scholarly journals Does thinner right entorhinal cortex underlie genetic liability to cannabis use?

2018 ◽  
Vol 48 (16) ◽  
pp. 2766-2775 ◽  
Author(s):  
Subhadip Paul ◽  
Sagnik Bhattacharyya
Keyword(s):  
Surface Area ◽  
Entorhinal Cortex ◽  
Cortical Thickness ◽  
Causal Effect ◽  
Cannabis Use ◽  
Genetic Liability ◽  
Polygenic Model ◽  
Sibling Pairs ◽  
The Right ◽  
Prospective Longitudinal

AbstractBackgroundAlthough alterations in medial temporal lobe structures have been previously associated with use of cannabis, one of the most widely used illicit drugs, whether such alterations are a cause or effect of cannabis use has been unclear.MethodsIn this cross-sectional observational study involving 404 twins/siblings, we have compared cortical thickness and surface area between groups of gender-matched sibling-pairs (concordant cannabis unexposed, concordant exposed and discordant for cannabis exposure) using permutation tests after controlling for potential confounds. Bi-variate polygenic model was used to assess the genetic and environmental contributions underlying cortical morphological phenotypes and frequency of cannabis use.ResultsCortical thickness of the right entorhinal cortex was significantly lower in the concordant exposed siblings compared to both discordant unexposed and discordant exposed groups [false discovery rate (FDR)-corrected, q < 0.05]. The association between the right entorhinal cortex thickness and frequency of cannabis use is due to the contribution of significant shared additive genetic (ρg = −0.19 ± 0.08; p = 0.02) factors but not unique environment (ρe = 0.05 ± 0.09; p = 0.53). Significantly lower surface area of the right entorhinal cortex in discordant exposed group compared with the discordant unexposed group furnishes preliminary evidence in support of causal effect of cannabis use (FDR-corrected, q < 0.05). However, bi-variate polygenic model-based analysis did not show any significant effect.ConclusionsShared genetic liability may underlie the association between cannabis exposure and thinner right entorhinal cortex. Prospective longitudinal studies are necessary to definitively disentangle the cause–effect relationships of cannabis use.

scholarly journals Inflammatory agents partially explain changes in cortical thickness and surface area related to body mass index in adolescence

2019 ◽  
Author(s):  
X. Prats-Soteras ◽  
M.A. Jurado ◽  
J. Ottino-González ◽  
I. García-García ◽  
B. Segura ◽  
...  
Keyword(s):  
Body Mass Index ◽  
Surface Area ◽  
Body Mass ◽  
Cortical Thickness ◽  
Serum Levels ◽  
Fusiform Gyrus ◽  
Precentral Gyrus ◽  
Superior Frontal Gyrus ◽  
Tnf Α ◽  
The Right

ABSTRACTBackground/ObjectivesExcessive body mass index (BMI) has been linked to a low-grade chronic inflammation state. Unhealthy BMI has also been related to neuroanatomical changes in adults. However, research in adolescents is relatively limited and has produced conflicting results. This study aims to address the relationship between BMI and adolescents’ brain structure as well as to test the role that inflammatory adipose-related agents might have over this putative link.MethodsWe studied structural MRI and serum levels of interleukin-6, tumor necrosis factor alpha (TNF-α), C-reactive protein and fibrinogen in 65 adolescents (aged 12-21 years). Relationships between BMI, cortical thickness and surface area were tested with a vertex-wise analysis. Subsequently, we used backward multiple linear regression models to explore the influence of inflammatory parameters in each brain-altered area.ResultsWe found a negative association between cortical thickness and BMI in the left lateral occipital cortex (LOC), the left fusiform gyrus and the right precentral gyrus as well as a positive relationship between surface area and BMI in the left rostral middle frontal gyrus and the right superior frontal gyrus. In addition, we found that higher fibrinogen serum concentrations were related to thinning within the left LOC (β = −0.45, p < 0.001) and the left fusiform gyrus (β = - 0.33, p = 0.035), while higher serum levels of TNF-α were associated to a greater surface area in the right superior frontal gyrus (β = 0.32, p = 0.045).ConclusionsThese results suggest that adolescents’ body mass increases are related with brain abnormalities in areas that could play a relevant role in some aspects of feeding behavior. Likewise, we have evidenced that these cortical changes were partially driven by inflammatory agents such as fibrinogen and TNF-α.

