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1.
  • Brus, Ole, et al. (författare)
  • Subjective Memory Immediately Following Electroconvulsive Therapy
  • 2017
  • Ingår i: Journal of ECT. - Philadelphia, USA : Lippincott Williams & Wilkins. - 1095-0680. ; 33:2, s. 96-103
  • Tidskriftsartikel (refereegranskat)abstract
    • Objectives: The aims of the present study were to describe the short-term rate of subjective memory worsening (SMW) and identify factors of importance for SMW in a large clinical sample treated for depression with electroconvulsive therapy (ECT).Methods: This register-based study included 1212 patients from the Swedish National Quality Register for ECT. Subjective memory worsening was defined as a 2-point worsening on the memory item of the Comprehensive Psychopathological Rating Scale from before to within 1 week after treatment. Associations between patient characteristics and treatment factors were examined using logistic regression.Results: Subjective memory worsening was experienced in 26%. It was more common in women than in men (31% vs 18%; P < 0.001) and more common in patients aged 18 to 39 years than in patients 65 years or older (32% vs 22%; P = 0.008). Patients with less subjective memory disturbances before ECT had a greater risk of SMW. Patients in remission after ECT had a lower risk of SMW. A brief pulse width stimulus gave higher risk of SMW compared with ultrabrief pulse (odds ratio, 1.61; 95% confidence interval, 1.05-2.47).Conclusions: Subjective memory worsening is reported by a minority of patients. However, young women are at risk of experiencing SMW. Ultrabrief pulse width stimulus could be considered for patients treated with unilateral electrode placement who experience SMW. Each patient should be monitored with regard to symptoms and adverse effects, and treatment should be adjusted on an individual basis to maximize the clinical effect and with efforts to minimize the cognitive adverse effects.
2.
  • Backlund, Lena, et al. (författare)
  • P2RX7: Expression Responds to Sleep Deprivation and Associates with Rapid Cycling in Bipolar Disorder Type 1
  • 2012
  • Ingår i: Plos One. - 1932-6203. ; 7:8
  • Tidskriftsartikel (refereegranskat)abstract
    • Context: Rapid cycling is a severe form of bipolar disorder with an increased rate of episodes that is particularly treatment-responsive to chronotherapy and stable sleep-wake cycles. We hypothesized that the P2RX7 gene would be affected by sleep deprivation and be implicated in rapid cycling. Objectives: To assess whether P2RX7 expression is affected by total sleep deprivation and if variation in P2RX7 is associated with rapid cycling in bipolar patients. Design: Gene expression analysis in peripheral blood mononuclear cells (PBMCs) from healthy volunteers and case-case and case-control SNP/haplotype association analyses in patients. Participants: Healthy volunteers at the sleep research center, University of California, Irvine Medical Center (UCIMC), USA (n = 8) and Swedish outpatients recruited from specialized psychiatric clinics for bipolar disorder, diagnosed with bipolar disorder type 1 (n = 569; rapid cycling: n = 121) and anonymous blood donor controls (n = 1,044). Results: P2RX7 RNA levels were significantly increased during sleep deprivation in PBMCs from healthy volunteers (p = 2.3*10(-9)). The P2RX7 rs2230912_A allele was more common (OR = 2.2, p = 0.002) and the ACGTTT haplotype in P2RX7 (rs1718119 to rs1621388) containing the protective rs2230912_G allele (OR = 0.45-0.49, p = 0.003-0.005) was less common, among rapid cycling cases compared to non-rapid cycling bipolar patients and blood donor controls. Conclusions: Sleep deprivation increased P2RX7 expression in healthy persons and the putatively low-activity P2RX7 rs2230912 allele A variant was associated with rapid cycling in bipolar disorder. This supports earlier findings of P2RX7 associations to affective disorder and is in agreement with that particularly rapid cycling patients have a more vulnerable diurnal system.
3.
  • Damberg, Mattias, et al. (författare)
  • Investigation of transcription factor AP-2 beta genotype in women with premenstrual dysphoric disorder.
