Research Group for Lifespan Changes in Brain and Cognition, Department of Psychology, University of Oslo, Oslo, Norway.
Departament de Medicina, Facultat de Medicina i Ciències de la Salut, Universitat de Barcelona, Barcelona, Spain.
Sleep. 2021 Nov 12;44(11). doi: 10.1093/sleep/zsab110.
A critical role linking sleep with memory decay and β-amyloid (Aβ) accumulation, two markers of Alzheimer's disease (AD) pathology, may be played by hippocampal integrity. We tested the hypotheses that worse self-reported sleep relates to decline in memory and intra-hippocampal microstructure, including in the presence of Aβ.
Two-hundred and forty-three cognitively healthy participants, aged 19-81 years, completed the Pittsburgh Sleep Quality Index once, and two diffusion tensor imaging sessions, on average 3 years apart, allowing measures of decline in intra-hippocampal microstructure as indexed by increased mean diffusivity. We measured memory decay at each imaging session using verbal delayed recall. One session of positron emission tomography, in 108 participants above 44 years of age, yielded 23 Aβ positive. Genotyping enabled control for APOE ε4 status, and polygenic scores for sleep and AD, respectively.
Worse global sleep quality and sleep efficiency related to more rapid reduction of hippocampal microstructure over time. Focusing on efficiency (the percentage of time in bed at night spent asleep), the relation was stronger in presence of Aβ accumulation, and hippocampal integrity decline mediated the relation with memory decay. The results were not explained by genetic risk for sleep efficiency or AD.
Worse sleep efficiency related to decline in hippocampal microstructure, especially in the presence of Aβ accumulation, and Aβ might link poor sleep and memory decay. As genetic risk did not account for the associations, poor sleep efficiency might constitute a risk marker for AD, although the driving causal mechanisms remain unknown.
睡眠与记忆衰退和β-淀粉样蛋白（Aβ）积累之间的关键联系，这两个都是阿尔茨海默病（AD）病理的标志物，可能与海马体的完整性有关。我们检验了以下假设：较差的自我报告睡眠与记忆和海马内微观结构的下降有关，包括在存在 Aβ的情况下。
243 名认知健康的参与者，年龄在 19-81 岁之间，平均每 3 年完成一次匹兹堡睡眠质量指数和两次弥散张量成像，以测量海马内微观结构的下降，指标为平均弥散度的增加。我们在每次成像时使用口头延迟回忆来测量记忆衰退。在 108 名年龄在 44 岁以上的参与者中进行了一次正电子发射断层扫描，其中 23 人 Aβ 阳性。基因分型使我们能够控制 APOE ε4 状态，以及睡眠和 AD 的多基因评分。
较差的整体睡眠质量和睡眠效率与海马体微观结构随时间的更快下降有关。在存在 Aβ 积累的情况下，关注效率（夜间躺在床上睡着的时间百分比），这种关系更强，海马体的完整性下降介导了与记忆衰退的关系。这些结果不能用睡眠效率或 AD 的遗传风险来解释。
较差的睡眠效率与海马体微观结构的下降有关，尤其是在存在 Aβ 积累的情况下，Aβ 可能将睡眠质量差和记忆衰退联系起来。由于遗传风险不能解释这些关联，较差的睡眠效率可能构成 AD 的风险标志物，尽管驱动这些关联的因果机制尚不清楚。