scholarly journals Distinctive Frontal and Occipitotemporal Surface Features in Neglectful Parenting

2021 ◽  
Vol 11 (3) ◽  
pp. 387
Author(s):  
Inmaculada León ◽  
María José Rodrigo ◽  
Ileana Quiñones ◽  
Juan Andrés Hernández-Cabrera ◽  
Lorna García-Pentón
Keyword(s):  
Surface Area ◽  
Cortical Thickness ◽  
Emotional Awareness ◽  
Emotional Availability ◽  
Middle Frontal Gyrus ◽  
Control Group ◽  
Direct Effects ◽  
The Right ◽  
The Brain

Although the brain signatures of adaptive human parenting are well documented, the cortical features associated with maladaptive caregiving are underexplored. We investigated whether cortical thickness and surface area vary in a small group of mothers who had neglected their children (24 in the neglect group, NG) compared to a control group of mothers with non-neglectful caregiving (21 in the control group, CG). We also tested whether the cortical differences were related to dyadic mother-child emotional availability (EA) in a play task with their children and whether alexithymia involving low emotional awareness that characterizes the NG could play a role in the cortical-EA associations. Whole-brain analysis of the cortical mantle identified reduced cortical thickness in the right rostral middle frontal gyrus and an increased surface area in the right lingual and lateral occipital cortices for the NG with respect to the CG. Follow-up path analysis showed direct effects of the right rostral middle frontal gyrus (RMFG) on the emotional availability (EA) and on the difficulty to identify feelings (alexithymia factor), with a marginal indirect RMFG-EA effect through this factor. These preliminary findings extend existing work by implicating differences in cortical features associated with neglectful parenting and relevant to mother-child interactive bonding.

scholarly journals T183. LOW LEVELS OF VITAMIN D ARE ASSOCIATED WITH REDUCED CORTICAL THICKNESS AND SURFACE AREA IN FRONTAL, TEMPORAL AND OCCIPITAL REGIONS IN FIRST-EPISODE PSYCHOSIS PATIENTS

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S301-S302
Author(s):  
Simone Ciufolini ◽  
John Lally ◽  
Brendon Stubbs ◽  
Shubulade Smith ◽  
Marta Di Forti ◽  
...  
Keyword(s):  
Vitamin D ◽  
Surface Area ◽  
Cortical Thickness ◽  
Brain Structure ◽  
First Episode Psychosis ◽  
First Episode ◽  
Vitamin D Levels ◽  
Episode Psychosis ◽  
Low Levels ◽  
The Right