  • 2005
  • Ingår i: Neuroscience letters. - 0304-3940. ; 377:1, s. 49-52
  • Tidskriftsartikel (refereegranskat)abstract
    • It has repeatedly been shown that the serotonergic system is involved in the symptomatology of premenstrual dysphoric disorder (PMDD). Women with PMDD are reported to differ from symptom-free controls with regard to serotonin-related biological markers. Evidence from family and twin studies suggests a genetic contribution to the aetiology of PMDD. The expression of human transcription factor AP-2beta in neural crest cell lineages and neuroectodermal cells suggests that this protein may be of importance for functional characteristics of neurons by regulating the expression of target genes. Within the monoaminergic systems, several genes have binding sites for AP-2beta in regulatory regions, suggesting an involvement of AP-2beta in these systems. The gene encoding AP-2beta is located on chromosome 6p12-p21.1 and includes a polymorphic region consisting of a variable number of [CAAA] repeats located in the second intron. We have earlier shown that AP-2beta genotype is associated with serotonergic phenotypes and that brainstem levels of AP-2beta correlate positively to serotonin metabolism in rat frontal cortex. The aim of this study was to investigate the relationship between PMDD and transcription factor AP-2beta genotype. The participants included 176 women with PMDD and 91 healthy controls. Genotyping was performed by polymerase chain reactions. We did not observe any differences in AP-2beta genotype frequencies between PMDD subjects and controls. Our results suggest that AP-2beta genotype is not a risk factor for PMDD. To our knowledge, this is the first study investigating transcription factor AP-2beta genotype in women with PMDD. Hence, these results should be considered preliminary until replicated.
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4.
  • de Jong, Simone, et al. (författare)
  • Applying polygenic risk scoring for psychiatric disorders to a large family with bipolar disorder and major depressive disorder
  • 2018
  • Ingår i: Communications Biology. - Nature Publishing Group. - 2399-3642. ; 1
  • Tidskriftsartikel (refereegranskat)abstract
    • Psychiatric disorders are thought to have a complex genetic pathology consisting of interplay of common and rare variation. Traditionally, pedigrees are used to shed light on the latter only, while here we discuss the application of polygenic risk scores to also highlight patterns of common genetic risk. We analyze polygenic risk scores for psychiatric disorders in a large pedigree (n ~ 260) in which 30% of family members suffer from major depressive disorder or bipolar disorder. Studying patterns of assortative mating and anticipation, it appears increased polygenic risk is contributed by affected individuals who married into the family, resulting in an increasing genetic risk over generations. This may explain the observation of anticipation in mood disorders, whereby onset is earlier and the severity increases over the generations of a family. Joint analyses of rare and common variation may be a powerful way to understand the familial genetics of psychiatric disorders.
5.
  • Henningsson, Susanne, et al. (författare)
  • Possible association between the androgen receptor gene and autism spectrum disorder.
  • 2009
  • Ingår i: Psychoneuroendocrinology. - 0306-4530. ; 34:5, s. 752-761
  • Tidskriftsartikel (refereegranskat)abstract
    • Autism is a highly heritable disorder but the specific genes involved remain largely unknown. The higher prevalence of autism in men than in women, in conjunction with a number of other observations, has led to the suggestion that prenatal brain exposure to androgens may be of importance for the development of this condition. Prompted by this hypothesis, we investigated the potential influence of variation in the androgen receptor (AR) gene on the susceptibility for autism. To this end, 267 subjects with autism spectrum disorder and 617 controls were genotyped for three polymorphisms in exon I of the AR gene: the CAG repeat, the GGN repeat and the rs6152 SNP. In addition, parents and affected siblings were genotyped for 118 and 32 of the cases, respectively. Case-control comparisons revealed higher prevalence of short CAG alleles as well as of the A allele of the rs6152 SNP in female cases than in controls, but revealed no significant differences with respect to the GGN repeat. Analysis of the 118 families using transmission disequilibrium test, on the other hand, suggested an association with the GGN polymorphism, the rare 20-repeat allele being undertransmitted to male cases and the 23-repeat allele being overtransmitted to female cases. Sequencing of the AR gene in 46 patients revealed no mutations or rare variants. The results tend some support for an influence of the studied polymorphisms on the susceptibility for autism, but argue against the possibility that mutations in the AR gene are common in subjects with this condition. (C) 2008 Elsevier Ltd. All rights reserved.
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6.
