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PLoS One. 2018 Jan 25;13(1):e0191281. doi: 10.1371/journal.pone.0191281. eCollection 2018.

APOEε4 and slow wave sleep in older adults.

Author information

1
Research Institute, California Pacific Medical Center, San Francisco, California, United States of America.
2
Departments of Psychiatry and Neurology, University of California San Francisco, San Francisco, California, United States of America.
3
Medical Center, San Francisco VA, San Francisco, California, United States of America.
4
Department of Epidemiology and Biostatistics University of California San Francisco, San Francisco, California, United States of America.
5
Department of Psychiatry, University of California San Diego, La Jolla, California, United States of America.
6
Division of Epidemiology and Community Health, University of Minnesota, Minneapolis, Minnesota, United States of America.
7
Center for Chronic Disease Outcomes Research, Minneapolis VA Medical Center, Minneapolis, Minnesota, United States of America.
8
Department of Medicine, University of Minnesota, Minneapolis, Minnesota, United States of America.
9
Department of Epidemiology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
10
Department of Medicine, University of California San Diego, La Jolla, California, United States of America.
11
Division of Sleep & Circadian Disorders, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
12
Departments of Medicine, Brigham and Women's Hospital and Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America.

Abstract

Slow wave (or stage N3) sleep has been linked to a variety of cognitive processes. However, the role of stage N3 in the elderly is debated. The link between stage N3 and episodic memory may be weakened or changed in the older adult population, possibly due to several altered mechanisms impacting the cellular structure of the brain. The bases for the age-related dissociation between stage N3 and cognition are not understood. Since APOEε4 status is the strongest genetic risk factor for cognitive decline, we assessed whether the ε4 allele is associated with stage N3 sleep. Participants were from the population-based Osteoporotic Fractures in Men (MrOS) cohort with polysomnography and APOEε4 genotype data (n = 2,302, 100% male, mean age 76.6 years). Sleep stages were objectively measured using overnight in-home polysomnography and central electroencephalogram data were used to score stage N3 sleep. Cognitive function was assessed using the Modified Mini Mental State Exam (3MS). The APOE rs429358 single nucleotide polymorphism, which defines the APOEε4 allele, was genotyped using a custom genotyping array. Total time in stage N3 sleep was significantly higher (p<0.0001) among the 40 MrOS participants carrying two copies of the ε4 allele (62±5.2 minutes) compared with 43±1.5 minutes for carriers of one ε4 allele (n = 515) and 40±0.8 minutes for ε4 non-carriers (n = 1747). All results were independent of sleep efficiency, number of sleep cycles, and apnea hypopnea index. These findings support an association between APOEε4 genotype and sleep stage N3 in the elderly. Increased total stage N3 duration among ε4/ε4 carriers does not appear to reflect compensation for prior cognitive decline and may reflect overactive downscaling of synapses during sleep. If confirmed, these results might in part explain the high risk of age-related cognitive decline and AD among APOE ε4/ε4 carriers.

PMID:
29370207
PMCID:
PMC5784964
DOI:
10.1371/journal.pone.0191281
[Indexed for MEDLINE]
Free PMC Article

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