Correction: No Evidence of Association between Childhood Urban Environment and Cortical Thinning in Psychotic Disorder.
Ontology highlight
ABSTRACT:
SUBMITTER: PLOS ONE Staff
PROVIDER: S-EPMC5436876 | biostudies-literature | 2017
REPOSITORIES: biostudies-literature
Publications
Correction: No Evidence of Association between Childhood Urban Environment and Cortical Thinning in Psychotic Disorder.
PloS one 20170518 5
[This corrects the article DOI: 10.1371/journal.pone.0166651.]. ...[more]
Similar Datasets
Project description:BackgroundThe alterations in cortical morphology, such as cortical thinning, observed in psychotic disorder, may be the outcome of interacting genetic and environmental effects. It has been suggested that urban upbringing may represent a proxy environmental effect impacting cortical thickness (CT). Therefore, the current study examined whether the association between group as a proxy genetic variable (patients with psychotic disorder [high genetic risk], healthy siblings of patients [intermediate risk] and healthy control subjects [average risk]) and CT was conditional on different levels of the childhood urban environment and whether this was sex-dependent.MethodsT1-weighted MRI scans were acquired from 89 patients with a psychotic disorder, 95 non-psychotic siblings of patients with psychotic disorder and 87 healthy control subjects. Freesurfer software was used to measure CT. Developmental urban exposure was classified as low, medium, and high, reflecting the population density and the number of moves between birth and the 15th birthday, using data from the Dutch Central Bureau of Statistics and the equivalent database in Belgium. Multilevel regression analyses were used to examine the association between group, sex, and urban upbringing (as well as their interactions) and cortical CT as the dependent variable.ResultsCT was significantly smaller in the patient group compared to the controls (B = -0.043, p <0.001), but not in the siblings compared to the controls (B = -0.013, p = 0.31). There was no main effect of developmental urbanicity on CT (B = 0.001, p = 0.91). Neither the three-way group × urbanicity × sex interaction (?2 = 3.73, p = 0.16), nor the two-way group × urbanicity interaction was significant (?2 = 0.51, p = 0.77).ConclusionThe negative association between (familial risk for) psychotic disorder and CT was not moderated by developmental urbanicity, suggesting that reduced CT is not the outcome of familial sensitivity to the proxy environmental factor 'urban upbringing'.
| S-EPMC5207533 | biostudies-literature
Project description:IMPORTANCE:Psychotic disorders (including schizophrenia, schizoaffective disorder, and psychotic bipolar disorder) are devastating illnesses characterized by breakdown in the integration of information processing. Recent advances in neuroimaging allow for the estimation of brain networks on the basis of intrinsic functional connectivity, but the specific network abnormalities in psychotic disorders are poorly understood. OBJECTIVE:To compare intrinsic functional connectivity across the cerebral cortex in patients with schizophrenia spectrum disorders or psychotic bipolar disorder and healthy controls. DESIGN, SETTING, AND PARTICIPANTS:We studied 100 patients from an academic psychiatric hospital (28 patients with schizophrenia, 32 patients with schizoaffective disorder, and 40 patients with bipolar disorder with psychosis) and 100 healthy controls matched for age, sex, race, handedness, and scan quality from December 2009 to October 2011. MAIN OUTCOMES AND MEASURES:Functional connectivity profiles across 122 regions that covered the entire cerebral cortex. RESULTS:Relative to the healthy controls, individuals with a psychotic illness had disruption across several brain networks, with preferential reductions in functional connectivity within the frontoparietal control network (P <?.05, corrected for family-wise error rate). This functionally defined network includes portions of the dorsolateral prefrontal cortex, posteromedial prefrontal cortex, lateral parietal cortex, and posterior temporal cortex. This effect was seen across diagnoses and persisted after matching patients and controls on the basis of scan quality. CONCLUSIONS AND RELEVANCE:Our study results support the view that cortical information processing is disrupted in psychosis and provides new evidence that disruptions within the frontoparietal control network may be a shared feature across both schizophrenia and affective psychosis.
