Neural anomalies during vigilance in schizophrenia: Diagnostic specificity and genetic associations.
Neural anomalies during vigilance in schizophrenia: Diagnostic specificity and genetic associations.
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DOI：
10.1016/j.nicl.2020.102414
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Sponheim SR
中科院分区：
文献类型：
--
作者：
Klein SD;Shekels LL;McGuire KA;Sponheim SR
比较精神分裂症先证者、双相先证者和亲属的视觉ERP。精神分裂症患者的N1增强预测更大的感知灵敏度。精神分裂症特异性N2缺陷可能反映了受损的视觉物体识别。精神分裂症的先证者和亲属显示减少P3 COMT基因型不同。双相先证者和亲属的性别依赖性异常较轻。警觉性受损是精神分裂症的核心认知缺陷，并可作为内表型（即，遗传责任）。我们在精神分裂症患者（N = 48）、双相情感障碍患者（N = 26）、精神分裂症患者的一级生物学亲属（N = 55）和双相情感障碍患者（N = 28）中使用了具有感知退化刺激的连续执行任务，以及健康对照组（N = 68）为了澄清先前报道的警觉缺陷和异常神经功能是否指示精神分裂症的遗传易感性，而不是严重精神分裂症的一般易感性，精神病理学我们还研究了儿茶酚-O-甲基转移酶基因的变异，以评估大脑反应是否与高阶认知相关的遗传变异有关。精神分裂症患者的亲属有一个增加率的误认非目标刺激的目标时，他们的感知相似，提示轮廓知觉的困难。更大的早期视觉反应（即，N1）与精神分裂症患者更好的任务表现相关，这与反映有益神经补偿的N1反应增强一致。此外，减少N2增强目标刺激是特定于精神分裂症。精神分裂症患者和一级亲属都表现出晚期认知反应（P3 b）降低，这预示着更差的表现。双相情感障碍患者的一级亲属表现出表现缺陷，并显示异常的神经反应，比精神分裂症的易感性和依赖于性别的个人温和。儿茶酚-O-甲基转移酶基因的变异与精神分裂症和双相情感障碍患者的P3 b有差异。精神分裂症的警觉性差是由未能增强早期视觉反应，对目标的中潜伏期脑反应的弱增强，以及可能与前额多巴胺能可用性相关的遗传变异相关的晚期认知反应的有限参与所特别预测的。实验结果说明了区分精神分裂症和双相情感障碍的特定神经功能，并提供了一个假定的内表型的证据，更广泛地区分精神分裂症和严重精神疾病的遗传易感性。
Compared visual ERPs in schizophrenia probands, bipolar probands, and relatives. Enhanced N1 in patients with schizophrenia predicted greater perceptual sensitivity. A schizophrenia specific N2 deficit may reflect impaired visual object recognition. Schizophrenia probands and relatives displayed reduced P3 varying by COMT genotype. Bipolar probands and relatives had milder abnormalities dependent on sex. Impaired vigilance is a core cognitive deficit in schizophrenia and may serve as an endophenotype (i.e., mark genetic liability). We used a continuous performance task with perceptually degraded stimuli in schizophrenia patients (N = 48), bipolar disorder patients (N = 26), first-degree biological relatives of schizophrenia patients (N = 55) and bipolar disorder patients (N = 28), as well as healthy controls (N = 68) to clarify whether previously reported vigilance deficits and abnormal neural functions were indicative of genetic liability for schizophrenia as opposed to a generalized liability for severe psychopathology. We also examined variation in the Catechol-O-methyltransferase gene to evaluate whether brain responses were related to genetic variation associated with higher-order cognition. Relatives of schizophrenia patients had an increased rate of misidentification of nontarget stimuli as targets when they were perceptually similar, suggestive of difficulties with contour perception. Larger early visual responses (i.e., N1) were associated with better task performance in patients with schizophrenia consistent with enhanced N1 responses reflecting beneficial neural compensation. Additionally, reduced N2 augmentation to target stimuli was specific to schizophrenia. Both patients with schizophrenia and first-degree relatives displayed reduced late cognitive responses (P3b) that predicted worse performance. First-degree relatives of bipolar patients exhibited performance deficits, and displayed aberrant neural responses that were milder than individuals with liability for schizophrenia and dependent on sex. Variation in the Catechol-O-methyltransferase gene was differentially associated with P3b in schizophrenia and bipolar groups. Poor vigilance in schizophrenia is specifically predicted by a failure to enhance early visual responses, weak augmentation of mid-latency brain responses to targets, and limited engagement of late cognitive responses that may be tied to genetic variation associated with prefrontal dopaminergic availability. Experimental results illustrate specific neural functions that distinguish schizophrenia from bipolar disorder and provides evidence for a putative endophenotype that differentiates genetic liability for schizophrenia from severe mental illness more broadly.
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儿茶酚-O-甲基转移酶（COMT）基因多态性和年轻女性乳腺癌风险。
影响因子：
8.8
作者：
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