Neurocognition in youth and young adults under age 30 at familial risk for schizophrenia: A quantitative and qualitative review
Neurocognition in youth and young adults under age 30 at familial risk for schizophrenia: A quantitative and qualitative review
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DOI：
10.1080/13546805.2012.676309
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发表时间：
2013-01-01
影响因子：
1.7
通讯作者：
Seidman, Larry J.
中科院分区：
文献类型：
--
作者：
Agnew-Blais, Jessica;Seidman, Larry J.
导论.神经认知功能障碍是精神分裂症的主要特征，在疾病的所有阶段都可以观察到。由于精神分裂症是已知的运行在家庭中，研究神经认知功能的一级，非精神病亲属已被广泛使用的策略，近50年来了解假定的遗传风险。研究非精神病性亲属（家族性高风险，或FHR）允许识别独立于与精神病相关的混淆的认知脆弱性标志物。方法.先前的荟萃分析已经阐明了精神病发病前、前驱期和发病后以及不分年龄的亲属中认知缺陷的水平和模式。然而，没有先前的定量分析专门针对精神分裂症患者的年轻一级亲属的研究，这些人没有通过高峰年龄疾病风险（70个个体测试和250个变量）。结论.一般来说，年轻的胎心率个体表现出与健康对照组相比，具有中度严重程度的赤字。最大的平均效应量（ES），基于至少三项独立研究中给出的测试，是对全量表智商的估计（d= 0.777），其次是词汇（d= 0.749）和单字阅读测试（d= 0.698）（通常用作智商的估计）。陈述性记忆，持续注意力，工作记忆和其他措施有更温和的ESs.Deficits比建立精神分裂症较轻，但往往严重的临床高风险或pupelis前驱参与者和年长的亲属在以前的荟萃分析检查。此外，虽然从更有限的文献评估，青年在FHR精神分裂症往往表现出更差的神经认知功能比那些在FHR情感性精神病。这表明，精神分裂症的遗传风险反映在阳性胎心率对认知能力的影响特别大。
Introduction. Neurocognitive dysfunction is a central feature of schizophrenia and is observed during all phases of the illness. Because schizophrenia is known to run in families, studying neurocognitive function in first-degree, nonpsychotic relatives has been a widely utilised strategy for almost 50 years for understanding presumed genetic risk. Studying nonpsychotic relatives (familial high-risk, or FHR) allows for identification of cognitive vulnerability markers independent of confounds associated with psychosis. Methods. Prior meta-analyses have elucidated the level and pattern of cognitive deficits in the premorbid, prodromal, and postonset periods of psychosis, and in relatives regardless of age. However, no prior quantitative analyses have specifically focused on studies of young first-degree relatives of individuals with schizophrenia who have not passed through the peak age illness risk (70 individual tests and 250 variables. Conclusions. In general, young FHR individuals demonstrated deficits with a moderate level of severity compared with healthy controls. The largest average effect sizes (ESs), based on tests given in at least three independent studies, were on estimates of Full Scale IQ (d= 0.777), followed by Vocabulary (d= 0.749) and single word reading tests (d= 0.698) (often used as estimates of IQ). Measures of declarative memory, sustained attention, working memory and others had more modest ESs. Deficits were milder than in established schizophrenia, but often as severe as in clinical high-risk or putatively prodromal participants and in older relatives examined in prior meta-analyses. Additionally, while assessed from a more limited literature, youth at FHR for schizophrenia tended to show worse neurocognitive functioning than those at FHR for affective psychosis. This suggests that genetic risk for schizophrenia as reflected in a positive FHR carries an especially heavy impact on cognitive ability.