1006737 SNP and cerebrospinal fluid (CSF) markers. We found a significant association between the risk allele in rs1006737 and a decreased CSF hyperphosphorylated tau/total tau ratio in patients with bipolar disorder, thus linking variation in the CACNA1C gene to a neurochemical marker of neuroaxonal plasticity in those with this disorder.
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39.
  • Jakobsson, Joel, et al. (författare)
  • Monocyte and microglial activation in patients with mood-stabilized bipolar disorder.
  • 2015
  • Ingår i: Journal of psychiatry & neuroscience : JPN. - : CMA Joule Inc.. - 1488-2434 .- 1180-4882. ; 40:2
  • Tidskriftsartikel (refereegranskat)abstract
    • Bipolar disorder is associated with medical comorbidities that have been linked to systemic inflammatory mechanisms. There is, however, limited evidence supporting a role of neuroinflammation in bipolar disorder. Here we tested whether microglial activation and associated tissue remodelling processes are related to bipolar disorder by analyzing markers in cerebrospinal fluid (CSF) and serum from patients and healthy controls.
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40.
  • Jildenstål, Pether, et al. (författare)
  • Agreement between frontal and occipital regional cerebral oxygen saturation in infants during surgery and general anesthesia an observational study
  • 2019
  • Ingår i: Pediatric Anesthesia. - : Wiley. - 1460-9592 .- 1460-9592 .- 1155-5645. ; 29:11, s. 1122-1127
  • Tidskriftsartikel (refereegranskat)abstract
    • Abstract Background: Advances in perioperative pediatric care have resulted in an increased number of procedures requiring anesthesia. During anesthesia and surgery, the patient is subjected to factors that affect the circulatory homeostasis, which can influence oxygenation of the brain. Near‐infrared spectroscopy (NIRS) is an easy applicable noninvasive method for monitoring of regional tissue oxygenation (rScO₂%). Alternate placements for NIRS have been investigated; however, no alternative cranial placements have been explored. Aim: To evaluate the agreement between frontal and occipital recordings of rScO₂% in infants using INVOSTM during surgery and general anesthesia. Method: A standard frontal monitoring of rScO₂% with NIRS was compared with occipital rScO₂% measurements in fifteen children at an age <1 year, ASA 1‐2, undergoing cleft lip and/or palate surgery during general anesthesia with sevoflurane. An agreement analysis was performed according to Bland and Altman. Results: Mean values of frontal and occipital rScO₂% at baseline were largely similar (70.7 ± 4.77% and 69.40 ± 5.04%, respectively). In the majority of the patients, the frontal and occipital recordings of rScO2 changed in parallel. There was a moderate positive correlation between frontal and occipital rScO₂% INVOS™ readings (rho[ρ]: 0.513, P < .01). The difference between frontal and occipital rScO₂ ranged from −31 to 28 with a mean difference (bias) of −0.15%. The 95% limit of agreement was −18.04%‐17.74%. The error between frontal and occipital rScO₂ recordings was 23%. Conclusion: The agreement between frontal and occipital recordings of brain rScO₂% in infants using INVOSTM during surgery and general anesthesia was acceptable. In surgical procedures where the frontal region of the head is not available for monitoring, occipital recordings of rScO₂% could be an option for monitoring.
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41.
