Neurobiological Highlights of Cognitive Impairment in Psychiatric Disorders.
Ontology highlight
ABSTRACT:
SUBMITTER: Morozova A
PROVIDER: S-EPMC8835608 | biostudies-literature | 2022 Jan
REPOSITORIES: biostudies-literature
Publications
Neurobiological Highlights of Cognitive Impairment in Psychiatric Disorders.
Morozova Anna A Zorkina Yana Y Abramova Olga O Pavlova Olga O Pavlov Konstantin K Soloveva Kristina K Volkova Maria M Alekseeva Polina P Andryshchenko Alisa A Kostyuk Georgiy G Gurina Olga O Chekhonin Vladimir V
International journal of molecular sciences 20220122 3
This review is focused on several psychiatric disorders in which cognitive impairment is a major component of the disease, influencing life quality. There are plenty of data proving that cognitive impairment accompanies and even underlies some psychiatric disorders. In addition, sources provide information on the biological background of cognitive problems associated with mental illness. This scientific review aims to summarize the current knowledge about neurobiological mechanisms of cognitive ...[more]
Similar Datasets
Project description:Integrating findings from genome-wide association studies with molecular datasets can develop insight into the underlying functional mechanisms responsible for trait-associated genetic variants. We have applied the principles of Mendelian randomization (MR) to investigate whether brain-derived gene expression (n = 1194) may be responsible for mediating the effect of genetic variants on eight cognitive and psychological outcomes (attention deficit hyperactivity disorder (ADHD), Alzheimer's disease, bipolar disorder, depression, intelligence, insomnia, neuroticism and schizophrenia). Transcriptome-wide analyses identified 83 genes associated with at least one outcome (PBonferroni < 6.72 × 10-6), with multiple-trait colocalization also implicating changes to brain-derived DNA methylation at nine of these loci. Comparing effects between outcomes identified evidence of enrichment which may reflect putative causal relationships, such as an inverse relationship between genetic liability towards schizophrenia risk and cognitive ability in later life. Repeating these analyses in whole blood (n = 31 684), we replicated 58.2% of brain-derived effects (based on P < 0.05). Finally, we undertook phenome-wide evaluations at associated loci to investigate pleiotropic effects with 700 complex traits. This highlighted pleiotropic loci such as FURIN (initially implicated in schizophrenia risk (P = 1.05 × 10-7)) which had evidence of an effect on 28 other outcomes, as well as genes which may have a more specific role in disease pathogenesis (e.g. SLC12A5 which only provided evidence of an effect on depression (P = 7.13 × 10-10)). Our results support the utility of whole blood as a valuable proxy for informing initial target identification but also suggest that gene discovery in a tissue-specific manner may be more informative. Finally, non-pleiotropic loci highlighted by our study may be of use for therapeutic translational endeavours.
| S-EPMC9990996 | biostudies-literature
Project description:A retrospective meta-analysis of magnetic resonance imaging voxel-based morphometry studies proposed that reduced gray matter volumes in the dorsal anterior cingulate and the left and right anterior insular cortex-areas that constitute hub nodes of the salience network-represent a common substrate for major psychiatric disorders. Here, we investigated the hypothesis that the common substrate serves as an intermediate phenotype to detect genetic risk variants relevant for psychiatric disease. To this end, after a data reduction step, we conducted genome-wide association studies of a combined common substrate measure in four population-based cohorts (n = 2271), followed by meta-analysis and replication in a fifth cohort (n = 865). After correction for covariates, the heritability of the common substrate was estimated at 0.50 (standard error 0.18). The top single-nucleotide polymorphism (SNP) rs17076061 was associated with the common substrate at genome-wide significance and replicated, explaining 1.2% of the common substrate variance. This SNP mapped to a locus on chromosome 5q35.2 harboring genes involved in neuronal development and regeneration. In follow-up analyses, rs17076061 was not robustly associated with psychiatric disease, and no overlap was found between the broader genetic architecture of the common substrate and genetic risk for major depressive disorder, bipolar disorder, or schizophrenia. In conclusion, our study identified that common genetic variation indeed influences the common substrate, but that these variants do not directly translate to increased disease risk. Future studies should investigate gene-by-environment interactions and employ functional imaging to understand how salience network structure translates to psychiatric disorder risk.
