Gray matter matters: The structure of the socially-anxious brain

Bas-Hoogendam, Janna Marie

doi:10.1016/j.ebiom.2020.102937

Cited by 4 publications

(3 citation statements)

References 11 publications

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“…Third, GMV is a complicated parameter that is different from other surface-based indices, such as cortical thickness, surface area, and cortical folding (gyrification index) [115]. Another reasonable interpretation for the discrepancies is that no changed GMV may be the result of cortical thinning with concurrent surface expansion or vice versa [115], as our recent study demonstrated dissociations in cortical thickness and surface area (i.e., decreased cortical thickness and increased cortical surface area) in SAD patients [22,116]. Fourth, differences in parameter settings on preprocessing and statistical analysis may also contribute to the heterogeneity.…”

Section: Comparison Between Our Results and Previous Findings And Pot...mentioning

confidence: 95%

“…Neuroscience plays a crucial role in a translational approach to inform the improvement and development of diagnostic and therapeutic strategies. In the future, along with the identification and confirmation of the close (even causal) relation between the GM structural/functional alterations and occurrence/progression of SAD, those identified regions could serve neural biomarkers for early diagnosis of SAD, as well as reliable and noninvasive tools for disorder prognosis and treatment efficacy assessment [31,116,119]. Furthermore, regions with GM abnormalities are potential therapeutic targets.…”

Section: Comparison Between Our Results and Previous Findings And Pot...mentioning

confidence: 96%

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Structural and functional deficits and couplings in the cortico-striato-thalamo-cerebellar circuitry in social anxiety disorder

et al. 2022

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Although functional and structural abnormalities in brain regions involved in the neurobiology of fear and anxiety have been observed in patients with social anxiety disorder (SAD), the findings have been heterogeneous due to small sample sizes, demographic confounders, and methodological differences. Besides, multimodal neuroimaging studies on structural-functional deficits and couplings are rather scarce. Herein, we aimed to explore functional network anomalies in brain regions with structural deficits and the effects of structure-function couplings on the SAD diagnosis. High-resolution structural magnetic resonance imaging (MRI) and resting-state functional MRI images were obtained from 49 non-comorbid patients with SAD and 53 demography-matched healthy controls. Whole-brain voxel-based morphometry analysis was conducted to investigate structural alterations, which were subsequently used as seeds for the resting-state functional connectivity analysis. In addition, correlation and mediation analyses were performed to probe the potential roles of structural-functional deficits in SAD diagnosis. SAD patients had significant gray matter volume reductions in the bilateral putamen, right thalamus, and left parahippocampus. Besides, patients with SAD demonstrated widespread resting-state dysconnectivity in cortico-striato-thalamo-cerebellar circuitry. Moreover, dysconnectivity of the putamen with the cerebellum and the right thalamus with the middle temporal gyrus/supplementary motor area partially mediated the effects of putamen/thalamus atrophy on the SAD diagnosis. Our findings provide preliminary evidence for the involvement of structural and functional deficits in cortico-striato-thalamo-cerebellar circuitry in SAD, and may contribute to clarifying the underlying mechanisms of structure-function couplings for SAD. Therefore, they could offer insights into the neurobiological substrates of SAD.

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Section: Comparison Between Our Results and Previous Findings And Pot...mentioning

confidence: 95%

Section: Comparison Between Our Results and Previous Findings And Pot...mentioning

confidence: 96%

Structural and functional deficits and couplings in the cortico-striato-thalamo-cerebellar circuitry in social anxiety disorder

et al. 2022

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“…described increased cortical thickness in the superior parietal cortex in SAD [121] , a finding confirmed by Zhao and colleagues [122] , although we and others could not replicate this finding in multiple samples of SAD patients [ 32 , 123 , 124 ]; cf. [125] . At the functional level, Kreifelts et al.…”

Section: Discussionmentioning

confidence: 99%

Intrinsic functional connectivity in families genetically enriched for social anxiety disorder – an endophenotype study

et al. 2021

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Background Social anxiety disorder (SAD) is a serious psychiatric condition with a high prevalence, and a typical onset during childhood/adolescence. The condition runs in families, but it is largely unknown which neurobiological characteristics transfer this genetic vulnerability (‘endophenotypes’). Using data from the Leiden Family Lab study on SAD, including two generations of families genetically enriched for SAD, we investigated whether social anxiety (SA) co-segregated with changes in intrinsic functional connectivity (iFC), and examined heritability. Methods Functional MRI data were acquired during resting-state in 109 individuals (56 males; mean age: 31·5, range 9·2-61·5 years). FSL's tool MELODIC was used to perform independent component analysis. Six networks of interest (default mode, dorsal attention, executive control, frontoparietal, limbic and salience) were identified at the group-level and used to generate subject-specific spatial maps. Voxel-wise regression models, with SA-level as predictor and voxel-wise iFC as candidate endophenotypes, were performed to investigate the association with SA, within masks of the networks of interest. Subsequently, heritability was estimated. Findings SA co-segregated with iFC within the dorsal attention network (positive association in left middle frontal gyrus and right postcentral gyrus) and frontoparietal network (positive association within left middle temporal gyrus) (cluster-forming-threshold z >2·3, cluster-corrected extent-threshold p <0·05). Furthermore, iFC of multiple voxels within these clusters was at least moderately heritable. Interpretation These findings provide initial evidence for increased iFC as candidate endophenotype of SAD, particularly within networks involved in attention. These changes might underlie attentional biases commonly present in SAD. Funding Leiden University Research Profile ‘Health, Prevention and the Human Lifecycle’.

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Genetic Vulnerability to Social Anxiety Disorder

Bas-Hoogendam

2024

Current Topics in Behavioral Neurosciences

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Gray matter matters: The structure of the socially-anxious brain

Cited by 4 publications

References 11 publications

Structural and functional deficits and couplings in the cortico-striato-thalamo-cerebellar circuitry in social anxiety disorder

Structural and functional deficits and couplings in the cortico-striato-thalamo-cerebellar circuitry in social anxiety disorder

Intrinsic functional connectivity in families genetically enriched for social anxiety disorder – an endophenotype study

Genetic Vulnerability to Social Anxiety Disorder

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