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Sökning: WFRF:(Landen M) > (2015-2019) > (2017)

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  • Föregående 12[3]4Nästa
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21.
  • Isgren, Anniella, et al. (författare)
  • Markers of neuroinflammation and neuronal injury in bipolar disorder: Relation to prospective clinical outcomes.
  • 2017
  • Ingår i: Brain, behavior, and immunity. - 1090-2139. ; 65, s. 195-201
  • Tidskriftsartikel (refereegranskat)abstract
    • Neuroimmune mechanisms have been linked to the pathophysiology of bipolar disorder based on studies of biomarkers in plasma, cerebrospinal fluid (CSF), and postmortem brain tissue. There are, however, no longitudinal studies investigating if CSF markers of neuroinflammation and neuronal injury predict clinical outcomes in patients with bipolar disorder. We have in previous studies found higher CSF concentrations of interleukin-8 (IL-8), monocyte chemoattractant protein 1 (MCP-1/CCL-2), chitinase-3-like protein 1 (CHI3L1/YKL-40), and neurofilament light chain (NF-L) in euthymic patients with bipolar disorder compared with controls. Here, we investigated the relationship of these CSF markers of neuroinflammation and neuronal injury with clinical outcomes in a prospective study. 77 patients with CSF analyzed at baseline were followed for 6-7years. Associations of baseline biomarkers with clinical outcomes (manic/hypomanic and depressive episodes, suicide attempts, psychotic symptoms, inpatient care, GAF score change) were investigated. Baseline MCP-1 concentrations were positively associated with manic/hypomanic episodes and inpatient care during follow-up. YKL-40 concentrations were negatively associated with manic/hypomanic episodes and with occurrence of psychotic symptoms. The prospective negative association between YKL-40 and manic/hypomanic episodes survived multiple testing correction. Concentrations of IL-8 and NF-L were not associated with clinical outcomes. High concentrations of these selected CSF markers of neuroinflammation and neuronal injury at baseline were not consistently associated with poor clinical outcomes in this prospective study. The assessed proteins may be involved in adaptive immune processes or reflect a state of vulnerability for bipolar disorder rather than being of predictive value for disease progression.
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23.
  • Lautner, Ronald, et al. (författare)
  • Preclinical effects of APOE ϵ4 on cerebrospinal fluid Aβ42 concentrations
  • 2017
  • Ingår i: Alzheimer's Research and Therapy. - BioMed Central. - 1758-9193. ; 9:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: From earlier studies it is known that the APOE ϵ2/ϵ3/ϵ4 polymorphism modulates the concentrations of cerebrospinal fluid (CSF) beta-amyloid1-42 (Aβ42) in patients with cognitive decline due to Alzheimer's disease (AD), as well as in cognitively healthy controls. Here, in a large cohort consisting solely of cognitively healthy individuals, we aimed to evaluate how the effect of APOE on CSF Aβ42 varies by age, to understand the association between APOE and the onset of preclinical AD. Methods: APOE genotype and CSF Aβ42 concentration were determined in a cohort comprising 716 cognitively healthy individuals aged 17-99 from nine different clinical research centers. Results: CSF concentrations of Aβ42 were lower in APOE ϵ4 carriers than in noncarriers in a gene dose-dependent manner. The effect of APOE ϵ4 on CSF Aβ42 was age dependent. The age at which CSF Aβ42 concentrations started to decrease was estimated at 50 years in APOE ϵ4-negative individuals and 43 years in heterozygous APOE ϵ4 carriers. Homozygous APOE ϵ4 carriers showed a steady decline in CSF Aβ42 concentrations with increasing age throughout the examined age span. Conclusions: People possessing the APOE ϵ4 allele start to show a decrease in CSF Aβ42 concentration almost a decade before APOE ϵ4 noncarriers already in early middle age. Homozygous APOE ϵ4 carriers might deposit Aβ42 throughout the examined age span. These results suggest that there is an APOE ϵ4-dependent period of early alterations in amyloid homeostasis, when amyloid slowly accumulates, that several years later, together with other downstream pathological events such as tau pathology, translates into cognitive decline.