Abstract Background Vitamin D is a neuro-steroid hormone important in brain development, maturation and function as it modulates the production of numerous brain growth factors. Indeed insufficient levels seem to compromise brain development and confer an increased risk of developing schizophrenia later on in life. Finally patients with first-episode psychosis tend to have lower levels of vitamin D than healthy controls. We aimed to explore: 1) The association between vitamin levels and brain structure (i.e. cortical thickness and surface area) in FEP individuals; 2) Differences in brain structure (i.e. cortical thickness and surface area) between FEP individuals with optimal and sub-optimal levels of Vitamin D. Methods Sample: 49 patients with first episode of psychosis (mean age: 27.8 SD ± 9.1 years) part of the BRC Psychosis Theme study on Genetics and Psychosis (GAP). Vitamin D: Vitamin D (serum 25-hydroxyvitamin D) levels were determined by immunoassay. Patients were considered to have sub-optimal levels if vitamin D concentration was below 20 ng/ml, with higher concentrations deemed optimal. Twenty patients had sub-optimal levels of Vitamin D whereas 29 had optimal Vitamin D concentration. Brain Structure: 3T MRI scan were used to evaluate the cortical thickness and the surface area in 49 FEP patients. FreeSurfer 5.3.0 was used to correlate Vitamin D levels with both cortical thickness and surface area in a vertex-by-vertex analysis. afterwards differences in cortical thickness and surface area between FEP participants with both optimal and sub-optimal Vitamin D levels were examined using a vertex-by-vertex General Linear Model analysis in FreeSurfer 5.3.0. Results were corrected for multiples comparison with Montecarlo simulation. Results Vitamin D levels positively correlated with cortical thickness in the left superior-frontal gyrus and surface area in the right peri-calcarine and right inferior-parietal gyrus (all p&lt;0.05 FWE corrected). FEP patients with sub-optimal levels of Vitamin D (below 20 ng/ml) had reduced cortical thickness in the right medial-orbitofrontal gyrus and lingual gyrus compared to those with optimal levels of Vitamin D (all p&lt;0.05 FWE corrected). Additionally, FEP patients with sub-optimal levels of Vitamin D had smaller surface areas in the cuneus, latero-orbitofrontal gyrus, pre- and post central gyri, superio-frontal gyrus, and inferio parietal gyrus in the right hemisphere than those with optimal levels (all p&lt;0.05 FWE corrected). Discussion Vitamin D levels are associated with reduced cortical thickness and smaller surface area in frontal, temporal, parietal and occipital brain regions in individuals with FEP. Interestingly, these areas complete their maturation well into late adolescence, thus potentially being exposed to low Vitamin D levels over a long period of time may contribute to specific brain structure in adulthood. The identification of a specific brain conformation associated to low levels of Vitamin D would promote greater understanding of the interface between physical and mental illness fostering the development of precision psychiatry.

scholarly journals Comparison of Surface Area and Cortical Thickness Asymmetry in the Human and Chimpanzee Brain

2020 ◽  
Author(s):  
Li Xiang ◽  
Timothy J Crow ◽  
William D Hopkins ◽  
Neil Roberts
Keyword(s):  
Human Brain ◽  
Surface Area ◽  
Cortical Thickness ◽  
Cognitive Abilities ◽  
Occipital Lobe ◽  
Superior Temporal Gyrus ◽  
Occipital Cortex ◽  
Neural Substrates ◽  
Precentral Gyrus ◽  
The Right

Abstract Comparative study of the structural asymmetry of the human and chimpanzee brain may shed light on the evolution of language and other cognitive abilities in humans. Here we report the results of vertex-wise and ROI-based analyses that compared surface area (SA) and cortical thickness (CT) asymmetries in 3D MR images obtained for 91 humans and 77 chimpanzees. The human brain is substantially more asymmetric than the chimpanzee brain. In particular, the human brain has 1) larger total SA in the right compared with the left cerebral hemisphere, 2) a global torque-like asymmetry pattern of widespread thicker cortex in the left compared with the right frontal and the right compared with the left temporo-parieto-occipital lobe, and 3) local asymmetries, most notably in medial occipital cortex and superior temporal gyrus, where rightward asymmetry is observed for both SA and CT. There is also 4) a prominent asymmetry specific to the chimpanzee brain, namely, rightward CT asymmetry of precentral cortex. These findings provide evidence of there being substantial differences in asymmetry between the human and chimpanzee brain. The unique asymmetries of the human brain are potential neural substrates for cognitive specializations, and the presence of significant CT asymmetry of precentral gyrus in the chimpanzee brain should be further investigated.

scholarly journals Sulcal thickness as a vulnerability indicator for schizophrenia

2007 ◽  
Vol 191 (3) ◽  
pp. 229-233 ◽  
Author(s):  
Vina M. Goghari ◽  
Kelly Rehm ◽  
Cameron S. Carter ◽  
Angus W. Macdonald
Keyword(s):  
Surface Area ◽  
Cortical Thickness ◽  
Hemispheric Asymmetry ◽  
Genetic Liability ◽  
Cortical Thinning ◽  
Vulnerability Indicator ◽  
Area And Volume

BackgroundPeople with schizophrenia may demonstrate cortical abnormalities, with gyri and sulci potentially being differentially affected.AimsTo measure frontal and temporal sulcal cortical thickness, surface area and volume in the non-psychotic relatives of patients with schizophrenia as a potential vulnerability indicator for the disorder.MethodAn automated parcellation method was used to measure the superior frontal, inferior frontal, cingulate, superior temporal and inferior temporal sulci in the relatives of patients (n=19) and controls (n=22).ResultsCompared with controls, relatives had reversed hemispheric asymmetry in their cingulate sulcal thickness and a bilateral reduction in their superior temporal sulcal thickness.ConclusionsCingulate and superior temporal sulcal thickness abnormalities may reflect neural abnormalities associated with the genetic liability to schizophrenia. Cortical thinning in these regions suggests that liability genes affect the dendrites, synapses or myelination process during the neurodevelopment of the cortical mantle.

