Is poorer sleep efficiency linked to faster changes in the hippocampus?

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The researchers proposed that hippocampal integrity may play a critical role in linking sleep with memory decay and β-amyloid (Aβ) accumulation, two markers of Alzheimer's disease (AD) pathology. They tested whether worse self-reported sleep was related to decline in memory and intra-hippocampal microstructure, including in the presence of Aβ.

In this longitudinal observational study, 243 cognitively healthy participants aged 19–81 completed the Pittsburgh Sleep Quality Index once and underwent two diffusion tensor imaging sessions an average of 3 years apart. Increased mean diffusivity was used as an index of decline in intra-hippocampal microstructure. Memory decay was measured at each imaging session using verbal delayed recall. A single positron emission tomography session in 108 participants older than 44 identified 23 as Aβ positive. Genotyping allowed the researchers to control for APOE ε4 status and polygenic scores for sleep and AD.

Worse overall sleep quality and sleep efficiency were associated with faster decline in hippocampal microstructure over time. Sleep efficiency was the percentage of time in bed at night spent asleep; its association with microstructural decline was stronger in the presence of Aβ accumulation, and decline in hippocampal integrity mediated its relationship with memory decay. Genetic risk for sleep efficiency or AD did not explain the results.

The researchers concluded that poorer sleep efficiency was associated with decline in hippocampal microstructure, especially in the presence of Aβ accumulation, and that Aβ might link poor sleep and memory decay. Because genetic risk did not account for the associations, poor sleep efficiency might be a risk marker for AD, although the causal mechanisms driving the associations remain unknown.