  • Jonsson, Lina, 1982, et al. (författare)
  • Characterisation of age and polarity at onset in bipolar disorder
  • 2021
  • Ingår i: British Journal of Psychiatry. - : Royal College of Psychiatrists. - 0007-1250 .- 1472-1465. ; 219:6, s. 659-669
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Studying phenotypic and genetic characteristics of age at onset (AAO) and polarity at onset (PAO) in bipolar disorder can provide new insights into disease pathology and facilitate the development of screening tools. Aims To examine the genetic architecture of AAO and PAO and their association with bipolar disorder disease characteristics. Method Genome-wide association studies (GWASs) and polygenic score (PGS) analyses of AAO (n = 12 977) and PAO (n = 6773) were conducted in patients with bipolar disorder from 34 cohorts and a replication sample (n = 2237). The association of onset with disease characteristics was investigated in two of these cohorts. Results Earlier AAO was associated with a higher probability of psychotic symptoms, suicidality, lower educational attainment, not living together and fewer episodes. Depressive onset correlated with suicidality and manic onset correlated with delusions and manic episodes. Systematic differences in AAO between cohorts and continents of origin were observed. This was also reflected in single-nucleotide variant-based heritability estimates, with higher heritabilities for stricter onset definitions. Increased PGS for autism spectrum disorder (beta = -0.34 years, s.e. = 0.08), major depression (beta = -0.34 years, s.e. = 0.08), schizophrenia (beta = -0.39 years, s.e. = 0.08), and educational attainment (beta = -0.31 years, s.e. = 0.08) were associated with an earlier AAO. The AAO GWAS identified one significant locus, but this finding did not replicate. Neither GWAS nor PGS analyses yielded significant associations with PAO. Conclusions AAO and PAO are associated with indicators of bipolar disorder severity. Individuals with an earlier onset show an increased polygenic liability for a broad spectrum of psychiatric traits. Systematic differences in AAO across cohorts, continents and phenotype definitions introduce significant heterogeneity, affecting analyses.
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42.
  • Karanti, Alina (Aikaterini), et al. (författare)
  • Patient educational level and management of bipolar disorder
  • 2021
  • Ingår i: Bjpsych Open. - : Royal College of Psychiatrists. - 2056-4724. ; 7:2
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Socioeconomic factors can affect healthcare management. Aims The aim was to investigate if patient educational attainment is associated with management of bipolar disorder. Method We included patients with bipolar disorder type 1 (n = 4289), type 2 (n = 4020) and not otherwise specified (n = 1756), from the Swedish National Quality Register for Bipolar Disorder (BipolaR). The association between patients' educational level and pharmacological and psychological interventions was analysed by binary logistic regression. We calculated odds ratios after adjusting for demographic and clinical variables. Results Higher education was associated with increased likelihood of receiving psychotherapy (adjusted odds ratio 1.34, 95% CI 91.22-1.46) and psychoeducation (adjusted odds ratio 1.18, 95% CI 1.07-1.46), but with lower likelihood of receiving first-generation antipsychotics (adjusted odds ratio 0.76, 95% CI 0.62-0.94) and tricyclic antidepressants (adjusted odds ratio 0.76, 95% CI 0.59-0.97). Higher education was also associated with lower risk for compulsory in-patient care (adjusted odds ratio 0.79, 95% CI 0.67-0.93). Conclusions Pharmacological and psychological treatment of bipolar disorder differ depending on patients' educational attainment. The reasons for these disparities remain to be explained.
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43.
  • Klamer, Daniel, 1976, et al. (författare)
  • Activation of a nitric-oxide-sensitive cAMP pathway with phencyclidine: elevated hippocampal cAMP levels are temporally associated with deficits in prepulse inhibition
  • 2005
  • Ingår i: Psychopharmacology (Berl). ; 179:2, s. 479-88
  • Tidskriftsartikel (refereegranskat)abstract
    • RATIONALE: Schizophrenic patients show deficits in pre-attentive information processing as evidenced, for example, by disrupted prepulse inhibition, a measure of sensorimotor gating. A similar disruption can be observed in animals treated with the psychotomimetic agent, phencyclidine (PCP). However, the mechanism by which PCP alters brain function has not been fully elucidated. Recent studies have demonstrated that certain behavioural and neurochemical effects of PCP in rats and mice are blocked by nitric oxide (NO) synthase inhibition, suggesting an important role for NO in the effects of PCP. OBJECTIVE: The aim of the present study was to investigate the effects of PCP on cAMP production in the ventral hippocampus and the role of NO in these effects using in vivo microdialysis in rats. Furthermore, the effects of PCP on acoustic startle reactivity and prepulse inhibition of acoustic startle were compared with changes in cAMP levels in the ventral hippocampus. RESULTS: Significant increases in cAMP levels were observed in the ventral hippocampus following both local infusion (10(-4) mol/l and 10(-3) mol/l) and systemic administration (2 mg/kg) of PCP. The PCP-induced changes in prepulse inhibition and startle reactivity were associated in magnitude and duration with the increase in cAMP levels in the hippocampus. Furthermore, systemic administration of the NO synthase inhibitor, L: -NAME (10 mg/kg), blocked both the changes in cAMP levels and the behavioural responses induced by PCP. CONCLUSIONS: These findings indicate that the effects of PCP on prepulse inhibition and startle reactivity are associated with an increase in cAMP levels in the ventral hippocampus, and that this change in cAMP response may be linked to the production of NO.