24.
  • 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. - 0001-690X. ; 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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25.
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26.
  • Pålsson, Erik, 1975-, et al. (författare)
  • Cerebrospinal fluid monoamine metabolite profiles in bipolar disorder, ADHD, and controls.
  • 2017
  • Ingår i: Journal of neural transmission (Vienna, Austria : 1996). - 1435-1463. ; 124:9
  • Tidskriftsartikel (refereegranskat)abstract
    • Alterations in monoaminergic signaling are suggested as key aspects of the pathophysiology in bipolar disorder and ADHD, but it is not known if the monoamine metabolic profile differs between these disorders. One method to study monoaminergic systems in humans is to measure monoamine end-point metabolite concentrations in cerebrospinal fluid (CSF). Here, we analyzed CSF monoamine metabolite concentrations in 103 adults with bipolar disorder, 72 adults with ADHD, and 113 controls. Individuals with bipolar disorder had significantly higher homovanillic acid (HVA, 264 ± 112 nmol/L, p < 0.001) and 5-hydroxyindoleacetic acid (5-HIAA, 116 ± 42 nmol/L, p = 0.001) concentration, but lower 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG, 38 ± 8 nmol/L, p < 0.001) concentrations than controls (HVA, 206 ± 70 nmol/L; 5-HIAA, 98 ± 31 nmol/L; and MHPG, 42 ± 7 nmol/L). Higher HVA concentrations were associated with a history of psychosis in the bipolar disorder sample. Subjects with ADHD had higher HVA (240 ± 94 nmol/L, p < 0.001) concentrations compared with controls. In addition, SSRI treatment was associated with lower 5-HIAA concentrations in both patient groups. A power analysis indicated that for within-group comparisons, only large effects would be reliably detectable. Thus, there may be moderate-to-small effects caused by medication that were not detected due to the limited size of the sub-groups in these analyses. In conclusion, the present study suggests disorder-specific alterations of CSF monoamine metabolite concentrations in patients with bipolar disorder and ADHD compared with controls; these differences were independent of acute symptoms and medication effects.
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27.
  • Song, Jie, et al. (författare)
  • Suicidal Behavior During Lithium and Valproate Treatment: A Within-Individual 8-Year Prospective Study of 50,000 Patients With Bipolar Disorder.
  • 2017
  • Ingår i: The American journal of psychiatry. - 1535-7228. ; 174:8, s. 795-802
  • Tidskriftsartikel (refereegranskat)abstract
    • Conclusions regarding lithium's antisuicidal effect for bipolar disorder have been limited due to nonrepresentative subjects and potential confounding factors, including varying severity of illness. Findings regarding the effect of valproate, the most common alternative to lithium, are inconsistent for suicidal behavior. This study investigated the associations of these two drugs with the risk of suicide-related events, and possible differences between drugs, by using within-individual designs in a register-based longitudinal cohort.Through linkage of multiple Swedish national registers, 51,535 individuals with bipolar disorder were followed from 2005 to 2013 for treatment with lithium and valproate. Stratified Cox regression was used to estimate the hazard ratios of suicide-related events during treated periods compared with untreated periods. For significant associations between medication and suicide-related events, the population attributable fraction was estimated to assess the public health impact for patients with bipolar disorder.During follow-up, 10,648 suicide-related events occurred. The incidence rate was significantly decreased by 14% during lithium treatment (hazard ratio 0.86, 95% confidence interval [CI] 0.78-0.95) but not during valproate treatment (hazard ratio 1.02, 95% CI 0.89-1.15). The difference in hazard ratios of suicide-related events between lithium and valproate was statistically significant. Estimates of the population attributable fraction suggested that 12% (95% CI 4%-20%) of suicide-related events could have been avoided if patients had taken lithium during the entire follow-up.The results suggest that lithium should be considered for patients with bipolar disorder with suspected suicidal intentions, although risk for suicide is only one of the considerations when providing clinical care.
