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Cardiorespiratory Fitness Modifies Influence of Sleep Problems on Cerebrospinal Fluid Biomarkers in an At-Risk Cohort.
J Alzheimers Dis. 2019; 69(1):111-121.JA

Abstract

BACKGROUND

Previous studies indicate that cardiorespiratory fitness (CRF) and sleep are each favorably associated with Alzheimer's disease (AD) pathophysiology, including reduced amyloid-β (Aβ) and tau pathology. However, few studies have examined CRF and sleep in the same analysis.

OBJECTIVE

To examine the relationship between sleep and core AD cerebrospinal fluid (CSF) biomarkers among at-risk healthy late-middle-aged adults and determine whether CRF modifies this association.

METHODS

Seventy-four adults (age = 64.38±5.48, 68.9% female) from the Wisconsin Registry for Alzheimer's Prevention participated. Sleep was evaluated using the Medical Outcomes Study Sleep Scale, specifically the Sleep Problems Index I (SPI), which incorporates domains of sleep disturbance, somnolence, sleep adequacy, and shortness of breath. Higher scores indicate greater sleep problems. To assess CRF, participants underwent a graded exercise test. CSF was collected via lumbar puncture, from which Aβ42, total-tau (t-tau), and phosphorylated-tau (p-tau) were immunoassayed. Regression analyses examined the association between SPI and CSF biomarkers, and the interaction between SPI and CRF on these same biomarkers, adjusting for relevant covariates.

RESULTS

Higher SPI scores were associated with greater p-tau (p = 0.027) and higher t-tau/Aβ42 (p = 0.021) and p-tau/Aβ42 (p = 0.009) ratios. Analyses revealed significant SPI*CRF interactions for t-tau (p = 0.016), p-tau (p = 0.008), and p-tau/Aβ42 (p = 0.041); with a trend for t-tau/Aβ42 (p = 0.061). Specifically, the relationship between poorer sleep and these biomarkers was significant among less fit individuals, but not among those who were more fit.

CONCLUSION

In a late-middle-aged at-risk cohort, CRF attenuated the association between poor sleep and levels of select CSF biomarkers. This suggests fitness may play an important role in preventing AD by protecting against pathology, even in impaired sleep.

Authors+Show Affiliations

Geriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA. Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Wisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.Neuroscience Training Program, University of Wisconsin-Madison, Madison, WI, USA. Wisconsin Center for Sleep Medicine and Research, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Department of Psychiatry, University of Wisconsin-Madison, Madison, WI, USA.Department of Kinesiology, University of Wisconsin School of Education, Madison, WI, USA.Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Wisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Department of Kinesiology, University of Wisconsin School of Education, Madison, WI, USA.Wisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.Geriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA. Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Department of Neurology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.Geriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA. Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sweden. Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK. UK Dementia Research Institute, London, UK.Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden. Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Sweden.Geriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA. Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Wisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Wisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Department of Neurology, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.Geriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA. Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Wisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.Department of Kinesiology, University of Wisconsin School of Education, Madison, WI, USA. Research Service, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA.Geriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA. Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Wisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.Geriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA. Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Wisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.

Pub Type(s)

