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Poor sleep is associated with CSF biomarkers of amyloid pathology in cognitively normal adults.
Neurology. 2017 Aug 01; 89(5):445-453.Neur

Abstract

OBJECTIVE

To determine the relationship between sleep quality and CSF markers of Alzheimer disease (AD) pathology in late midlife.

METHODS

We investigated the relationship between sleep quality and CSF AD biomarkers in a cohort enriched for parental history of sporadic AD, the Wisconsin Registry for Alzheimer's Prevention. A total of 101 participants (mean age 62.9 ± 6.2 years, 65.3% female) completed sleep assessments and CSF collection and were cognitively normal. Sleep quality was measured with the Medical Outcomes Study Sleep Scale. CSF was assayed for biomarkers of amyloid metabolism and plaques (β-amyloid 42 [Aβ42]), tau pathology (phosphorylated tau [p-tau] 181), neuronal/axonal degeneration (total tau [t-tau], neurofilament light [NFL]), neuroinflammation/astroglial activation (monocyte chemoattractant protein-1 [MCP-1], chitinase-3-like protein 1 [YKL-40]), and synaptic dysfunction/degeneration (neurogranin). To adjust for individual differences in total amyloid production, Aβ42 was expressed relative to Aβ40. To assess cumulative pathology, CSF biomarkers were expressed in ratio to Aβ42. Relationships among sleep scores and CSF biomarkers were assessed with multiple regression, controlling for age, sex, time between sleep and CSF measurements, and CSF assay batch.

RESULTS

Worse subjective sleep quality, more sleep problems, and daytime somnolence were associated with greater AD pathology, indicated by lower CSF Aβ42/Aβ40 and higher t-tau/Aβ42, p-tau/Aβ42, MCP-1/Aβ42, and YKL-40/Aβ42. There were no significant associations between sleep and NFL or neurogranin.

CONCLUSIONS

Self-report of poor sleep was associated with greater AD-related pathology in cognitively healthy adults at risk for AD. Effective strategies exist for improving sleep; therefore sleep health may be a tractable target for early intervention to attenuate AD pathogenesis.