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28.
  • Sparding, Timea, et al. (författare)
  • Personality traits in bipolar disorder and influence on outcome.
  • 2017
  • Ingår i: BMC psychiatry. - 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 2 years. 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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29.
  • van Hulzen, Kimm J E, et al. (författare)
  • Genetic Overlap Between Attention-Deficit/Hyperactivity Disorder and Bipolar Disorder: Evidence From Genome-wide Association Study Meta-analysis.
  • 2017
  • Ingår i: Biological psychiatry. - 1873-2402. ; 82:9, s. 634-641
  • Tidskriftsartikel (refereegranskat)abstract
    • Attention-deficit/hyperactivity disorder (ADHD) and bipolar disorder (BPD) are frequently co-occurring and highly heritable mental health conditions. We hypothesized that BPD cases with an early age of onset (≤21 years old) would be particularly likely to show genetic covariation with ADHD.Genome-wide association study data were available for 4609 individuals with ADHD, 9650 individuals with BPD (5167 thereof with early-onset BPD), and 21,363 typically developing controls. We conducted a cross-disorder genome-wide association study meta-analysis to identify whether the observed comorbidity between ADHD and BPD could be due to shared genetic risks.We found a significant single nucleotide polymorphism-based genetic correlation between ADHD and BPD in the full and age-restricted samples (rGfull = .64, p = 3.13 × 10(-14); rGrestricted = .71, p = 4.09 × 10(-16)). The meta-analysis between the full BPD sample identified two genome-wide significant (prs7089973 = 2.47 × 10(-8); prs11756438 = 4.36 × 10(-8)) regions located on chromosomes 6 (CEP85L) and 10 (TAF9BP2). Restricting the analyses to BPD cases with an early onset yielded one genome-wide significant association (prs58502974 = 2.11 × 10(-8)) on chromosome 5 in the ADCY2 gene. Additional nominally significant regions identified contained known expression quantitative trait loci with putative functional consequences for NT5DC1, NT5DC2, and CACNB3 expression, whereas functional predictions implicated ABLIM1 as an allele-specific expressed gene in neuronal tissue.The single nucleotide polymorphism-based genetic correlation between ADHD and BPD is substantial, significant, and consistent with the existence of genetic overlap between ADHD and BPD, with potential differential genetic mechanisms involved in early and later BPD onset.
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30.
  • Landen, Jaren W., et al. (författare)
  • Ponezumab in mild-to-moderate Alzheimer's disease : Randomized phase II PET-PIB study
  • 2017
  • Ingår i: Alzheimer's and Dementia: Translational Research and Clinical Interventions. - John Wiley and Sons Inc.. ; 3:3, s. 393-401
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction The safety, pharmacokinetics, and effect on peripheral and central amyloid β (Aβ) of multiple doses of ponezumab, an anti-Aβ monoclonal antibody, were characterized in subjects with mild-to-moderate Alzheimer's disease treated for 1 year. Methods Subjects were aged ≥50 years with Mini–Mental State Examination scores 16 to 26. Cohort Q was randomized to ponezumab 10 mg/kg (n = 12) or placebo (n = 6) quarterly. Cohort M was randomized to a loading dose of ponezumab 10 mg/kg or placebo, followed by monthly ponezumab 7.5 mg/kg (n = 12) or placebo (n = 6), respectively. Results Ponezumab was generally well tolerated. Plasma concentrations increased dose dependently, but cerebrospinal fluid (CSF) penetration was low. Plasma Aβ increased dose dependently with ponezumab, but CSF biomarkers, brain amyloid burden, cognition, and function were not affected. Conclusions Both ponezumab dosing schedules were generally safe and well tolerated but did not alter CSF biomarkers, brain amyloid burden, or clinical outcomes.
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