Is Risk of Alzheimer’s Linked to Specific Sleep Patterns?

Summary: Sleep disturbances may be an outcome of Alzheimer’s in those with a genetic predisposition, but not a cause of dementia. Those with genetic risk factors for Alzheimer’s tend to have shorter sleep durations and are more likely to be early risers but are less likely to suffer from insomnia.

Source: AAN

Disturbed sleep patterns do not cause Alzheimer’s disease but people who are at high genetic risk of developing Alzheimer’s disease may be more likely to be a “morning person,” have shorter sleep duration and other measures of sleep disturbance and are less likely to have insomnia, according to a study published in the August 19, 2020, online issue of Neurology.

“We know that people with Alzheimer’s disease often report depression and various sleep problems, like insomnia,” said study author Abbas Dehghan, Ph.D., of Imperial College London in the United Kingdom. “We wanted to find out if there are causal relationships between different sleep patterns and depression and Alzheimer’s.”

To evaluate the relationship between different sleep patterns, major depressive disorder, and Alzheimer’s disease, researchers analyzed the result of different genetic studies collected from databases that included: 21,982 people diagnosed with Alzheimer’s disease who were compared to 41,944 without Alzheimer’s disease; 9,240 with major depressive disorder who were compared to 9,519 without major depressive disorder; and 446,118 people with measurements of sleep-related characteristics.

Risk of Alzheimer’s was determined based on genetic studies where Alzheimer’s was diagnosed by autopsy or clinical examination.

Researchers analysed the genetic information using a study design called Mendelian randomization that can determine if there is cause and effect.

Researchers found no evidence that sleep-related characteristics caused Alzheimer’s disease. They also found no evidence of cause and effect between major depressive disorder and Alzheimer’s.

This shows an old man sleeping
Researchers found no evidence that sleep-related characteristics caused Alzheimer’s disease. Image is in the public domain.

Researchers did find a small association between the following: people with twice the genetic risk for Alzheimer’s disease were 1% more likely to call themselves “morning people” compared to people at lower genetic risk; and people with twice the genetic risk of Alzheimer’s had a 1% lower risk of insomnia. However, this effect of this association is small and shows only a possible link, not cause and effect.

A limitation of the study was that most of the people in the study were of European ancestry, so the results may not apply to the people of different ethnicity.

Funding: This study was supported by U.K. Dementia Research Institute and the NIHR Imperial College Healthcare Trust.

About this aging research article

Source:
AAN
Contacts:
M.A. Rosko – AAN
Image Source:
The image is in the public domain.

Original Research: Closed access
“Sleep, major depressive disorder and Alzheimer’s disease: A Mendelian randomisation study” by Jian Huang, Verena Zuber, Paul M. Matthews, et al. Neurology.


Abstract

Sleep, major depressive disorder and Alzheimer’s disease: A Mendelian randomisation study

Objective
To explore the causal relationships between sleep, major depressive disorder (MDD), and Alzheimer’s disease (AD).

Methods
We conducted bi-directional 2-sample Mendelian randomisation analyses. Genetic associations were obtained from the largest genome-wide association studies currently available in UK Biobank (N = 446,118), the Psychiatric Genomics Consortium (N = 18,759), and the International Genomics of Alzheimer’s Project (N = 63,926). We used the inverse variance weighted Mendelian randomisation method to estimate causal effects, and weighted median and MR-Egger for sensitivity analyses to test for pleiotropic effects.

Results
We found that higher risk of AD was significantly associated with being a “morning person” (OR = 1.01, p = 0.001), shorter sleep duration (self-reported: β = −0.006, p = 1.9 × 10−4; accelerometer-based: β = −0.015, p = 6.9 × 10−5), less likely to report long sleep (β = −0.003, p = 7.3 × 10−7), earlier timing of the least active 5 hours (β = −0.024, p = 1.7 × 10−13), and a smaller number of sleep episodes (β = −0.025, p = 5.7 × 10−14) after adjusting for multiple comparisons. We also found that higher risk of AD was associated with lower risk of insomnia (OR = 0.99, p = 7 × 10−13). However, we did not find evidence either that these abnormal sleep patterns were causally related to AD or for a significant causal relationship between MDD and risk of AD.

Conclusion
We found that AD may causally influence sleep patterns. However, we did not find evidence supporting a causal role of disturbed sleep patterns for AD or evidence for a causal relationship between MDD and AD.

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