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Sleep Quality May Affect Alzheimer’s Risk
Two new studies link sleep quality with the risk for Alzheimer’s disease (AD) and AD-related pathology in the brain.
In one study, researchers report that shorter sleep duration and poor sleep quality are associated with increased deposition of amyloid in the brain, changes linked to the development of AD.
“As evidence of this association accumulates, intervention trials will be needed to determine whether optimizing sleep can prevent or slow AD progression,” the researchers, with lead author Adam P. Spira, PhD, from The Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, conclude.
In a separate report, researchers led by Andrew S.P. Lim, MD, from the Division of Neurology, Department of Medicine at Sunnybrook Health Sciences Center, University of Toronto, Ontario, Canada, found that better sleep consolidation appears to attenuate the effect of the apolipoprotein E (APOE) genotype on incident AD, as well as the development of neurofibrillary tangle pathology in the brain.
“Assessment of sleep consolidation may identify APOE + individuals at high risk for incident AD, and interventions to enhance sleep consolidation should be studied as potentially useful means to reduce the risk of AD and development of neurofibrillary tangles in APOE ε4+ individuals,” they conclude.
Both papers were published online October 21 in JAMA Neurology.
Poor Sleep Quality
Prior studies have linked disturbed sleep to cognitive impairment in older adults, and patients with AD have been shown to spend more time awake in bed and have more fragmented sleep than those without AD. A previous report showed that cerebro-spinal fluid amyloid-β (Aβ) levels in young people increased with time awake and decreased with time asleep, the authors point out.
To see whether poor sleep contributes to the neuropathologic changes underlying AD, Dr. Spira and colleagues used data on community-dwelling people participating in the Baltimore Longitudinal Study of Aging (BLSA) to examine the association between self-reported sleep quality and Aβ burden in the brain, measured using positron emission tomography (PET) with carbon-11 labeled Pittsburgh compound B (PiB).
This neuroimaging substudy of BLSA is a cross-sectional study of 70 adults, mean age 76 (range, 53 to 91) years. Sleep variables were self-reported, and Aβ was measured by using PiB-PET distribution volume ratios (DVR).
After adjustment for potential confounders, the researchers found that shorter sleep duration was associated with great Aβ burden, measured both by mean cortical DVR (B = 0.08 [95% confidence interval (CI), 0.03 – 0.14]; P = .005) and precuneus DVR (B = 0.11 [95% CI, 0.03 – 0.18]; P = .007).
Reports of lower sleep quality were also associated with a greater Aβ burden measured by precuneus DVR (B = 0.08 [95% CI, 0.01 – 0.15]; P = .03).
The researchers caution that the cross-sectional design used in this study means they can’t determine the direction of this association: that is, whether disturbed sleep causes increased Aβ deposition or vice versa.
“Additional studies with objective sleep measures are needed to determine whether sleep disturbance causes or accelerates Alzheimer disease,” they note. If sleep disturbance is found to cause Aβ, that could have “significant public health implications,” they add, because insomnia can be treated.
Sleep Consolidation and AD Risk
In a separate report, researchers looked at the relationship between poor sleep consolidation, defined as the interruption of sleep by repeated awakenings, and the risk for AD conferred by the APOE ε4 risk allele, as well as the burden of AD pathology (in this instance, both Aβ and neurofibrillary tangles identified upon autopsy).
Study participants, 698 community-dwelling people without dementia, were taking part in the Rush Memory and Aging Project, a prospective, longitudinal cohort study with annual evaluations up to 6 years of follow-up. Mean age of participants was 81.7 years, and 77% of participants were women.
The researchers used up to 10 days of actigraphic recording to ascertain the degree of sleep consolidation among participants and determined their APOE genotype. Over that time, 201 participants died and Aβ and neurofibrillary tangles were identified by using immunohistochemistry.
During follow-up, 98 participants developed AD. The researchers found that better sleep consolidation attenuated the effect of the ε4 allele on the risk for incident AD (hazard ratio, 0.67 [95% CI, 0.46 – 0.97; P = .04] per allele per 1–standard deviation increase in sleep consolidation).
“In a series of linear mixed-effect models, better sleep consolidation also attenuated the effect of the ε4 allele on the annual rate of cognitive decline,” the authors write.
Among those who died, the researchers found that better sleep consolidation mitigated the negative effect of the ε4 allele on the density of neurofibrillary tangles (NFTs) density at death, “which accounted for its beneficial effects on the association between APOE and cognition proximate to death,” they conclude.
“These findings highlight a thus far unappreciated biological and clinical link between sleep, APOE biology, NFTs, and AD.”
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