Independent inheritance of cognition and bipolar disorder in a family sample

IF 1.6 3区 医学 Q3 GENETICS & HEREDITY
Alexander D'Amico, Heejong Sung, Alejandro Arbona-Lampaya, Ally Freifeld, Katie Hosey, Joshua Garcia, Ley Lacbawan, Emily Besançon, Layla Kassem, Nirmala Akula, Emma E. M. Knowles, Dwight Dickinson, Francis J. McMahon
{"title":"Independent inheritance of cognition and bipolar disorder in a family sample","authors":"Alexander D'Amico,&nbsp;Heejong Sung,&nbsp;Alejandro Arbona-Lampaya,&nbsp;Ally Freifeld,&nbsp;Katie Hosey,&nbsp;Joshua Garcia,&nbsp;Ley Lacbawan,&nbsp;Emily Besançon,&nbsp;Layla Kassem,&nbsp;Nirmala Akula,&nbsp;Emma E. M. Knowles,&nbsp;Dwight Dickinson,&nbsp;Francis J. McMahon","doi":"10.1002/ajmg.b.33001","DOIUrl":null,"url":null,"abstract":"<p>Cognitive deficits in people with bipolar disorder (BD) may be the result of the illness or its treatment, but they could also reflect genetic risk factors shared between BD and cognition. We investigated this question using empirical genetic relationships within a sample of patients with BD and their unaffected relatives. Participants with bipolar I, II, or schizoaffective disorder (“narrow” BD, <i>n</i> = 69), related mood disorders (“broad” BD, <i>n</i> = 135), and their clinically unaffected relatives (<i>n</i> = 227) completed five cognitive tests. General cognitive function (<i>g</i>) was quantified via principal components analysis (PCA). Heritability and genetic correlations were estimated with SOLAR-Eclipse. Participants with “narrow” or “broad” diagnoses showed deficits in <i>g</i>, although affect recognition was unimpaired. Cognitive performance was significantly heritable (<i>h</i><sup>2</sup> = 0.322 for g, <i>p</i> &lt; 0.005). Coheritability between psychopathology and <i>g</i> was small (0.0184 for narrow and 0.0327 for broad) and healthy relatives of those with BD were cognitively unimpaired. In this family sample, cognitive deficits were present in participants with BD but were not explained by substantial overlaps in genetic determinants of mood and cognition. These findings support the view that cognitive deficits in BD are largely the result of the illness or its treatment.</p>","PeriodicalId":7673,"journal":{"name":"American Journal of Medical Genetics Part B: Neuropsychiatric Genetics","volume":"198 1","pages":""},"PeriodicalIF":1.6000,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ajmg.b.33001","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"American Journal of Medical Genetics Part B: Neuropsychiatric Genetics","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/ajmg.b.33001","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
引用次数: 0

Abstract

Cognitive deficits in people with bipolar disorder (BD) may be the result of the illness or its treatment, but they could also reflect genetic risk factors shared between BD and cognition. We investigated this question using empirical genetic relationships within a sample of patients with BD and their unaffected relatives. Participants with bipolar I, II, or schizoaffective disorder (“narrow” BD, n = 69), related mood disorders (“broad” BD, n = 135), and their clinically unaffected relatives (n = 227) completed five cognitive tests. General cognitive function (g) was quantified via principal components analysis (PCA). Heritability and genetic correlations were estimated with SOLAR-Eclipse. Participants with “narrow” or “broad” diagnoses showed deficits in g, although affect recognition was unimpaired. Cognitive performance was significantly heritable (h2 = 0.322 for g, p < 0.005). Coheritability between psychopathology and g was small (0.0184 for narrow and 0.0327 for broad) and healthy relatives of those with BD were cognitively unimpaired. In this family sample, cognitive deficits were present in participants with BD but were not explained by substantial overlaps in genetic determinants of mood and cognition. These findings support the view that cognitive deficits in BD are largely the result of the illness or its treatment.

Abstract Image

家族样本中认知和躁郁症的独立遗传。
双相情感障碍(BD)患者的认知缺陷可能是疾病或其治疗的结果,但也可能反映了双相情感障碍和认知之间共有的遗传风险因素。我们利用双相情感障碍患者及其未受影响亲属样本中的经验遗传关系研究了这一问题。患有双相情感障碍 I、II 或分裂情感障碍("狭义 "BD,n = 69)、相关情绪障碍("广义 "BD,n = 135)的参与者及其临床上未受影响的亲属(n = 227)完成了五项认知测试。一般认知功能(g)通过主成分分析(PCA)进行量化。利用 SOLAR-Eclipse 对遗传率和遗传相关性进行了估计。诊断为 "狭义 "或 "广义 "的受试者在 g 方面表现出缺陷,但情感识别能力未受影响。认知表现具有明显的遗传性(g=0.322,p
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
5.90
自引率
7.10%
发文量
40
审稿时长
4-8 weeks
期刊介绍: Neuropsychiatric Genetics, Part B of the American Journal of Medical Genetics (AJMG) , provides a forum for experimental and clinical investigations of the genetic mechanisms underlying neurologic and psychiatric disorders. It is a resource for novel genetics studies of the heritable nature of psychiatric and other nervous system disorders, characterized at the molecular, cellular or behavior levels. Neuropsychiatric Genetics publishes eight times per year.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信