Social cognition in 22q11.2 deletion syndrome and idiopathic developmental neuropsychiatric disorders.
Social cognition in 22q11.2 deletion syndrome and idiopathic developmental neuropsychiatric disorders.
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DOI：
10.1186/s11689-021-09363-4
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发表时间：
2021-04-17
影响因子：
4.9
通讯作者：
Bearden CE
中科院分区：
文献类型：
--
作者：
Jalal R;Nair A;Lin A;Eckfeld A;Kushan L;Zinberg J;Karlsgodt KH;Cannon TD;Bearden CE
22q11.2缺失综合征(22q11DS)是一种常见的反复发作的神经遗传学疾病，与发育性神经精神障碍和智能障碍的风险增加有关。患有22q11DS的儿童和成人通常表现出明显的社会功能障碍和神经认知障碍，自闭症谱系障碍(ASD)和精神病的发病率都较高。然而，在22q11DS中，社会认知的基本过程与认知能力之间的关系还没有得到很好的研究。在这里，我们研究了22q11DS患者与多组特发性神经精神障碍患者的社会认知差异，并典型地发展为健康对照(HC)。此外，我们还考察了智力功能的差异及其与社会认知能力的关系。最后，我们考察了社会认知能力与现实社会行为之间的关系。我们检测了273名参与者的社会认知和智力功能(平均年龄=17.74±5.18%女性=44.3%)：50名患有22q11DS，49名青年首发精神病(FEP)，48名临床高危精神病(CHR)，24名ASD参与者，102名HC。社会认知使用社会推理意识测验(TASIT)进行评估，而互惠的社会行为则通过社会反应量表(SRS)上的父母/照顾者评分进行评估。参与者还接受了韦克斯勒简明智力量表第二版(WASI-II)的测试，以评估智力功能。在控制智力功能后，22q11DS组的社会认知能力显著低于CHR、FEP和HC组，但与ASD组相比没有差异。在TASIT和智商之间的社会认知之间发现了显著的正相关。相反，对于任何群体，TASIT和现实世界社会行为(SRS)之间没有发现显著的关系。我们的发现表明，即使在对全球智力功能进行调整后，22q11DS患者的社会认知缺陷在整个年龄范围内也比特发性神经精神疾病更加突出。这些结果有助于我们理解22q11DS与特发性神经精神障碍相比在智力和社会方面的脆弱性。我们发现智力和社会认知之间存在很强的相关性，这一发现强调了在社会技能干预中考虑神经认知缺陷并为22q11DS和其他智力障碍人群量身定做这些现有治疗模式的重要性。网上版载有补充材料，可在10.1186/s11689-021-09363-4查阅。
22q11.2 deletion syndrome (22q11DS) is a common recurrent neurogenetic condition associated with elevated risk for developmental neuropsychiatric disorders and intellectual disability. Children and adults with 22q11DS often exhibit marked social impairment as well as neurocognitive deficits, and have elevated rates of both autism spectrum disorder (ASD) and psychosis. However, the relationship between the basic processes of social cognition and cognitive ability has not been well studied in 22q11DS. Here, we examined differences in social cognition in 22q11DS, relative to multiple groups of idiopathic neuropsychiatric disorders, and typically developing healthy controls (HC). Additionally, we examined differences in intellectual functioning and its relationship to social cognitive abilities. Finally, we examined the relationship between social cognitive abilities and real-world social behavior. We examined social cognition and intellectual functioning in 273 participants (mean age = 17.74 ± 5.18% female = 44.3%): 50 with 22q11DS, 49 youth with first episode psychosis (FEP), 48 at clinical high-risk (CHR) for psychosis, 24 participants with ASD, and 102 HC. Social cognition was assessed using The Awareness of Social Inference Test (TASIT), while reciprocal social behavior was assessed via parent/caregiver ratings on the Social Responsiveness Scale (SRS). Participants were also administered the Wechsler Abbreviated Scale of Intelligence, 2nd edition (WASI-II) to assess intellectual functioning. The 22q11DS group exhibited significantly lower social cognitive abilities compared to CHR, FEP, and HC groups after controlling for intellectual functioning, but not in comparison to the ASD group. Significant positive correlations were found between social cognition, as measured by the TASIT and IQ across groups. In contrast, no significant relationships were found between TASIT and real-world social behavior (SRS) for any group. Our findings indicate social cognitive deficits are more prominent in 22q11DS than idiopathic neuropsychiatric conditions across the age range, even after adjusting for global intellectual function. These results contribute to our understanding of the intellectual and social vulnerabilities of 22q11DS in comparison to idiopathic neuropsychiatric disorders. Our findings of robust associations between intellectual ability and social cognition emphasizes the importance of accounting for neurocognitive deficits in social skills interventions and tailoring these existing treatment models for 22q11DS and other populations with intellectual impairment. The online version contains supplementary material available at 10.1186/s11689-021-09363-4.
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影响因子：
4.5
作者：
Addington J;Cadenhead KS;Cornblatt BA;Mathalon DH;McGlashan TH;Perkins DO;Seidman LJ;Tsuang MT;Walker EF;Woods SW;Addington JA;Cannon TD
通讯作者：
Cannon TD
影响因子：
10.6
作者：
Constantino, JN;Todd, RD
通讯作者：
Todd, RD
影响因子：
2
作者：
Bassett, AS;Chow, EWC;Gatzoulis, MA
通讯作者：
Gatzoulis, MA
影响因子：
3.6
作者：
de Wilde, Amber;Koot, Hans M.;van Lier, Pol A. C.
通讯作者：
van Lier, Pol A. C.
影响因子：
1.7
作者：
Dehn, Milton J.
通讯作者：
Dehn, Milton J.