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Authors+Show Affiliations

Sprecher KE
From the Department of Medicine and Neuroscience Training Program (K.E.S.) and Wisconsin Alzheimer's Disease Research Center (C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.), University of Wisconsin-Madison; Wisconsin Alzheimer's Institute (R.L.K., C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.); Geriatric Research Education and Clinical Center (C.M.C., O.C.O., S.A., S.C.J., B.B.B.), Wm. S. Middleton Veterans Hospital, Madison, WI; Institute of Neuroscience and Physiology (H.Z., K.B.), University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; and Department of Psychiatry and Human Behavior (R.M.B.), University of California, Irvine. ksprecher@wisc.edu.
Koscik RL
From the Department of Medicine and Neuroscience Training Program (K.E.S.) and Wisconsin Alzheimer's Disease Research Center (C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.), University of Wisconsin-Madison; Wisconsin Alzheimer's Institute (R.L.K., C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.); Geriatric Research Education and Clinical Center (C.M.C., O.C.O., S.A., S.C.J., B.B.B.), Wm. S. Middleton Veterans Hospital, Madison, WI; Institute of Neuroscience and Physiology (H.Z., K.B.), University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; and Department of Psychiatry and Human Behavior (R.M.B.), University of California, Irvine.
Carlsson CM
From the Department of Medicine and Neuroscience Training Program (K.E.S.) and Wisconsin Alzheimer's Disease Research Center (C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.), University of Wisconsin-Madison; Wisconsin Alzheimer's Institute (R.L.K., C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.); Geriatric Research Education and Clinical Center (C.M.C., O.C.O., S.A., S.C.J., B.B.B.), Wm. S. Middleton Veterans Hospital, Madison, WI; Institute of Neuroscience and Physiology (H.Z., K.B.), University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; and Department of Psychiatry and Human Behavior (R.M.B.), University of California, Irvine.
Zetterberg H
From the Department of Medicine and Neuroscience Training Program (K.E.S.) and Wisconsin Alzheimer's Disease Research Center (C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.), University of Wisconsin-Madison; Wisconsin Alzheimer's Institute (R.L.K., C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.); Geriatric Research Education and Clinical Center (C.M.C., O.C.O., S.A., S.C.J., B.B.B.), Wm. S. Middleton Veterans Hospital, Madison, WI; Institute of Neuroscience and Physiology (H.Z., K.B.), University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; and Department of Psychiatry and Human Behavior (R.M.B.), University of California, Irvine.
Blennow K
From the Department of Medicine and Neuroscience Training Program (K.E.S.) and Wisconsin Alzheimer's Disease Research Center (C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.), University of Wisconsin-Madison; Wisconsin Alzheimer's Institute (R.L.K., C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.); Geriatric Research Education and Clinical Center (C.M.C., O.C.O., S.A., S.C.J., B.B.B.), Wm. S. Middleton Veterans Hospital, Madison, WI; Institute of Neuroscience and Physiology (H.Z., K.B.), University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; and Department of Psychiatry and Human Behavior (R.M.B.), University of California, Irvine.
Okonkwo OC
From the Department of Medicine and Neuroscience Training Program (K.E.S.) and Wisconsin Alzheimer's Disease Research Center (C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.), University of Wisconsin-Madison; Wisconsin Alzheimer's Institute (R.L.K., C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.); Geriatric Research Education and Clinical Center (C.M.C., O.C.O., S.A., S.C.J., B.B.B.), Wm. S. Middleton Veterans Hospital, Madison, WI; Institute of Neuroscience and Physiology (H.Z., K.B.), University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; and Department of Psychiatry and Human Behavior (R.M.B.), University of California, Irvine.
Sager MA
From the Department of Medicine and Neuroscience Training Program (K.E.S.) and Wisconsin Alzheimer's Disease Research Center (C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.), University of Wisconsin-Madison; Wisconsin Alzheimer's Institute (R.L.K., C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.); Geriatric Research Education and Clinical Center (C.M.C., O.C.O., S.A., S.C.J., B.B.B.), Wm. S. Middleton Veterans Hospital, Madison, WI; Institute of Neuroscience and Physiology (H.Z., K.B.), University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; and Department of Psychiatry and Human Behavior (R.M.B.), University of California, Irvine.
Asthana S
From the Department of Medicine and Neuroscience Training Program (K.E.S.) and Wisconsin Alzheimer's Disease Research Center (C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.), University of Wisconsin-Madison; Wisconsin Alzheimer's Institute (R.L.K., C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.); Geriatric Research Education and Clinical Center (C.M.C., O.C.O., S.A., S.C.J., B.B.B.), Wm. S. Middleton Veterans Hospital, Madison, WI; Institute of Neuroscience and Physiology (H.Z., K.B.), University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; and Department of Psychiatry and Human Behavior (R.M.B.), University of California, Irvine.
Johnson SC
From the Department of Medicine and Neuroscience Training Program (K.E.S.) and Wisconsin Alzheimer's Disease Research Center (C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.), University of Wisconsin-Madison; Wisconsin Alzheimer's Institute (R.L.K., C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.); Geriatric Research Education and Clinical Center (C.M.C., O.C.O., S.A., S.C.J., B.B.B.), Wm. S. Middleton Veterans Hospital, Madison, WI; Institute of Neuroscience and Physiology (H.Z., K.B.), University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; and Department of Psychiatry and Human Behavior (R.M.B.), University of California, Irvine.
Benca RM
From the Department of Medicine and Neuroscience Training Program (K.E.S.) and Wisconsin Alzheimer's Disease Research Center (C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.), University of Wisconsin-Madison; Wisconsin Alzheimer's Institute (R.L.K., C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.); Geriatric Research Education and Clinical Center (C.M.C., O.C.O., S.A., S.C.J., B.B.B.), Wm. S. Middleton Veterans Hospital, Madison, WI; Institute of Neuroscience and Physiology (H.Z., K.B.), University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; and Department of Psychiatry and Human Behavior (R.M.B.), University of California, Irvine.
Bendlin BB
From the Department of Medicine and Neuroscience Training Program (K.E.S.) and Wisconsin Alzheimer's Disease Research Center (C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.), University of Wisconsin-Madison; Wisconsin Alzheimer's Institute (R.L.K., C.M.C., O.C.O., M.A.S., S.A., S.C.J., B.B.B.); Geriatric Research Education and Clinical Center (C.M.C., O.C.O., S.A., S.C.J., B.B.B.), Wm. S. Middleton Veterans Hospital, Madison, WI; Institute of Neuroscience and Physiology (H.Z., K.B.), University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK; and Department of Psychiatry and Human Behavior (R.M.B.), University of California, Irvine.

