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Neural and neurocognitive markers of vulnerability to gambling disorder: a study of unaffected siblings.

ABSTRACT: Psychological and neurobiological markers in individuals with gambling disorder (GD) could reflect transdiagnostic vulnerability to addiction or neuroadaptive consequences of long-term gambling. Using an endophenotypic approach to identify vulnerability markers, we tested the biological relatives of cases with GD. Male participants seeking treatment for GD (n?=?20) were compared with a male control group (n?=?18). Biological siblings of cases with GD (n?=?17, unrelated to the current GD group) were compared with a separate control group (n?=?19) that overlapped partially with the GD control group. Participants completed a comprehensive assessment of clinical scales, neurocognitive functioning, and fMRI of unexpected financial reward. The GD group displayed elevated levels of self-report impulsivity and delay discounting, and increased risk-taking on the Cambridge Gamble Task. We did not observe impaired motor impulsivity on the stop-signal task. Siblings of GD showed some overlapping effects; namely, elevated impulsivity (negative urgency) and increased risk-taking on the Cambridge Gamble Task. We did not observe any differences in the neural response to win outcomes, either in the GD or sibling analysis compared with their control group. Within the GD group, activity in the thalamus and caudate correlated negatively with gambling severity. Increased impulsivity and risk-taking in GD are present in biological relatives of cases with GD, suggesting these markers may represent pre-existing vulnerability to GD.

SUBMITTER: Limbrick-Oldfield EH

PROVIDER: S-EPMC6901470 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature

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Neural and neurocognitive markers of vulnerability to gambling disorder: a study of unaffected siblings.

Limbrick-Oldfield Eve H EH Mick Inge I Cocks Rachel E RE Flechais Remy S A RSA Turton Samuel S Lingford-Hughes Anne A Bowden-Jones Henrietta H Clark Luke L

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology 20191009 2

Psychological and neurobiological markers in individuals with gambling disorder (GD) could reflect transdiagnostic vulnerability to addiction or neuroadaptive consequences of long-term gambling. Using an endophenotypic approach to identify vulnerability markers, we tested the biological relatives of cases with GD. Male participants seeking treatment for GD (n = 20) were compared with a male control group (n = 18). Biological siblings of cases with GD (n = 17, unrelated to the current GD group) w ...[more]

PMID: 31597159

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Project description:IntroductionResponse inhibition is one of the executive functions impaired in attention-deficit/hyperactivity disorder (ADHD). Increasing evidence indicates that altered functional and structural neural connectivity are part of the neurobiological basis of ADHD. Here, we investigated if adolescents with ADHD show altered functional connectivity during response inhibition compared to their unaffected siblings and healthy controls.MethodsResponse inhibition was assessed using the stop signal paradigm. Functional connectivity was assessed using psycho-physiological interaction analyses applied to BOLD time courses from seed regions within inferior- and superior frontal nodes of the response inhibition network. Resulting networks were compared between adolescents with ADHD (N = 185), their unaffected siblings (N = 111), and controls (N = 125).ResultsControl subjects showed stronger functional connectivity than the other two groups within the response inhibition network, while subjects with ADHD showed relatively stronger connectivity between default mode network (DMN) nodes. Stronger connectivity within the response inhibition network was correlated with lower ADHD severity, while stronger connectivity with the DMN was correlated with increased ADHD severity. Siblings showed connectivity patterns similar to controls during successful inhibition and to ADHD subjects during failed inhibition. Additionally, siblings showed decreased connectivity with the primary motor areas as compared to both participants with ADHD and controls.DiscussionSubjects with ADHD fail to integrate activation within the response inhibition network and to inhibit connectivity with task-irrelevant regions. Unaffected siblings show similar alterations only during failed stop trials, as well as unique suppression of motor areas, suggesting compensatory strategies. These findings support the role of altered functional connectivity in understanding the neurobiology and familial transmission of ADHD.