| S-EPMC8007575 | biostudies-literature
Project description:ImportanceMany psychiatric disorders can be conceptualized as disorders of brain maturation during childhood and adolescence. Discovering the neurobiological underpinnings of brain maturation may elucidate molecular pathways of vulnerability and resilience to such disorders.ObjectiveTo investigate the underlying neurobiological mechanisms of age-associated cortical thinning during maturation and their implications for psychiatric disorders.Design, setting, and participantsThis multicohort analysis used data from 3 community-based studies. The Saguenay Youth Study provided data from 1024 adolescents who were recruited at a single site in Quebec, Canada. The IMAGEN cohort provided data from 1823 participants who were recruited in 8 European cities. The Brazil High Risk Cohort Study for the Development of Childhood Psychiatric Disorders provided data from 815 participants who were recruited in 2 Brazilian cities. Cortical thickness was estimated from the results of magnetic resonance imaging (MRI) scans, and age-associated cortical thinning was estimated in 34 cortical regions. Gene expression from the Allen Human Brain Atlas was aligned with the same regions. Similarities in the interregional profiles of gene expression and the profiles of age-associated cortical thinning were measured. The involvement of dendrites, dendritic spines, and myelin was tested using 3 gene panels. Enrichment for genes associated with psychiatric disorders was tested among the genes associated with thinning and their coexpression networks. Data analysis was conducted between March and October 2019.Main outcomes and measuresMRI-derived estimates of age-associated cortical thinning and gene expression in 34 cortical regions.ResultsA total of 3596 individuals aged 9 to 21 years were included in this study. Of those, 1803 participants (50.1%) were female, and the mean (SD) age was 15.2 (2.6) years. Interregional profiles of age-associated cortical thinning were associated with interregional gradients in the expression of genes associated with dendrites, dendritic spines, and myelin; the variance in thinning explained by the gene panels across different points ranged from 0.45% to 10.55% for the dendrite panel, 0.00% to 9.98% for the spine panel, and 0.19% to 26.39% for the myelin panel. These genes and their coexpression networks were enriched for genes associated with several psychiatric disorders.Conclusions and relevanceIn this study, genetic similarity between interregional variation in cortical thinning during maturation and multiple psychiatric disorders suggests overlapping molecular underpinnings. This finding adds to the understanding of the neurodevelopmental mechanisms of psychiatric disorders.
| S-EPMC7301307 | biostudies-literature
Project description:BackgroundAutomatic biases, such as attentional biases and avoidance and interpretative biases, have been purported to be responsible for several psychiatric disorders. Gamification has been considered for cognitive bias modification, mainly to address the core issues of diminishing motivation to train over time, as bias modification intervention tasks tend to be highly repetitive. While a prior review has suggested how gamification strategies could be applied to such tasks, there remains a lack of systematic evaluation of gamified cognitive bias modification interventions in the literature.ObjectiveThe objective of this review is to understand the overall effectiveness of a gamified approach for cognitive bias modification and inform future research that seeks to integrate gamification technologies into existing conventional bias modification interventions.MethodsTo identify the relevant articles for our review, the following search terminologies were used: ("cognitive bias" OR "attention bias" OR "interpret* bias" OR "approach bias" OR "avoidance bias") AND ("training" OR "modification" OR "practice" OR "therapy") AND ("gamification" OR "game elements" OR "game" OR "gaming" OR "game mechanics"). PubMed, MEDLINE, PsycINFO, and Scopus databases were searched systematically for articles published after 2000. Articles were included if they described a gamified cognitive bias modification task and included participants with underlying psychopathological symptoms. Data were systematically extracted from the identified articles, and a qualitative synthesis was performed.ResultsFour studies evaluated gamified cognitive bias modification interventions. Two studies included participants with anxiety symptoms, one with affective symptoms, and one with alcohol problems. The conventional visual probe task paradigm was used in 3 studies, and the attentional visual search task paradigm was used in the last study. We found gaming elements incorporated to include that of animations, sounds, feedback, and a point-scoring system for response time and difficulty. Of the 4 identified studies, only 2 reported their gamified interventions to be effective.ConclusionsOur review is the first to systematically synthesize the evidence for gamified cognitive bias modification interventions. The results arising from our review should be considered in the future design and conceptualization of gamified cognitive bias modification interventions.International registered report identifier (irrid)RR2-10.2196/10154.