Cortical thickness, cortical surface area and subcortical volumes in schizophrenia and bipolar disorder patients with cannabis use

2018 ◽  
Vol 28 (1) ◽  
pp. 37-47 ◽  
Author(s):  
Cecilie Bhandari Hartberg ◽  
Elisabeth H. Lange ◽  
Trine Vik Lagerberg ◽  
Unn K. Haukvik ◽  
Ole A. Andreassen ◽  
...  
Keyword(s):  
Bipolar Disorder ◽  
Surface Area ◽  
Cortical Thickness ◽  
Cannabis Use ◽  
Cortical Surface ◽  
Cortical Surface Area ◽  
Subcortical Volumes

scholarly journals Understanding the nature of association between anxiety phenotypes and anorexia nervosa: a triangulation approach

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
E. Caitlin Lloyd ◽  
Hannah M. Sallis ◽  
Bas Verplanken ◽  
Anne M. Haase ◽  
Marcus R. Munafò
Keyword(s):  
Anorexia Nervosa ◽  
Longitudinal Study ◽  
Anxiety Disorder ◽  
Anxiety Disorders ◽  
Causal Effect ◽  
Causal Effects ◽  
Observational Research ◽  
Genome Wide Association Studies ◽  
Genetic Liability ◽  
Depressed Affect

Abstract Background Evidence from observational studies suggests an association between anxiety disorders and anorexia nervosa (AN), but causal inference is complicated by the potential for confounding in these studies. We triangulate evidence across a longitudinal study and a Mendelian randomization (MR) study, to evaluate whether there is support for anxiety disorder phenotypes exerting a causal effect on AN risk. Methods Study One assessed longitudinal associations of childhood worry and anxiety disorders with lifetime AN in the Avon Longitudinal Study of Parents and Children cohort. Study Two used two-sample MR to evaluate: causal effects of worry, and genetic liability to anxiety disorders, on AN risk; causal effects of genetic liability to AN on anxiety outcomes; and the causal influence of worry on anxiety disorder development. The independence of effects of worry, relative to depressed affect, on AN and anxiety disorder outcomes, was explored using multivariable MR. Analyses were completed using summary statistics from recent genome-wide association studies. Results Study One did not support an association between worry and subsequent AN, but there was strong evidence for anxiety disorders predicting increased risk of AN. Study Two outcomes supported worry causally increasing AN risk, but did not support a causal effect of anxiety disorders on AN development, or of AN on anxiety disorders/worry. Findings also indicated that worry causally influences anxiety disorder development. Multivariable analysis estimates suggested the influence of worry on both AN and anxiety disorders was independent of depressed affect. Conclusions Overall our results provide mixed evidence regarding the causal role of anxiety exposures in AN aetiology. The inconsistency between outcomes of Studies One and Two may be explained by limitations surrounding worry assessment in Study One, confounding of the anxiety disorder and AN association in observational research, and low power in MR analyses probing causal effects of genetic liability to anxiety disorders. The evidence for worry acting as a causal risk factor for anxiety disorders and AN supports targeting worry for prevention of both outcomes. Further research should clarify how a tendency to worry translates into AN risk, and whether anxiety disorder pathology exerts any causal effect on AN.

scholarly journals Genetic Liability to Cannabis Use Disorder and COVID-19 Hospitalization

2021 ◽  
Author(s):  
Alexander S. Hatoum ◽  
Claire L. Morrison ◽  
Sarah M.C. Colbert ◽  
Evan A. Winiger ◽  
Emma C. Johnson ◽  
...  
Keyword(s):  
Cannabis Use ◽  
Cannabis Use Disorder ◽  
Genetic Liability
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