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44.
  • Klamer, Daniel, 1976, et al. (författare)
  • Antagonism of the nitric oxide synthase inhibitor, L-NAME, of the effects of phencyclidine on latent inhibition in taste aversion conditioning
  • 2005
  • Ingår i: Behav Brain Res. ; 161:1, s. 60-8
  • Tidskriftsartikel (refereegranskat)abstract
    • Latent inhibition (LI) is a behavioural procedure used to evaluate the potential propsychotic and antipsychotic properties of psychoactive drugs. In the present study, a conditioned taste aversion (CTA) procedure was used to investigate the effects of the nitric oxide (NO) synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), and the psychotomimetic drugs, phencyclidine (PCP) and d-amphetamine (d-AMP) on LI. PCP (2 mg/kg) and d-AMP (0.5 mg/kg) were both found to enhance LI in this procedure. The effect of d-AMP on LI was less pronounced and this drug also caused a weak disruption of taste aversion conditioning. Pretreatment with L-NAME (10 mg/kg) blocked the LI enhancing effect of PCP on LI but not that of d-AMP. L-NAME by itself caused an attenuation of LI. L-NAME has been shown to block also other behavioural and biochemical effects of PCP in previous studies and these results and the present findings suggest that at least some of the effects PCP are dependent on NO and possibly also that some NOS inhibitors may exert antipsychotic properties.
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45.
  •  
46.
  • Klamer, Daniel, 1976, et al. (författare)
  • Habituation of acoustic startle is disrupted by psychotomimetic drugs: differential dependence on dopaminergic and nitric oxide modulatory mechanisms
  • 2004
  • Ingår i: Psychopharmacology (Berl). ; 176:3-4, s. 440-50
  • Tidskriftsartikel (refereegranskat)abstract
    • RATIONALE: A deficit in attention and information processing has been considered a central feature in schizophrenia, which might lead to stimulus overload and cognitive fragmentation. It has been shown that patients with schizophrenia display a relative inability to gate incoming stimuli. Thus, patients repeatedly subjected to acoustic startle-eliciting stimuli habituate less to these stimuli than controls. Furthermore, schizophrenia-like symptoms can be induced by pharmacological manipulations in humans by psychotomimetic drugs, e.g. phencyclidine (PCP) and D-amphetamine (D-AMP). Recent studies show that the behavioural and biochemical effects of PCP in rodents are blocked by nitric oxide synthase (NOS) inhibitors, suggesting that NO plays an important role in at least the pharmacological effects of PCP. OBJECTIVES: The first aim of the present study was to investigate if PCP, MK-801 and D-AMP impair habituation of acoustic startle in mice. Secondly, we examine the effect of the NOS inhibitor, L-NAME, and the dopamine receptor antagonist, haloperidol, on drug-induced deficit in habituation. RESULTS: PCP (4 mg/kg), MK-801 (0.4 mg/kg) and D-AMP (5.0 mg/kg), impaired habituation of the acoustic startle response in mice. This effect was reversed by the NOS inhibitor, L-NAME. The typical antipsychotic, haloperidol, reversed the effects of PCP and D-AMP, but not that of MK-801. CONCLUSIONS: The finding that PCP, MK-801 and D-AMP impair habituation in mice is consistent with the idea that these treatments model certain filter deficits seen in schizophrenic patients. Furthermore, the present results suggest that NO is critically involved in these effects on habituation, whereas that of dopamine is less clear.
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47.