Project description:Objective: Previous studies suggest that abnormal brain structure and function may be neuroimaging endophenotypes of obsessive-compulsive disorder (OCD). Comparing the intrinsic brain activity of OCD patients and their unaffected siblings will help to further understand the susceptibility to, and pathological mechanisms of, OCD. We used a case-control study design aiming to establish whether the abnormal regional homogeneity (ReHo) found in OCD patients also exists in their unaffected siblings. Method: Fifteen unmedicated OCD patients, 15 of their unaffected siblings, and 30 healthy controls (HCs) received resting-state functional magnetic resonance imaging (r-s fMRI) scanning and clinical evaluation. We used the ReHo method to analyze the inter-regional synchronized activity of all participants. One-way analysis of covariance with post hoc tests was used to compare the ReHo maps across groups. A Pearson correlation analysis was conducted to assess the correlations between clinical characteristics and abnormal ReHo in OCD patients. Results: Relative to HCs, OCD patients and their unaffected siblings showed overlapping higher ReHo values in the right dorsolateral prefrontal cortex (DLPFC). Patients with OCD showed increased ReHo in left middle frontal gyrus (MFG) relative to both their unaffected siblings and HCs. In addition to the right DLPFC and left MFG, OCD patients, compared with HCs, also showed abnormal ReHo in other regions, including higher ReHo in the right superior parietal cortex and lower ReHo in the left inferior parietal cortex, right parahippocampal region, left thalamus, and right inferior temporal cortex. Compared with HCs, the unaffected siblings of patients with OCD had significantly higher ReHo in the right inferior parietal cortex, right MFG, and right supplementary motor area. There was no association between clinical symptoms and abnormal ReHo values in OCD patients. Conclusions: This study found overlapping higher ReHo values in the right DLPFC of OCD patients and their unaffected siblings. Our results suggest that the higher ReHo in the right DLPFC may be a potential neuroimaging endophenotype, which may reflect an increased genetic risk of OCD.

Project description:BACKGROUND:Altered structural network-connectivity has been reported in psychotic disorder but whether these alterations are associated with genetic vulnerability, and/or with phenotypic variation, has been less well examined. This study examined i) whether differences in network-connectivity exist between patients with psychotic disorder, siblings of patients with psychotic disorder and controls, and ii) whether network-connectivity alterations vary with (subclinical) symptomatology. METHODS:Network-connectivity measures (global efficiency (GE), density, local efficiency (LE), clustering coefficient (CC)) were derived from diffusion weighted imaging (DWI) and were compared between 85 patients with psychotic disorder, 93 siblings without psychotic disorder and 80 healthy comparison subjects using multilevel regression models. In patients, associations between Positive and Negative Syndrome Scale (PANSS) symptoms and topological measures were examined. In addition, interactions between subclinical psychopathology and sibling/healthy comparison subject status were examined in models of topological measures. RESULTS:While there was no main effect of group with respect to GE, density, LE and CC, siblings had a significantly higher CC compared to patients (B = 0.0039, p = .002). In patients, none of the PANSS symptom domains were significantly associated with any of the four network-connectivity measures. The two-way interaction between group and SIR-r positive score in the model of LE was significant (χ2 = 6.24, p = .01, df = 1). In the model of CC, the interactions between group and respectively SIS-r positive (χ2 = 5.59, p = .02, df = 1) and negative symptom scores (χ2 = 4.71, p = .03, df = 1) were significant. Stratified analysis showed that, in siblings, decreased LE and CC was significantly associated with increased SIS-r positive scores (LE: B = -0.0049, p = .003, CC: B = -0.0066, p = .01) and that decreased CC was significantly associated with increased SIS-r negative scores (B = -0.012, p = .003). There were no significant interactions between group and SIS-r scores in the models of GE and density. CONCLUSION:The findings indicate absence of structural network-connectivity alterations in individuals with psychotic disorder and in individuals at higher than average genetic risk for psychotic disorder, in comparison with healthy subjects. The differential subclinical symptom-network connectivity associations in siblings with respect to controls may be a sign of psychosis vulnerability in the siblings.

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Neural and neurocognitive markers of vulnerability to gambling disorder: a study of unaffected siblings.

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Neural and neurocognitive markers of vulnerability to gambling disorder: a study of unaffected siblings.

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