MeSH

Amyloid beta-PeptidesBiomarkersChemokine CCL2Chitinase-3-Like Protein 1FemaleHumansLongitudinal StudiesMaleMental Status ScheduleMiddle AgedNeurofilament ProteinsNuclear ProteinsPeptide FragmentsPhosphorylationRNA-Binding ProteinsSelf ReportSleepSleep Wake Disorderstau Proteins

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28679595

Citation

Sprecher, Kate E., et al. "Poor Sleep Is Associated With CSF Biomarkers of Amyloid Pathology in Cognitively Normal Adults." Neurology, vol. 89, no. 5, 2017, pp. 445-453.
Sprecher KE, Koscik RL, Carlsson CM, et al. Poor sleep is associated with CSF biomarkers of amyloid pathology in cognitively normal adults. Neurology. 2017;89(5):445-453.
Sprecher, K. E., Koscik, R. L., Carlsson, C. M., Zetterberg, H., Blennow, K., Okonkwo, O. C., Sager, M. A., Asthana, S., Johnson, S. C., Benca, R. M., & Bendlin, B. B. (2017). Poor sleep is associated with CSF biomarkers of amyloid pathology in cognitively normal adults. Neurology, 89(5), 445-453. https://doi.org/10.1212/WNL.0000000000004171
Sprecher KE, et al. Poor Sleep Is Associated With CSF Biomarkers of Amyloid Pathology in Cognitively Normal Adults. Neurology. 2017 Aug 1;89(5):445-453. PubMed PMID: 28679595.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Poor sleep is associated with CSF biomarkers of amyloid pathology in cognitively normal adults. AU - Sprecher,Kate E, AU - Koscik,Rebecca L, AU - Carlsson,Cynthia M, AU - Zetterberg,Henrik, AU - Blennow,Kaj, AU - Okonkwo,Ozioma C, AU - Sager,Mark A, AU - Asthana,Sanjay, AU - Johnson,Sterling C, AU - Benca,Ruth M, AU - Bendlin,Barbara B, Y1 - 2017/07/05/ PY - 2016/08/28/received PY - 2017/04/14/accepted PY - 2017/7/7/pubmed PY - 2017/8/5/medline PY - 2017/7/7/entrez SP - 445 EP - 453 JF - Neurology JO - Neurology VL - 89 IS - 5 N2 - OBJECTIVE: To determine the relationship between sleep quality and CSF markers of Alzheimer disease (AD) pathology in late midlife. METHODS: We investigated the relationship between sleep quality and CSF AD biomarkers in a cohort enriched for parental history of sporadic AD, the Wisconsin Registry for Alzheimer's Prevention. A total of 101 participants (mean age 62.9 ± 6.2 years, 65.3% female) completed sleep assessments and CSF collection and were cognitively normal. Sleep quality was measured with the Medical Outcomes Study Sleep Scale. CSF was assayed for biomarkers of amyloid metabolism and plaques (β-amyloid 42 [Aβ42]), tau pathology (phosphorylated tau [p-tau] 181), neuronal/axonal degeneration (total tau [t-tau], neurofilament light [NFL]), neuroinflammation/astroglial activation (monocyte chemoattractant protein-1 [MCP-1], chitinase-3-like protein 1 [YKL-40]), and synaptic dysfunction/degeneration (neurogranin). To adjust for individual differences in total amyloid production, Aβ42 was expressed relative to Aβ40. To assess cumulative pathology, CSF biomarkers were expressed in ratio to Aβ42. Relationships among sleep scores and CSF biomarkers were assessed with multiple regression, controlling for age, sex, time between sleep and CSF measurements, and CSF assay batch. RESULTS: Worse subjective sleep quality, more sleep problems, and daytime somnolence were associated with greater AD pathology, indicated by lower CSF Aβ42/Aβ40 and higher t-tau/Aβ42, p-tau/Aβ42, MCP-1/Aβ42, and YKL-40/Aβ42. There were no significant associations between sleep and NFL or neurogranin. CONCLUSIONS: Self-report of poor sleep was associated with greater AD-related pathology in cognitively healthy adults at risk for AD. Effective strategies exist for improving sleep; therefore sleep health may be a tractable target for early intervention to attenuate AD pathogenesis. SN - 1526-632X UR - https://www.unboundmedicine.com/medline/citation/28679595/full_citation L2 - http://www.neurology.org/cgi/pmidlookup?view=long&pmid=28679595 DB - PRIME DP - Unbound Medicine ER -