Individuals With a High Genetic Risk for Alzheimer’s Disease Have Altered Sleep Patterns


Alzheimer’s disease (AD) had a significant correlation with sleep patterns, according to results from a genome-wide association study, published in Neurology.

Databases from the United Kingdom Biobank (n=446,118), the International Genomics of Alzheimer’s Project (n=63,926), and the Psychiatric Genomics Consortium (n=18,759) were combined for bi-directional two-sample Mendelian randomization analyses. Sleep phenotypes were self-reported or measured using an accelerometer. Insomnia was defined as difficulty falling asleep or maintaining sleep. AD was diagnosed during a clinical examination or a post-mortem autopsy. Major depressive disorder was clinically defined.

Individuals who had a high genetic risk for AD were more likely to report being a morning person (odd’s ratio [OR], 1.01; 95% CI, 1.01-1.02; P =.001). They were more likely to self-report short sleep durations (β, -0.006; 95% CI, -0.010 to -0.002; P =7.3×10) and less likely to self-report long sleep (β, -0.003; 95% CI, -0.005 to -0.001; P =7.3×10).

Those with a higher genetic risk for AD had smaller numbers of sleep episodes (β, -0.025; 95% CI, -0.031 to -0.019; P =5.7×10) with the least active 5 hours of sleep occurring earlier in the night (β, -0.024; 95% CI, -0.030 to -0.018; P =1.7×10), as measured by an accelerometer.

A high genetic risk for AD was associated with a lower risk for insomnia (OR, 0.99; 95% CI, 0.991-0.995; P =7.0×10).

After removing single nucleotide polymorphisms (SNPs) from the apolipoprotein E (APOE) gene from the analyses, the significant relationships between AD and sleep duration were no longer significant.

The investigators observed no significant correlations between major depressive disorder and sleep patterns.

Limitations of the study were the mixture of data types. The investigators had differing power for self-reported and accelerometer data. Also, the Mendelian randomization analysis assumes a lifetime exposure to risk factors which may have contributed to an overestimation of the effects.

The study authors concluded that they found evidence to support a relationship between AD and sleep disturbances. However, without further study it remains unclear whether AD was the cause of the altered sleep patterns.

Disclosure: One author declared industry affiliations. Please refer to the original article for a full list of disclosures.

Reference

Huang J, Zuber V, Matthews P M, et al. Sleep, major depressive disorder and Alzheimer’s disease: a Mendelian randomisation study. Neurology. 2020;10.1212/ WNL.0000000000010463.



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