| S-EPMC6229516 | biostudies-literature
Project description:Neurologic impairment persisting months after acute severe SARS-CoV-2 infection has been described because of several pathogenic mechanisms, including persistent systemic inflammation. The objective of this study is to analyze the selective involvement of the different cognitive domains and the existence of related biomarkers. Cross-sectional multicentric study of patients who survived severe infection with SARS-CoV-2 consecutively recruited between 90 and 120 days after hospital discharge. All patients underwent an exhaustive study of cognitive functions as well as plasma determination of pro-inflammatory, neurotrophic factors and light-chain neurofilaments. A principal component analysis extracted the main independent characteristics of the syndrome. 152 patients were recruited. The results of our study preferential involvement of episodic and working memory, executive functions, and attention and relatively less affectation of other cortical functions. In addition, anxiety and depression pictures are constant in our cohort. Several plasma chemokines concentrations were elevated compared with both, a non-SARS-Cov2 infected cohort of neurological outpatients or a control healthy general population. Severe Covid-19 patients can develop an amnesic and dysexecutive syndrome with neuropsychiatric manifestations. We do not know if the deficits detected can persist in the long term and if this can trigger or accelerate the onset of neurodegenerative diseases.
| S-EPMC8894467 | biostudies-literature
Project description:BackgroundAlthough cognitive impairment is a core symptom of schizophrenia related to poorer outcomes in different functional domains, it still remains a major therapeutic challenge. To date, no comprehensive treatment guidelines for cognitive impairment in schizophrenia are implemented.MethodsThe aim of the present guidance paper is to provide a comprehensive meta-review of the current available evidence-based treatments for cognitive impairment in schizophrenia. The guidance is structured into three sections: pharmacological treatment, psychosocial interventions, and somatic treatments.ResultsBased on the reviewed evidence, this European Psychiatric Association guidance recommends an appropriate pharmacological management as a fundamental starting point in the treatment of cognitive impairment in schizophrenia. In particular, second-generation antipsychotics are recommended for their favorable cognitive profile compared to first-generation antipsychotics, although no clear superiority of a single second-generation antipsychotic has currently been found. Anticholinergic and benzodiazepine burdens should be kept to a minimum, considering the negative impact on cognitive functioning. Among psychosocial interventions, cognitive remediation and physical exercise are recommended for the treatment of cognitive impairment in schizophrenia. Noninvasive brain stimulation techniques could be taken into account as add-on therapy.ConclusionsOverall, there is definitive progress in the field, but further research is needed to develop specific treatments for cognitive impairment in schizophrenia. The dissemination of this guidance paper may promote the development of shared guidelines concerning the treatment of cognitive functions in schizophrenia, with the purpose to improve the quality of care and to achieve recovery in this population.
| S-EPMC9532218 | biostudies-literature
Project description:BackgroundImpairment in a wide range of cognitive abilities has been consistently reported in individuals with schizophrenia. Both neurocognitive and social cognitive deficits are thought to underlie severe functional disabilities associated with schizophrenia. Despite the key role in schizophrenia outcome, cognition is still poorly assessed in both research and clinical settings.MethodsIn this guidance paper, we provide a systematic review of the scientific literature and elaborate several recommendations for the assessment of cognitive functions in schizophrenia both in research settings and in real-world clinical practice.ResultsExpert consensus and systematic reviews provided guidance for the optimal assessment of cognitive functions in schizophrenia. Based on the reviewed evidence, we recommend a comprehensive and systematic assessment of neurocognitive and social cognitive domains in schizophrenia, in all phases of the disorder, as well as in subjects at risk to develop psychosis. This European Psychiatric Association guidance recommends not only the use of observer reports but also self-reports and interview-based cognitive assessment tools. The guidance also provides a systematic review of the state of the art of assessment in the first episode of psychosis patients and in individuals at risk for psychosis.ConclusionThe comprehensive review of the evidence and the recommendations might contribute to advance the field, allowing a better cognitive assessment, and avoiding overlaps with other psychopathological dimensions. The dissemination of this guidance paper may promote the development of shared guidelines concerning the assessment of cognitive functions in schizophrenia, with the purpose to improve the quality of care and to obtain recovery.
