High-Quality Sleep Mitigates ABCA7-Related Generalization Deficits in Healthy Older African Americans.
High-Quality Sleep Mitigates ABCA7-Related Generalization Deficits in Healthy Older African Americans.
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DOI：
10.3233/jad-230043
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发表时间：
2023
影响因子：
4
通讯作者：
Gluck, Mark A.
中科院分区：
文献类型：
--
作者：
Sinha, Neha;Fausto, Bernadette A.;Mander, Bryce;Gluck, Mark A.
睡眠不足和阿尔茨海默病(AD)对老年非裔美国人的影响不成比例。阿尔茨海默病的遗传易感性进一步增加了这一人群中认知能力下降的风险。除载脂蛋白Eɛ4外，ABCA7rs115550680是与非裔美国人晚发性阿尔茨海默病相关的最强遗传位点。虽然睡眠和ABCA7 rs115550680独立影响晚年的认知结果，但我们对这两个因素对认知功能的相互作用知之甚少。我们研究了睡眠和ABCA7rs115550680对老年非裔美国人海马区依赖认知功能的相互作用。114名认知健康的老年非裔美国人接受了ABCA7风险的基因分型(n = 57名风险“G”等位基因携带者；n = 57名非携带者)，回答生活方式问卷，并完成认知电池。通过自我报告的睡眠质量(差、一般、好)来评估睡眠。协变量包括年龄和受教育年限。使用ANCOVA，我们发现，报告睡眠质量较差或一般的风险基因携带者对先前学习(AD的认知标志)的概括明显低于他们的非风险基因携带者。相反，在报告良好睡眠质量的个体中，泛化表现没有与基因型相关的差异。这些结果表明，睡眠质量可能对阿尔茨海默病的遗传风险具有神经保护作用。未来的研究将采用更严格的方法，调查睡眠神经生理学在与ABCA7相关的AD的发病和进展中的机制作用。还需要继续开发针对具有特定AD遗传风险特征的种族群体的非侵入性睡眠干预措施。
Both sleep deficiencies and Alzheimer’s disease (AD) disproportionately affect older African Americans. Genetic susceptibility to AD further compounds risk for cognitive decline in this population. Aside from APOE ɛ4, ABCA7 rs115550680 is the strongest genetic locus associated with late-onset AD in African Americans. While sleep and ABCA7 rs115550680 independently influence late-life cognitive outcomes, we know too little about the interplay between these two factors on cognitive function. We investigated the interaction between sleep and ABCA7 rs115550680 on hippocampal-dependent cognitive function in older African Americans. One-hundred fourteen cognitively healthy older African Americans were genotyped for ABCA7 risk (n = 57 carriers of risk “G” allele; n = 57 non-carriers), responded to lifestyle questionnaires, and completed a cognitive battery. Sleep was assessed via a self-reported rating of sleep quality (poor, average, good). Covariates included age and years of education. Using ANCOVA, we found that carriers of the risk genotype who reported poor or average sleep quality demonstrated significantly poorer generalization of prior learning—a cognitive marker of AD—compared to their non-risk counterparts. Conversely, there was no genotype-related difference in generalization performance in individuals who reported good sleep quality. These results indicate that sleep quality may be neuroprotective against genetic risk for AD. Future studies employing more rigorous methodology should investigate the mechanistic role of sleep neurophysiology in the pathogenesis and progression of AD associated with ABCA7. There is also need for the continued development of non-invasive sleep interventions tailored to racial groups with specific AD genetic risk profiles.