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| 33. |
- Lycke Brandt, Christine, et al.
(författare)
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Working memory networks and activation patterns in schizophrenia and bipolar disorder : comparison with healthy controls
- 2014
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Ingår i: British Journal of Psychiatry. - 0007-1250 .- 1472-1465. ; 204:4, s. 290-298
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Schizophrenia and bipolar disorder are severe mental disorders with overlapping genetic and clinical characteristics, including cognitive impairments. An important question is whether these disorders also have overlapping neuronal deficits.AIMS: To determine whether large-scale brain networks associated with working memory, as measured with functional magnetic resonance imaging (fMRI), are the same in both schizophrenia and bipolar disorder, and how they differ from those in healthy individuals.METHOD: Patients with schizophrenia (n = 100) and bipolar disorder (n = 100) and a healthy control group (n = 100) performed a 2-back working memory task while fMRI data were acquired. The imaging data were analysed using independent component analysis to extract large-scale networks of task-related activations.RESULTS: Similar working memory networks were activated in all groups. However, in three out of nine networks related to the experimental task there was a graded response difference in fMRI signal amplitudes, where patients with schizophrenia showed greater activation than those with bipolar disorder, who in turn showed more activation than healthy controls. Secondary analysis of the patient groups showed that these activation patterns were associated with history of psychosis and current elevated mood in bipolar disorder.CONCLUSIONS: The same brain networks were related to working memory in schizophrenia, bipolar disorder and controls. However, some key networks showed a graded hyperactivation in the two patient groups, in line with a continuum of neuronal abnormalities across psychotic disorders.
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| 34. |
- Mullins, Niamh, et al.
(författare)
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Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors
- 2022
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Ingår i: Biological Psychiatry. - : Elsevier. - 0006-3223 .- 1873-2402. ; 91:3, s. 313-327
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders.METHODS: We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors.RESULTS: Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged.CONCLUSIONS: Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.
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| 36. |
- Onyeka, I. N., et al.
(författare)
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Comorbidity of Physical Disorders Among Patients With Severe Mental Illness With and Without Substance Use Disorders: A Systematic Review and Meta-Analysis
- 2019
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Ingår i: Journal of Dual Diagnosis. - : Informa UK Limited. - 1550-4263 .- 1550-4271. ; 15:3, s. 192-206
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Physical disorders in patients with severe mental illness (SMI) are common and they tend to be underdiagnosed by clinicians, which might lead to negative treatment outcomes. The presence of substance use disorders could further aggravate the situation. There are existing systematic reviews on physical disorders among individuals with SMI in general but none of these previous reviews stratified their findings by substance use disorder status. This study aimed to synthesize the evidence on the frequency of comorbid physical disorders among patients with SMI with or without substance use disorders. Methods: We searched for studies published in English between 1988 and 2017 in MEDLINE, Embase, CINAHL, PsycINFO, Global Health, Web of Science, Scopus, WHO Global Health Library (Global Index Medicus), Google Scholar, OpenGrey, the Grey Literature Report, Cochrane Library, International Standardized Randomized Controlled Trial Number Registry, WHO International Clinical Trials Registry Platform, ClinicalTrials.gov, Australian and New Zealand Clinical Trials Registry, and PROSPERO. There was no geographical restriction and the target population was adults (>= 18 years) with diagnosed SMI including schizophrenia, bipolar disorder, and other psychotic illnesses. The outcome of interest was physical disorder. Results: A total of 6,994 records were retrieved. Only 30 papers (representing 24 studies) met our inclusion criteria and 13 studies were included in the meta-analysis. The prevalence of most of the reported physical disorders was higher in SMI patients with substance use disorders than in those without substance use disorders. When ranked according to pooled prevalence level, hypertension (35.6%), tardive dyskinesia (35.4%), and hepatitis C (26.9%) were the most prevalent physical disorders among SMI patients with substance use disorders. For SMI patients without substance use disorders, hypertension (32.5%), tardive dyskinesia (25.1%), and endocrine disease (19.0%) were more common. Estimates for diabetes (7.5% vs. 7.5%) and cardiovascular diseases (11.8% vs. 11.3%) were similar across groups. Conclusions: Physical disorders among SMI patients vary by substance use disorder status. Clinicians managing SMI in patients should screen for physical disorders and substance use disorders and provide treatment or referral. Registration: International Prospective Register of Systematic Reviews (PROSPERO) registration number CRD42017072286.
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| 37. |
- Satizabal, Claudia L., et al.
(författare)
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Genetic architecture of subcortical brain structures in 38,851 individuals
- 2019
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Ingår i: Nature Genetics. - : Nature Publishing Group. - 1061-4036 .- 1546-1718. ; 51:11, s. 1624-
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Tidskriftsartikel (refereegranskat)abstract
- Subcortical brain structures are integral to motion, consciousness, emotions and learning. We identified common genetic variation related to the volumes of the nucleus accumbens, amygdala, brainstem, caudate nucleus, globus pallidus, putamen and thalamus, using genome-wide association analyses in almost 40,000 individuals from CHARGE, ENIGMA and UK Biobank. We show that variability in subcortical volumes is heritable, and identify 48 significantly associated loci (40 novel at the time of analysis). Annotation of these loci by utilizing gene expression, methylation and neuropathological data identified 199 genes putatively implicated in neurodevelopment, synaptic signaling, axonal transport, apoptosis, inflammation/infection and susceptibility to neurological disorders. This set of genes is significantly enriched for Drosophila orthologs associated with neurodevelopmental phenotypes, suggesting evolutionarily conserved mechanisms. Our findings uncover novel biology and potential drug targets underlying brain development and disease.
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