| S-EPMC4435541 | biostudies-literature
Project description:Childhood maltreatment (CM) is a non-specific risk factor for eating disorders (ED) and is associated with a greater severity in their clinical presentation and poorer treatment outcome. These data suggest that maltreated people with ED may be biologically other than clinically different from non-maltreated people. The aim of the present study was to investigate cortical thickness (CT), a possible biomarker of neurodevelopment, in people with ED with or without history of CM and in healthy women. Twenty-four healthy women, 26 with anorexia nervosa and 24 with bulimia nervosa underwent a 3T MRI scan. All participants filled in the childhood trauma questionnaire. All neuroimaging data were processed by FreeSurfer. Twenty-four participants with ED were identified as maltreated and 26 participants with ED as non-maltreated. All healthy women were non-maltreated. Compared to healthy women, maltreated people with ED showed lower CT in the left rostral anterior cingulate gyrus, while compared to people with ED without history of CM showed lower CT values in the left superior frontal and in right caudal middle frontal and superior parietal gyri. No significant differences emerged in CT measures between healthy women and people with ED without history of CM. The present findings show for the first time that in adult people with ED childhood maltreatment is associated with cortical thinning in areas implicated in the modulation of brain processes that are acknowledged to play a role in the psychopathology of ED.
| S-EPMC10070200 | biostudies-literature
Project description:BackgroundChildhood is considered the most important phase of human development; within it the period from birth to 5 years of age is particularly critical, given the speed at which changes occur. The context where children live can influence early childhood developmnent (ECD) by providing or limiting opportunities to learn, play and establish social interactions. This study explored the associations between characteristics of the urban environment and ECD in 2,194 children aged 36 to 59 months living in urban municipalities in Mexico.MethodsWe obtained ECD information from the 2015 Survey of Boys, Girls, and Women (ENIM, for its Spanish acronym), measured with the Early Childhood Development Index. The urban environment was evaluated at the municipal level, considering variables from five environment domains: physical, social, service, socioeconomic, and governance. Multilevel logistic models were fitted to assess the association between urban environment characteristics and the inadequacy of ECD in general and by specific development domains: learning, socio-emotional, physical, and alpha-numeric.ResultsInadequate ECD was inversely associated with the availability of libraries (OR = 0.55, 95% CI: 0.43, 0.72), and positively associated with population density (OR = 1.01, 95% CI: 1.01-1.02). For the specific ECD domains, inadequate socio-emotional development was inversely associated with the availability of libraries (OR = 0.66, 95% CI: 0.51, 0.85). Inadequate literacy-numeracy knowledge was associated inversely with the availability of daycare centers (OR = 0.56, 95% CI: 0.32, 0.97), and directly associated with the number of hospitals and clinics (OR = 1.87, 95% CI: 1.29, 2.72). Finally, the marginalization index was positively associated with inadequacy in the learning domain (OR = 1.80, 95% CI: 1.06, 3.03).ConclusionsSome aspects of the urban environment associated with ECD, suggest that intervening in the urban context could improve overall child development. Investment in resources oriented to improve socio-emotional development and literacy (such as libraries and daycare), could foster ECD in Mexico.
| S-EPMC8598011 | biostudies-literature
Project description:In vivo structural neuroimaging can reliably identify changes to cortical morphology and its regional variation but cannot yet relate these changes to specific cortical layers. We propose, however, that by synthesizing principles of cortical organization, including relative contributions of different layers to sulcal and gyral thickness, regional patterns of variation in thickness of different layers across the cortical sheet and profiles of layer variation across functional hierarchies, it is possible to develop indirect morphological measures as markers of more specific cytoarchitectural changes. We developed four indirect measures sensitive to changes specifically occurring in supragranular cortical layers, and applied these to test the hypothesis that supragranular layers are disproportionately affected in schizophrenia. Our findings from the four different measures converge to indicate a predominance of supragranular thinning in schizophrenia, independent of medication and illness duration. We propose that these indirect measures offer novel ways of identifying layer-specific cortical changes, offering complementary in vivo observations to existing post-mortem studies.