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

Language

eng

PubMed ID

30958346

Citation

Law, Lena L., et al. "Cardiorespiratory Fitness Modifies Influence of Sleep Problems On Cerebrospinal Fluid Biomarkers in an At-Risk Cohort." Journal of Alzheimer's Disease : JAD, vol. 69, no. 1, 2019, pp. 111-121.
Law LL, Sprecher KE, Dougherty RJ, et al. Cardiorespiratory Fitness Modifies Influence of Sleep Problems on Cerebrospinal Fluid Biomarkers in an At-Risk Cohort. J Alzheimers Dis. 2019;69(1):111-121.
Law, L. L., Sprecher, K. E., Dougherty, R. J., Edwards, D. F., Koscik, R. L., Gallagher, C. L., Carlsson, C. M., Zetterberg, H., Blennow, K., Asthana, S., Sager, M. A., Hermann, B. P., Johnson, S. C., Cook, D. B., Bendlin, B. B., & Okonkwo, O. C. (2019). Cardiorespiratory Fitness Modifies Influence of Sleep Problems on Cerebrospinal Fluid Biomarkers in an At-Risk Cohort. Journal of Alzheimer's Disease : JAD, 69(1), 111-121. https://doi.org/10.3233/JAD-180291
Law LL, et al. Cardiorespiratory Fitness Modifies Influence of Sleep Problems On Cerebrospinal Fluid Biomarkers in an At-Risk Cohort. J Alzheimers Dis. 2019;69(1):111-121. PubMed PMID: 30958346.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cardiorespiratory Fitness Modifies Influence of Sleep Problems on Cerebrospinal Fluid Biomarkers in an At-Risk Cohort. AU - Law,Lena L, AU - Sprecher,Kate E, AU - Dougherty,Ryan J, AU - Edwards,Dorothy F, AU - Koscik,Rebecca L, AU - Gallagher,Catherine L, AU - Carlsson,Cynthia M, AU - Zetterberg,Henrik, AU - Blennow,Kaj, AU - Asthana,Sanjay, AU - Sager,Mark A, AU - Hermann,Bruce P, AU - Johnson,Sterling C, AU - Cook,Dane B, AU - Bendlin,Barbara B, AU - Okonkwo,Ozioma C, PY - 2019/4/9/pubmed PY - 2020/9/10/medline PY - 2019/4/9/entrez KW - Alzheimer’s disease KW - amyloid-β protein KW - biomarkers KW - cardiorespiratory fitness KW - cerebrospinal fluid KW - sleep KW - tau protein SP - 111 EP - 121 JF - Journal of Alzheimer's disease : JAD JO - J Alzheimers Dis VL - 69 IS - 1 N2 - BACKGROUND: Previous studies indicate that cardiorespiratory fitness (CRF) and sleep are each favorably associated with Alzheimer's disease (AD) pathophysiology, including reduced amyloid-β (Aβ) and tau pathology. However, few studies have examined CRF and sleep in the same analysis. OBJECTIVE: To examine the relationship between sleep and core AD cerebrospinal fluid (CSF) biomarkers among at-risk healthy late-middle-aged adults and determine whether CRF modifies this association. METHODS: Seventy-four adults (age = 64.38±5.48, 68.9% female) from the Wisconsin Registry for Alzheimer's Prevention participated. Sleep was evaluated using the Medical Outcomes Study Sleep Scale, specifically the Sleep Problems Index I (SPI), which incorporates domains of sleep disturbance, somnolence, sleep adequacy, and shortness of breath. Higher scores indicate greater sleep problems. To assess CRF, participants underwent a graded exercise test. CSF was collected via lumbar puncture, from which Aβ42, total-tau (t-tau), and phosphorylated-tau (p-tau) were immunoassayed. Regression analyses examined the association between SPI and CSF biomarkers, and the interaction between SPI and CRF on these same biomarkers, adjusting for relevant covariates. RESULTS: Higher SPI scores were associated with greater p-tau (p = 0.027) and higher t-tau/Aβ42 (p = 0.021) and p-tau/Aβ42 (p = 0.009) ratios. Analyses revealed significant SPI*CRF interactions for t-tau (p = 0.016), p-tau (p = 0.008), and p-tau/Aβ42 (p = 0.041); with a trend for t-tau/Aβ42 (p = 0.061). Specifically, the relationship between poorer sleep and these biomarkers was significant among less fit individuals, but not among those who were more fit. CONCLUSION: In a late-middle-aged at-risk cohort, CRF attenuated the association between poor sleep and levels of select CSF biomarkers. This suggests fitness may play an important role in preventing AD by protecting against pathology, even in impaired sleep. SN - 1875-8908 UR - https://www.unboundmedicine.com/medline/citation/30958346/Cardiorespiratory_Fitness_Modifies_Influence_of_Sleep_Problems_on_Cerebrospinal_Fluid_Biomarkers_in_an_At_Risk_Cohort_ L2 - https://content.iospress.com/openurl?genre=article&id=doi:10.3233/JAD-180291 DB - PRIME DP - Unbound Medicine ER -