  • Hollis, Chris, et al. (författare)
  • Methylphenidate and the risk of psychosis in adolescents and young adults a population-based cohort study
  • 2019
  • Ingår i: Lancet psychiatry. - Elsevier. - 2215-0374. ; 6:8, s. 651-658
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: There is a clinical concern that prescribing methylphenidate, the most common pharmacological treatment for attention-deficit hyperactivity disorder (ADHD), might increase the risk of psychotic events, particularly in young people with a history of psychosis. We aimed to determine whether the risk of psychotic events increases immediately after initiation of methylphenidate treatment or, in the longer term, 1 year after treatment initiation in adolescents and young adults with and without a previously diagnosed psychotic disorder.Methods: In this cohort study, we used population-based observational data from the Swedish Prescribed Drug Register, the National Patient Register, and the Total Population Register, three population-based registers containing data on all individuals in Sweden, to attain data on sex, birth, death, migration, medication use, and psychotic events for all eligible participants. We screened individuals on these registers to identify those receiving methylphenidate treatment, and who were aged 12-30 years at the start of treatment, for their inclusion in the study. We used a within-individual design to compare the incidence of psychotic events in these individuals during the 12-week periods immediately before and after methylphenidate initiation. Longer term risk was assessed by comparing the incidence of psychotic events 12 weeks before methylphenidate initiation and during a 12-week period one calendar year before the initiation of methylphenidate with the incidence of these events during the 12-week period one calendar year after methylphenidate initiation. We estimated the incidence rate ratios (IRR) and 95% CIs of psychotic events after the initation of methylphenidate treatment, relative to the events before treatment, which were defined as any hospital visit (inpatient admission or outpatient attendance, based on data from the National Patient Register) because of psychosis, using the International Classification of Diseases version 10 definition. Analyses were stratified by whether the individual had a history of psychosis.Findings: We searched the Swedish Prescribed Drug Register to find eligible individuals who had received methylphenidate between Jan 1, 2007 and June 30, 2012. 61 814 individuals were screened, of whom 23 898 (38.7%) individuals were assessed and 37 916 (61.3%) were excluded from the study because they were outside of the age criteria at the start of treatment, they had immigrated, emigrated, or died during the study period, or because they were administered other ADHD medications. The median age at methylphenidate initiation was 17 years, and a history of psychosis was reported in 479 (2.0%) participants. The IRR of psychotic events in the 12-week period after initiation of methylphenidate treatment relative to that in the 12-week period before treatment start was 1.04 (95% CI 0.80-1.34) in adolescents and young adults without a history of psychosis and 0.95 (0.69-1.30) among those with a history of psychosis.Interpretation: Contrary to clinical concerns, we found no evidence that initiation of methylphenidate treatment increases the risk of psychotic events in adolescents and young adults, including in those individuals with a history of psychosis. Our study should reassure clinicians considering initiating methylphenidate treatment for ADHD in adolescents and young adults, and it challenges the widely held view in clinical practice that methylphenidate should be avoided, or its use restricted, in individuals with a history of psychosis.
7.
  • Holm, Jonas, et al. (författare)
  • Improvement of cycloid psychosis following electroconvulsive therapy
  • 2017
  • Ingår i: Nordic Journal of Psychiatry. - TAYLOR & FRANCIS LTD. - 0803-9488. ; 71:6, s. 405-410
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: The treatment of choice for cycloid psychosis has traditionally been electroconvulsive therapy (ECT), but there is a lack of studies on its effectiveness.Aims: The primary aim of this register study was to determine the rates of remission and response after ECT for cycloid psychosis. The secondary aim was to examine possible predictors of outcome.Methods: Data were obtained from the National Quality Register for ECT in Sweden. The study population was patients (n=42) who received ECT for acute polymorphic psychotic disorder without symptoms of schizophrenia or for cycloid psychosis between 2011-2015 in 13 hospitals. Remission and response rates were calculated using Clinical Global Impression-Severity (CGI-S) and -Improvement scores, respectively. Variables with possible predictive value were tested using Chi-square and Fishers exact test.Results: The response rate was 90.5%. The remission rate was 45.2%. Of 42 patients, 40 improved their CGI-S score after ECT (pamp;lt;0.001). The mean number of ECT treatments was 2.5 for non-responders and 7.0 for responders (p=0.010). The mean number of ECT treatments did not differ significantly between remitters and non-remitters (7.2 vs 6.1, p=0.31). None of the other investigated potential predictors was statistically significantly associated with outcome.Conclusions: ECT is an effective treatment for cycloid psychosis. Future studies need to compare the outcome of ECT to that of other treatment strategies. Clinical implications: The high response rate with ECT indicates that cycloid psychosis is a clinically useful diagnosis.
8.
