Obstructive Sleep Apnea and Its Treatment in Aging: Effects on Alzheimer’s disease Biomarkers, Cognition, Brain Structure and Neurophysiology

Here we review the impact of obstructive sleep apnea (OSA) on biomarkers of Alzheimer's disease (AD) pathogenesis, neuroanatomy, cognition and neurophysiology, and present the research investigating the effects of continuous positive airway pressure (CPAP) therapy. OSA is associated with an inc...

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Published inNeurobiology of disease Vol. 145; p. 105054
Main Authors Mullins, Anna E., Kam, Korey, Parekh, Ankit, Bubu, Omonigho M., Osorio, Ricardo S., Varga, Andrew W.
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.11.2020
Elsevier
Subjects
ADNI
AHI
CPAP
AHI3A
PPG
PiB
MSLT
PVT
SDB
PCO2
EDS
MMSE
P-tau
CSF
KC
ApoE
T-tau
OSA
SWA
ISF
qEEG
AD
ESS
PSG
SpO2
AHI4
ERPs
mPFC
MCI
OSAS
PET
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Abstract Here we review the impact of obstructive sleep apnea (OSA) on biomarkers of Alzheimer's disease (AD) pathogenesis, neuroanatomy, cognition and neurophysiology, and present the research investigating the effects of continuous positive airway pressure (CPAP) therapy. OSA is associated with an increase in AD markers amyloid-β and tau measured in cerebrospinal fluid (CSF), by Positron Emission Tomography (PET) and in blood serum. There is some evidence suggesting CPAP therapy normalizes AD biomarkers in CSF but since mechanisms for amyloid-β and tau production/clearance in humans are not completely understood, these findings remain preliminary. Deficits in the cognitive domains of attention, vigilance, memory and executive functioning are observed in OSA patients with the magnitude of impairment appearing stronger in younger people from clinical settings than in older community samples. Cognition improves with varying degrees after CPAP use, with the greatest effect seen for attention in middle age adults with more severe OSA and sleepiness. Paradigms in which encoding and retrieval of information are separated by periods of sleep with or without OSA have been done only rarely, but perhaps offer a better chance to understand cognitive effects of OSA than isolated daytime testing. In cognitively normal individuals, changes in EEG microstructure during sleep, particularly slow oscillations and spindles, are associated with biomarkers of AD, and measures of cognition and memory. Similar changes in EEG activity are reported in AD and OSA, such as “EEG slowing” during wake and REM sleep, and a degradation of NREM EEG microstructure. There is evidence that CPAP therapy partially reverses these changes but large longitudinal studies demonstrating this are lacking. A diagnostic definition of OSA relying solely on the Apnea Hypopnea Index (AHI) does not assist in understanding the high degree of inter-individual variation in daytime impairments related to OSA or response to CPAP therapy. We conclude by discussing conceptual challenges to a clinical trial of OSA treatment for AD prevention, including inclusion criteria for age, OSA severity, and associated symptoms, the need for a potentially long trial, defining relevant primary outcomes, and which treatments to target to optimize treatment adherence.
AbstractList Here we review the impact of obstructive sleep apnea (OSA) on biomarkers of Alzheimer's disease (AD) pathogenesis, neuroanatomy, cognition and neurophysiology, and present the research investigating the effects of continuous positive airway pressure (CPAP) therapy. OSA is associated with an increase in AD markers amyloid-β and tau measured in cerebrospinal fluid (CSF), by Positron Emission Tomography (PET) and in blood serum. There is some evidence suggesting CPAP therapy normalizes AD biomarkers in CSF but since mechanisms for amyloid-β and tau production/clearance in humans are not completely understood, these findings remain preliminary. Deficits in the cognitive domains of attention, vigilance, memory and executive functioning are observed in OSA patients with the magnitude of impairment appearing stronger in younger people from clinical settings than in older community samples. Cognition improves with varying degrees after CPAP use, with the greatest effect seen for attention in middle age adults with more severe OSA and sleepiness. Paradigms in which encoding and retrieval of information are separated by periods of sleep with or without OSA have been done only rarely, but perhaps offer a better chance to understand cognitive effects of OSA than isolated daytime testing. In cognitively normal individuals, changes in EEG microstructure during sleep, particularly slow oscillations and spindles, are associated with biomarkers of AD, and measures of cognition and memory. Similar changes in EEG activity are reported in AD and OSA, such as “EEG slowing” during wake and REM sleep, and a degradation of NREM EEG microstructure. There is evidence that CPAP therapy partially reverses these changes but large longitudinal studies demonstrating this are lacking. A diagnostic definition of OSA relying solely on the Apnea Hypopnea Index (AHI) does not assist in understanding the high degree of inter-individual variation in daytime impairments related to OSA or response to CPAP therapy. We conclude by discussing conceptual challenges to a clinical trial of OSA treatment for AD prevention, including inclusion criteria for age, OSA severity, and associated symptoms, the need for a potentially long trial, defining relevant primary outcomes, and which treatments to target to optimize treatment adherence.
ArticleNumber 105054
Author Parekh, Ankit
Mullins, Anna E.
Kam, Korey
Bubu, Omonigho M.
Osorio, Ricardo S.
Varga, Andrew W.
AuthorAffiliation b Center for Brain Health, Department of Psychiatry, NYU Langone Medical Center, New York, NY, 10016, USA
a Mount Sinai Integrative Sleep Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA
AuthorAffiliation_xml – name: a Mount Sinai Integrative Sleep Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA
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Author_xml – sequence: 1
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  surname: Mullins
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– sequence: 2
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  surname: Kam
  fullname: Kam, Korey
  organization: Mount Sinai Integrative Sleep Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
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  givenname: Omonigho M.
  surname: Bubu
  fullname: Bubu, Omonigho M.
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  givenname: Andrew W.
  orcidid: 0000-0002-3668-3371
  surname: Varga
  fullname: Varga, Andrew W.
  email: andrew.varga@mssm.edu
  organization: Mount Sinai Integrative Sleep Center, Division of Pulmonary, Critical Care, and Sleep Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32860945$$D View this record in MEDLINE/PubMed
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Fri Aug 16 21:59:47 EDT 2024
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Sat Sep 28 08:34:38 EDT 2024
Fri Feb 23 02:48:04 EST 2024
IsDoiOpenAccess true
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Keywords ADNI
AHI
CPAP
AHI3A
PPG
PiB
MSLT
PVT
SDB
PCO2
EDS
MMSE
P-tau
CSF
KC
ApoE
T-tau
OSA
SWA
ISF
qEEG
AD
ESS
PSG
SpO2
AHI4
ERPs
mPFC
MCI
OSAS
PET
Language English
License This is an open access article under the CC BY-NC-ND license.
Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.
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ObjectType-Feature-3
content type line 23
ObjectType-Review-2
Equal contributions
ORCID 0000-0002-3668-3371
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PublicationTitle Neurobiology of disease
PublicationTitleAlternate Neurobiol Dis
PublicationYear 2020
Publisher Elsevier Inc
Elsevier
Publisher_xml – name: Elsevier Inc
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Snippet Here we review the impact of obstructive sleep apnea (OSA) on biomarkers of Alzheimer's disease (AD) pathogenesis, neuroanatomy, cognition and neurophysiology,...
Here we review the impact of obstructive sleep apnea (OSA) on biomarkers of Alzheimer’s disease (AD) pathogenesis, neuroanatomy, cognition and neurophysiology,...
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Title Obstructive Sleep Apnea and Its Treatment in Aging: Effects on Alzheimer’s disease Biomarkers, Cognition, Brain Structure and Neurophysiology
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