| S-EPMC4872401 | biostudies-literature
Project description:Previous neuroimaging studies have revealed that both gray matter (GM) and white matter (WM) are altered in several morphological aspects in schizophrenia patients. Although several studies reported associations between GM and WM alterations in restricted regions, the existence of a global association between GM and WM pathologies is unknown. Considering the wide distribution of GM morphological changes and the profound genetic background of WM abnormalities, it would be natural to postulate a global association between pathologies of GM and WM in schizophrenia. In this investigation, we studied 35 schizophrenia patients and 35 healthy control subjects using T1-weighted magnetic resonance imaging and diffusion tensor imaging (DTI) and investigated the association between GM thickness and WM fractional anisotropy (FA) as a proxy of pathology in each tissue. To investigate cortical thickness, surface-based analysis was used. The mean cortical thickness for the whole brain was computed for each hemisphere, and group comparisons were performed. For DTI data, mean FA for the whole brain was calculated, and group comparisons were performed. Subsequently, the correlation between mean cortical thickness and mean FA was investigated. Results showed that the mean cortical thickness was significantly thinner, and the mean FA was significantly lower in schizophrenia patients. Only in the patient group the mean cortical thickness and mean FA showed significant positive correlations in both hemispheres. This correlation remained significant even after controlling for demographic and clinical variables. Thus, our results indicate that the GM and WM pathologies of schizophrenia are intertwined at the global level.
| S-EPMC3932083 | biostudies-other
Project description:Background:Over the course of the last 30 years, autism spectrum disorder (ASD) diagnoses have increased, thus identifying a large group of aging individuals with ASD. Currently, little is known regarding how aging will affect these individual's neuroanatomy, compared to the neurotypical (NT) population. Because of the anatomical overlap of ASD-related cortical pathology and age-related cortical thinning, both following an anterior-to-posterior severity gradient, we hypothesize adults with ASD will show larger age-related cortical thinning than NT adults. Methods:We analyzed cortical measurements using available data from the multi-site Autism Brain Imaging Data Exchange I (ABIDE I; n=282) and our own cohort of middle-age to older adults with and without ASD (n=47) mostly available in ABIDE II (n=35). We compared correlations between cortical measures and age in right-handed adults with ASD (n=157) and similar NT adults (n = 172), controlling for IQ and site. Participants were 18 to 64 years of age (mean=29.8 years; median=26 years). Results:We found significant differences between diagnosis groups in the relationship between age and cortical thickness for areas of left frontal lobe (pars opercularis), temporal lobe (inferior gyrus, middle gyrus, banks of the superior temporal sulcus, and entorhinal cortex), parietal lobe (inferior gyrus), and lateral occipital lobe. For all areas, adults with ASD showed a greater negative correlation between age and cortical thickness than NT adults. Conclusion:As hypothesized, adults with ASD demonstrated exacerbated age-related cortical thinning, compared to NT adults. These differences were the largest and most extensive in the left temporal lobe. Future longitudinal work is warranted to investigate whether differences in brain age trajectories will translate to unique behavioral needs in older adults with ASD.
| S-EPMC7304569 | biostudies-literature
Project description:Importance: Persistent nightmares in childhood have been prospectively associated with psychosis and borderline personality disorder (BPD) in adolescence. However, the extent to which this association is also true for behavioral sleep problems is still unknown, and the potential mechanisms are unexplored.Objective: To examine the prospective associations between several parent-reported sleep problems in early childhood and psychotic and BPD symptoms at 11 to 13 years of age and the potential mediation of the associations by depression at 10 years of age.Design, setting, and participants: This cohort study assessed 13 488 participants in the Avon Longitudinal Study of Parents and Children birth cohort who were followed up for more than 13 years. Pregnant women from Avon, United Kingdom, with expected dates of delivery from April 1, 1991, to December 31, 1992, were invited to take part in the study. Data analysis was conducted from May 1 to December 31, 2019.Main outcomes and measures: Psychotic experiences at 12 to 13 years of age were assessed using the Psychosis-Like Symptom Interview, and BPD symptoms at 11 to 12 years of age were tested using the UK Childhood Interview for DSM-IV Borderline Personality Disorder. Parent-reported nighttime sleep duration, night awakening