  • Klamer, Daniel, 1976, et al. (författare)
  • Prefrontal NMDA receptor antagonism reduces impairments in pre-attentive information processing.
  • 2011
  • Ingår i: European Neuropsychopharmacology. - 0924-977X. ; 21:3, s. 248-253
  • Tidskriftsartikel (refereegranskat)abstract
    • A well established theory proposes that glutamate signalling via the NMDA receptor is compromised in patients with schizophrenia. Deficits related to NMDA receptor signalling can be observed in several brain regions including the prefrontal cortex (PFC), an area extensively linked to the cognitive dysfunction in this disease and notably affected by NMDA receptor antagonists such as phencyclidine (PCP). In addition, a number of studies suggest that normalizing of PFC function could constitute a treatment rationale for schizophrenia. To further study the role of PFC function we investigated the effect of local PFC NMDA receptor blockade on impaired prepulse inhibition (PPI) induced by systemic administration of PCP. Mice received prefrontal injections of PCP (0.01, 0.1 or 1 mM) before PCP treatment (5 mg/kg) and were thereafter tested for PPI. PCP induced deficits in PPI were ameliorated by prefrontal PCP (0.1 mM) treatment whereas PPI was not affected by prefrontal cortex PCP administration per se at any of the doses tested. Taken together, inhibition of NMDA receptors in the PFC does not seem to be enough to impair PPI per se but NMDA receptor mediated signalling in the PFC may be a key factor for the PPI-disruptive effects of global NMDA receptor inhibition. This indicates that targeting PFC NMDA receptor signalling may have potential as a treatment target for schizophrenia although further studies are needed to understand pharmacology and pathophysiological role of PFC NMDA receptors.
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48.
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49.
  • Larsson, F., et al. (författare)
  • Bipolar disorder type 1 was the most stable bipolar subdiagnosis
  • 2021
  • Ingår i: Lakartidningen. - 1652-7518. ; 118
  • Tidskriftsartikel (refereegranskat)abstract
    • DSM-IV subcategorises bipolar disorders into type 1, type 2, and a third not otherwise specified (NOS) category. Although previous works suggest that these subtypes remain reasonably stable over time, it is unclear if subdiagnoses endure over time or if patients are commonly recategorized within the spectrum in a real-world clinical setting. We assessed subdiagnostic stability in 6,374 individuals with bipolar disorder using data from the Swedish national quality assurance register for bipolar disorders (BipoläR). Diagnoses at baseline registration - that could occur at any time point during the course of illness - were compared with diagnoses at follow-up registration 3 years later. Changes in subdiagnoses were analysed in relation to clinical setting, diagnostic procedure, and patient features. We found that 74 %, 67 %, and 47 % of patients diagnosed with bipolar disorder type 1, type 2, and NOS, respectively, retained the same subdiagnosis at the 3-year follow-up. The following factors were associated with higher rate of subdiagnostic transitions: previous suicide attempts, unemployment or low psychosocial function, treatment with antidepressants, and comorbid anxiety, neuropsychiatric, or personality disorder. Conversely, use and duration of mood stabilizer treatment, the use of structured diagnostic instruments, and treatment at an outpatient unit specialized in managing affective disorders were associated with lower likelihood of subdiagnostic transitions. Our findings confirm that bipolar disorder type 1 is the most stable subdiagnostic group, but findings also indicate a significant degree of subdiagnostic instability, particularly in the NOS group.
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50.
  • Larsson, Ingrid, et al. (författare)
  • Dietary intake, resting energy expenditure, and eating behavior in women with and without polycystic ovary syndrome.
  • 2016
  • Ingår i: Clinical nutrition (Edinburgh, Scotland). - : Elsevier BV. - 1532-1983 .- 0261-5614. ; 35:1, s. 213-218
  • Tidskriftsartikel (refereegranskat)abstract
    • Data on dietary intake, meal patterns, and eating attitudes from women with polycystic ovary syndrome (PCOS) is limited despite the fact that PCOS is associated with obesity. We aimed to test the hypothesis that women with PCOS display altered dietary intakes and eating behaviors compared to controls.
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