Sleep Disturbances, Cognitive Status, and Biomarkers of Dementia.


Journal

Journal of Alzheimer's disease : JAD
ISSN: 1875-8908
Titre abrégé: J Alzheimers Dis
Pays: Netherlands
ID NLM: 9814863

Informations de publication

Date de publication:
2022
Historique:
pubmed: 30 8 2022
medline: 19 10 2022
entrez: 29 8 2022
Statut: ppublish

Résumé

While sleep disturbances appear to be risk factors in Alzheimer's disease (AD) progression, information such as the prevalence across dementia severity and the influence on the trajectory of cognitive decline is unclear. We evaluate the hypotheses that the prevalence of insomnia differs by cognitive impairment, that sleep disturbances track with AD biomarkers, and that longitudinal changes in sleep disorders affect cognition. We used the National Alzheimer's Coordinating Center Database to determine the prevalence of clinician-identified insomnia and nighttime behaviors in normal, mild cognitive impairment (MCI), and demented individuals. We evaluated mean Montreal Cognitive Assessment (MoCA) scores, hippocampal volumes (HV), and CSF phosphorylated tau:amyloid-β ratios at first visit using analysis of variance with age as a covariate. In longitudinal evaluations, we assessed changes in MoCA scores and HV in insomnia and nighttime behaviors between the first and last visits. Prevalence of insomnia was 14%, 16%, and 11% for normal, MCI, and dementia groups. Prevalence of nighttime behaviors was 14%, 21%, and 29% respectively. Insomnia patients had higher MoCA scores, larger HV, and lower pTauBeta than individuals without insomnia, indicating less neurodegeneration. In contrast, nighttime behaviors were associated with worse cognition, smaller HV, and higher pTauBeta. Similar findings were seen between longitudinal associations of sleep disorders and cognition and HV. Our findings suggest that insomnia is unreliably recognized in patients with cognitive impairment. Nighttime behaviors may better indicate the presence of sleep disturbances and have diagnostic specificity in AD over insomnia.

Sections du résumé

BACKGROUND
While sleep disturbances appear to be risk factors in Alzheimer's disease (AD) progression, information such as the prevalence across dementia severity and the influence on the trajectory of cognitive decline is unclear.
OBJECTIVE
We evaluate the hypotheses that the prevalence of insomnia differs by cognitive impairment, that sleep disturbances track with AD biomarkers, and that longitudinal changes in sleep disorders affect cognition.
METHODS
We used the National Alzheimer's Coordinating Center Database to determine the prevalence of clinician-identified insomnia and nighttime behaviors in normal, mild cognitive impairment (MCI), and demented individuals. We evaluated mean Montreal Cognitive Assessment (MoCA) scores, hippocampal volumes (HV), and CSF phosphorylated tau:amyloid-β ratios at first visit using analysis of variance with age as a covariate. In longitudinal evaluations, we assessed changes in MoCA scores and HV in insomnia and nighttime behaviors between the first and last visits.
RESULTS
Prevalence of insomnia was 14%, 16%, and 11% for normal, MCI, and dementia groups. Prevalence of nighttime behaviors was 14%, 21%, and 29% respectively. Insomnia patients had higher MoCA scores, larger HV, and lower pTauBeta than individuals without insomnia, indicating less neurodegeneration. In contrast, nighttime behaviors were associated with worse cognition, smaller HV, and higher pTauBeta. Similar findings were seen between longitudinal associations of sleep disorders and cognition and HV.
CONCLUSION
Our findings suggest that insomnia is unreliably recognized in patients with cognitive impairment. Nighttime behaviors may better indicate the presence of sleep disturbances and have diagnostic specificity in AD over insomnia.

Identifiants

pubmed: 36031904
pii: JAD220664
doi: 10.3233/JAD-220664
doi:

Substances chimiques

Amyloid beta-Peptides 0
Biomarkers 0
tau Proteins 0

Types de publication

Journal Article Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S. Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1367-1374

Subventions

Organisme : NIA NIH HHS
ID : P50 AG016574
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG049638
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG016573
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG005133
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG005146
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG047266
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG066546
Pays : United States
Organisme : NINDS NIH HHS
ID : U24 NS107182
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG010161
Pays : United States
Organisme : NIA NIH HHS
ID : P20 AG068077
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG010129
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG053760
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG010124
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG033514
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG010133
Pays : United States
Organisme : NIA NIH HHS
ID : U01 AG016976
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG005136
Pays : United States
Organisme : NIA NIH HHS
ID : SB1 AG037357
Pays : United States
Organisme : NIA NIH HHS
ID : P20 AG068082
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG019610
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG012300
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG008051
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG023501
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG072959
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG005681
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG028383
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG008702
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG047270
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG005138
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG005131
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG072958
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG005142
Pays : United States
Organisme : NIA NIH HHS
ID : P20 AG068053
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG008017
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG047366
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG013854
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG025688
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG013846
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG068128
Pays : United States
Organisme : NIA NIH HHS
ID : P30 AG035982
Pays : United States
Organisme : NIA NIH HHS
ID : P50 AG005134
Pays : United States
Organisme : NIA NIH HHS
ID : P20 AG068024
Pays : United States

Auteurs

Ifrah Zawar (I)

Comprehensive Epilepsy Program, Department of Neurology, University of Virginia, Charlottesville, VA, USA.

Meghan K Mattos (MK)

UVA Section of Geriatrics, School of Nursing, University of Virginia, Charlottesville, VA, USA.

Carol Manning (C)

Memory Disorders Program, Department of Neurology, University of Virginia, Charlottesville, VA, USA.

Mark Quigg (M)

Comprehensive Epilepsy Program, Department of Neurology, University of Virginia, Charlottesville, VA, USA.
UVA Section of Geriatrics, School of Nursing, University of Virginia, Charlottesville, VA, USA.

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Classifications MeSH