  • Hukic, Dzana Sudic, et al. (författare)
  • Cognitive Manic Symptoms in Bipolar Disorder Associated with Polymorphisms in the DAOA and COMT Genes
  • 2013
  • Ingår i: PLoS ONE. - Public Library of Science. - 1932-6203. ; 8:7
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: Bipolar disorder is characterized by severe mood symptoms including major depressive and manic episodes. During manic episodes, many patients show cognitive dysfunction. Dopamine and glutamate are important for cognitive processing, thus the COMT and DAOA genes that modulate the expression of these neurotransmitters are of interest for studies of cognitive function. Methodology: Focusing on the most severe episode of mania, a factor was found with the combined symptoms of talkativeness, distractibility, and thought disorder, considered a cognitive manic symptoms (CMS) factor. 488 patients were genotyped, out of which 373 (76%) had talkativeness, 269 (55%) distractibility, and 372 (76%) thought disorder. 215 (44%) patients were positive for all three symptoms, thus showing CMS (Table 1). As population controls, 1,044 anonymous blood donors (ABD) were used. Case-case and case-control design models were used to investigate genetic associations between cognitive manic symptoms in bipolar 1 disorder and SNPs in the COMT and DAOA genes. Results: The finding of this study was that cognitive manic symptoms in patients with bipolar 1 disorder was associated with genetic variants in the DAOA and COMT genes. Nominal association for DAOA SNPs and COMT SNPs to cognitive symptoms factor in bipolar 1 disorder was found in both allelic (Table 2) and haplotypic (Table 3) analyses. Genotypic association analyses also supported our findings. However, only one association, when CMS patients were compared to ABD controls, survived correction for multiple testing by max (T) permutation. Data also suggested interaction between SNPs rs2391191 in DAOA and rs5993883 in COMT in the case-control model. Conclusion: Identifying genes associated with cognitive functioning has clinical implications for assessment of prognosis and progression. Our finding are consistent with other studies showing genetic associations between the COMT and DAOA genes and impaired cognition both in psychiatric disorders and in the general population.
9.
  • Karanti, Alina, et al. (författare)
  • Gender differences in the treatment of patients with bipolar disorder: A study of 7354 patients
  • 2015
  • Ingår i: Journal of Affective Disorders. - 0165-0327. ; 174, s. 303-309
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Gender differences in treatment that are not supported by empirical evidence have been reported in several areas of medicine. Here, the aim was to evaluate potential gender differences in the treatment for bipolar disorder. Methods: Data was collected from the Swedish National Quality Assurance Register for bipolar disorder (BipolaR). Baseline registrations from the period 2004-2011 of 7354 patients were analyzed. Multiple logistic regression analysis was used to study the impact of gender on interventions. Results: Women were more often treated with antidepressants, lamotrigine, electroconvulsive therapy, benzodiazepines, and psychotherapy. Men were more often treated with lithium. There were no gender differences in treatment with mood stabilizers as a group, neuroleptics, or valproate. Subgroup analyses revealed that ECT was more common in women only in the bipolar l subgroup. Contrariwise, lamotrigine was more common in women only in the bipolar II subgroup. Limitations: As BipolaR contains data on outpatient treatment of persons with bipolar disorder in Sweden, it is unclear if these Findings translate to inpatient care and to outpatient treatment in other countries. Conclusions: Men and women with bipolar disorder receive different treatments in routine clinical settings in Sweden. Gender differences in level of functioning, bipolar subtype, or severity of bipolar disorder could not explain the higher prevalence of pharmacological treatment, electroconvulsive therapy, and psychotherapy in women. Our results suggest that clinicians treatment decisions are to some extent unduly influenced by patients gender. (C) 2014 Elsevier B.V. All rights reserved.
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10.
  • Landen, Mikael, et al. (författare)
  • Short Onset of Action of a Serotonin Reuptake Inhibitor When Used to Reduce Premenstrual Irritability.
  • 2009
  • Ingår i: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. - 0893-133X. ; 34:3, s. 585-92
  • Tidskriftsartikel (refereegranskat)abstract
    • Several studies suggest that serotonin reuptake inhibitors (SRIs) exert a more rapid effect when used for the treatment of symptoms such as anger and irritability then when used for depression, obsessive-compulsive disorder, or anxiety. In line with this, premenstrual irritability can be effectively dampened by intermittent administration of an SRI, from ovulation to menstruation, indicating an onset of action of 10 days or less. How fast this effect appears, in terms of hours or days, is of considerable theoretical interest, but has previously not been studied in detail. To explore this issue, 22 women with marked premenstrual irritability, who previously had responded to paroxetine, were given this compound during two menstrual cycles and placebo during one cycle in a double-blind, cross-over fashion. The women were asked to start medication in the midst of the luteal phase when irritability had been intense for 2 days. The paroxetine cycles differed significantly from the placebo cycle as early as 14 h after drug intake with respect to the number of subjects experiencing sustained reduction in irritability. When the different cycles were compared with respect to irritability-rating scores for each time of assessment, the difference was significant at day 3. The side effect nausea had an even more rapid onset (4 h), but usually disappeared within 4 days. To summarize, this controlled trial shows that an SRI reduces premenstrual irritability already within a few days after the onset of treatment.
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