| S-EPMC9532219 | biostudies-literature
Project description:Psychiatric diseases, such as schizophrenia, bipolar disorder, autism spectrum disorder, and major depressive disorder, place a huge health burden on society. Cognitive impairment is one of the core characteristics of psychiatric disorders and a vital determinant of social function and disease recurrence in patients. This review thus aims to explore the underlying molecular mechanisms of cognitive impairment in major psychiatric disorders and identify valuable biomarkers for diagnosis, treatment and prevention of patients.
| S-EPMC9666407 | biostudies-literature
Project description:BackgroundGeneral cognitive function predicts psychiatric illness across the life course. This study examines the role of pleiotropy in explaining the link between cognitive function and psychiatric disorder.MethodsWe used two large genome-wide association study data sets on cognitive function-one from older age, n = 53,949, and one from childhood, n = 12,441. We also used genome-wide association study data on educational attainment, n = 95,427, to examine the validity of its use as a proxy phenotype for cognitive function. Using a new method, linkage disequilibrium regression, we derived genetic correlations, free from the confounding of clinical state between psychiatric illness and cognitive function.ResultsWe found a genetic correlation of .711 (p = 2.26e-12) across the life course for general cognitive function. We also showed a positive genetic correlation between autism spectrum disorder and cognitive function in childhood (rg = .360, p = .0009) and for educational attainment (rg = .322, p = 1.37e-5) but not in older age. In schizophrenia, we found a negative genetic correlation between older age cognitive function (rg = -.231, p = 3.81e-12) but not in childhood or for educational attainment. For Alzheimer's disease, we found negative genetic correlations with childhood cognitive function (rg = -.341, p = .001), educational attainment (rg = -.324, p = 1.15e-5), and with older age cognitive function (rg = -.324, p = 1.78e-5).ConclusionsThe pleiotropy exhibited between cognitive function and psychiatric disorders changed across the life course. These age-dependent associations might explain why negative selection has not removed variants causally associated with autism spectrum disorder or schizophrenia.
| S-EPMC4974237 | biostudies-literature
Project description:BACKGROUND:Cognitive biases refer to automatic attentional or interpretational tendencies, which result in individuals with addictive disorders to automatically attend to substance-related stimuli and those with anxiety disorders to attend to threatening stimuli. To date, several studies have examined the efficacy of cognitive bias modification, and meta-analytical studies have synthesized the evidence for overall efficacy. The clinical utility of cognitive bias modification interventions has previously been limited to the confines of a laboratory, but recent advances in Web technologies can change this. OBJECTIVE:This scoping review aimed to determine the scope of Web-based cognitive bias interventions and highlight their effectiveness. METHODS:Databases (PubMed and MEDLINE, EMBASE, PsycINFO, ScienceDirect, and Cochrane Central) were searched from inception to December 5, 2017. The following search terminologies were used: ("attention bias" OR "cognitive bias" OR "approach bias" OR "avoidance bias" OR "interpretative bias") AND ("Internet" OR "Web" OR "Online"). The methods for this scoping review are based on the previously published protocol. For the synthesis of the evidence, a narrative synthesis was undertaken, as a meta-analysis was not appropriate, given the lack of reported effect sizes and the heterogeneity in the outcomes reported. RESULTS:Of the 2674 unique articles identified, we identified 22 randomized controlled studies that met our inclusion criteria: alcohol use disorder (n=2), tobacco use disorder (n=2), depressive disorder (n=3), anxiety and depressive symptoms in adolescents (n=3), obsessive-compulsive disorder (OCD; n=2), social anxiety disorder (n=9), and anxiety disorder (n=1). The sample sizes of these studies ranged from 16 to 434 participants. There is preliminary evidence to suggest that Web-based interventions could reduce biases among adolescents with heightened symptoms of anxiety and depression and among individuals with OCD. CONCLUSIONS:This is the first scoping review that mapped out the scope of cognitive bias modification interventions for psychiatric disorders. Web-based interventions have been applied predominantly for social anxiety and addictive disorders. Larger cohorts must be used in future studies to better determine the effectiveness of Web-based cognitive bias interventions. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID):RR1-10.2196/10427.
| S-EPMC6915808 | biostudies-literature