frequency, bedtime, and regularity of sleep routines were assessed when the child was 6, 18, and 30 months and 3.5, 4.8, and 5.8 years of age.Results: Data were available on 7155 participants (3718 girls [52%]) who reported on BPD symptoms and 6333 (3280 boys [52%]) who reported on BPD symptoms. Higher night awakening frequency at 18 months of age (odds ratio [OR], 1.13; 95% CI, 1.01-1.26) and less regular sleep routines at 6 months (OR, 0.68; 95% CI, 0.50-0.93), 30 months (OR, 0.64; 95% CI, 0.44-0.95), and 5.8 years (OR, 0.32; 95% CI, 0.19-0.53) of age were significantly associated with psychotic experiences in adolescence, whereas shorter nighttime sleep duration (OR, 0.78; 95% CI, 0.66-0.92) and later bedtime at 3.5 years of age (OR, 1.32; 95% CI, 1.09-1.60) were significantly associated with BPD symptoms. Results of mediation analysis were consistent with all these associations, except for later bedtime at 3.5 years and BPD in adolescence, which had no association. Depression at 10 years of age mediated the associations between frequent night awakenings at 18 months of age (bias-corrected estimate, -0.005; 95% CI, -0.008 to -0.002; P?=?.002) and irregular sleep routines at 5.8 years of age (bias-corrected estimate, -0.006; 95% CI, -0.010 to -0.003; P?=?.003) with psychosis.Conclusions and relevance: The findings suggest that some behavioral sleep problems in childhood are distinctively associated with the onset of psychosis and BPD in adolescence, following different pathways. Furthermore, depression at 10 years of age may mediate only the association with psychosis. These findings contribute to the design of more personalized interventions in psychosis and BPD.
| S-EPMC7330826 | biostudies-literature
Project description:The aim of this study is to determine whether structural MRI measures are associated with clinical impairment and progression to a Lewy body disease in patients with idiopathic REM sleep behavior disorder (iRBD). Twenty-seven patients with iRBD in addition to patients with de novo PD and healthy controls were included from the Parkinson's Progression Markers Initiative. Patients with iRBD were followed for up to 3 years. Clinical and MRI measures were compared across groups and the association between clinical features and structural MRI was assessed in iRBD patients. Cox regression analyses were applied to identify risk factors for progressing to a Lewy body disease in iRBD. Our results showed that, at baseline, iRBD patients showed parietal and occipital cortical thinning, compared to controls. They also showed worse motor and non-motor abilities, some of which correlated with motor, frontal or temporal cortical thinning. At follow-up, six (22%) iRBD patients were diagnosed with a Lewy body disorder. These patients showed cortical thinning in frontal, occipital and parietal areas compared to iRBD non-converters. Cortical thinning was a significant predictor for future development of a Lewy body disorder (HR: 0.784; 95% CI: 0.640-0.960; p = 0.02). We conclude that cortical thinning is associated with worse motor and non-motor abilities, and predicts conversion to a Lewy body disorder in iRBD, suggesting it could be used to select candidates for clinical trials to delay the onset of neurodegenerative disease.
| S-EPMC6499806 | biostudies-literature
Project description:BackgroundPosttraumatic stress disorder (PTSD) can be a source of significant social and daily distress in autism spectrum disorder (ASD). Compared to typically developed (TD) individuals, people with ASD are at an increased risk of adverse childhood experiences (ACEs), which can result in abnormal neuronal development. However, whether or how ACEs influence abnormal neural development and PTSD symptoms in ASD has not been fully elucidated.MethodsThirty-nine TD individuals and 41 individuals with ASD underwent T1-weighted magnetic resonance imaging and neurite orientation dispersion and density imaging (NODDI), with axonal and dendritic densities assessed in terms of the orientation dispersion index and neurite density index (NDI), respectively. Voxel-based analyses were performed to explore the brain regions associated with PTSD symptoms, and the relationships between the severity of ACEs and PTSD symptoms and NODDI parameters in the extracted brain regions were examined.ResultsThere was a significant positive association between PTSD symptom severity and NDI in the bilateral supplementary motor area; right superior frontal, left supramarginal, and right superior temporal gyrus; and right precuneus in the ASD group, but not in the TD group. ACE severity was significantly associated with NDI in the right superior frontal and left supramarginal gyrus and right precuneus in the ASD group. Moreover, NDI in the right precuneus mainly predicted the severity of PTSD symptoms in the ASD group, but not the TD group.ConclusionThese results suggest that ACE-associated higher neurite density is of clinical importance in the pathophysiology of PTSD symptoms in ASD.
| S-EPMC10515392 | biostudies-literature