Evidence map›Paper›PMID 30958346›Full record

ArticleJournal of Alzheimer's disease : JAD2019

Cardiorespiratory Fitness Modifies Influence of Sleep Problems on Cerebrospinal Fluid Biomarkers in an At-Risk Cohort.

Lena L Law, Kate E Sprecher, Ryan J Dougherty, Dorothy F Edwards, Rebecca L Koscik, Catherine L Gallagher, Cynthia M Carlsson, Henrik Zetterberg, Kaj Blennow, Sanjay Asthana and 6 more

Open access · greenAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Article
  3. Modifiable Risk Factors for Alzheimer's Disease.Frontiers in aging neuroscience · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 3 countries.

Lena L LawGeriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA.
Kate E SprecherNeuroscience Training Program, University of Wisconsin-Madison, Madison, WI, USA.
Ryan J DoughertyDepartment of Kinesiology, University of Wisconsin School of Education, Madison, WI, USA.
Dorothy F EdwardsWisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Rebecca L KoscikWisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Catherine L GallagherGeriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA.
Cynthia M CarlssonGeriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA.
Henrik ZetterbergClinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Kaj BlennowClinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Sanjay AsthanaGeriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA.
Mark A SagerWisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Bruce P HermannWisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Sterling C JohnsonGeriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA.
Dane B CookDepartment of Kinesiology, University of Wisconsin School of Education, Madison, WI, USA.
Barbara B BendlinGeriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA.
Ozioma C OkonkwoGeriatric Research Education and Clinical Center, William S. Middleton Memorial Veterans Hospital, Madison, WI, USA.
University of Wisconsin–Madison · USGeriatric Research Education and Clinical Center · USWilliam S. Middleton Memorial Veterans Hospital · USUK Dementia Research Institute · GBUniversity of Gothenburg · SE

Funding

University of Wisconsin Institute for Clinical and Translational ResearchUL1TR002373 · NCATS · UNIVERSITY OF WISCONSIN-MADISON · PI ELIZABETH S BURNSIDE, Allan R. Brasier · 2017 to 2026
$75.9M
Wisconsin Registry for Alzheimer's Prevention: Sex Differences in DNA MethylationR01AG027161 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI Nathaniel Ark Chin, Sterling C Johnson · 2007 to 2026
$35.6M
INSTITUTIONAL CTSA (UW-MADISON): CLINICAL TRIALSUL1RR025011 · NCRR · UNIVERSITY OF WISCONSIN-MADISON · PI DREZNER, MARC KENNETH · 2007 to 2011
$29.5M
The Longitudinal Course of Neural Function and Amyloid in People At Risk for ADR01AG021155 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI Sterling C Johnson · 2004 to 2026
$27.0M
Wisconsin Registry for Alzheimer's PreventionRF1AG027161 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI JOHNSON, STERLING C · 2018 to 2018
$18.8M
Wisconsin Alzheimer's Disease Research CenterP50AG033514 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI ASTHANA, SANJAY · 2009 to 2018
$16.2M
White matter degeneration: biomarkers in preclinical Alzheimer's DiseaseR01AG037639 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI BENDLIN, BARBARA BRIGITTA · 2012 to 2023
$5.3M
Statin Effects on Beta-Amyloid and Cerebral Perfusion in Adults at Risk for ADR01AG031790 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI CARLSSON, CYNTHIA M · 2009 to 2013
$1.6M
Early detection of asymptomatic middle-age adults at risk for ADK23AG045957 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI OKONKWO, OZIOMA C · 2013 to 2017
$884k
White matter degeneration: biomarkers in preclinical Alzheimer's DiseaseR56AG037639 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI BENDLIN, BARBARA BRIGITTA · 2017 to 2017
$759k
Apnea and local sleep: Mechanism and intervention in preclinical Alzheimer'sR56AG052698 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI BENCA, RUTH M, BENDLIN, BARBARA BRIGITTA · 2016 to 2016
$748k
Genetic and Lifestyle Determinants of Cognitive Resilience in MidlifeR21AG051858 · NIA · UNIVERSITY OF WISCONSIN-MADISON · PI OKONKWO, OZIOMA C · 2016 to 2017
$441k
NCATS NIH HHS UL1 TR002373NCRR NIH HHS UL1 RR025011NIA NIH HHS F31 AG048732NIA NIH HHS K23 AG045957NIA NIH HHS P50 AG033514NIA NIH HHS R01 AG021155NIA NIH HHS R01 AG027161NIA NIH HHS R01 AG031790NIA NIH HHS R01 AG037639NIA NIH HHS R21 AG051858NIA NIH HHS R56 AG037639NIA NIH HHS R56 AG052698NIA NIH HHS RF1 AG027161
6 · The paper itself

Abstract

backgroundPrevious 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.

objectiveTo 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.

methodsSeventy-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.

resultsHigher 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.

conclusionIn 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.

Indexed as

AgedAlzheimer DiseaseAmyloid beta-PeptidesBiomarkersCardiorespiratory FitnessFemaleHumansMaleMiddle AgedPeptide FragmentsPhosphorylationSleepSleep Wake Disorderstau ProteinsAmyloid beta-PeptidesBiomarkersPeptide Fragmentstau ProteinsAlzheimer’s diseaseamyloid-β proteinbiomarkerscardiorespiratory fitnesscerebrospinal fluidsleeptau protein

Identifiers

PMID30958346
PMCPMC6675618
OpenAlexW2929889837

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.