Alzheimer's disease cerebrospinal fluid biomarkers predict cognitive decline in lewy body dementia

ABSTRACT Introduction Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta 1‐42, total tau, and tau phosphorylated at threonine 181 reflect Alzheimer's disease neuropathology antemortem. In PD, low C...

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Published inMovement disorders Vol. 31; no. 8; pp. 1203 - 1208
Main Authors Abdelnour, Carla, van Steenoven, Inger, Londos, Elisabet, Blanc, Frédéric, Auestad, Bjørn, Kramberger, Milica G., Zetterberg, Henrik, Mollenhauer, Brit, Boada, Mercè, Aarsland, Dag
Format Journal Article
LanguageEnglish
Published United States Blackwell Publishing Ltd 01.08.2016
Wiley Subscription Services, Inc
Wiley
Subjects
a-beta
Aged
Aged, 80 and over
alpha-synuclein
Alzheimer Disease - cerebrospinal fluid
Alzheimer Disease - physiopathology
Alzheimer's disease
Amyloid beta-Peptides - cerebrospinal fluid
Biomarkers
bodies
Cerebrospinal fluid
Clinical Medicine
Cognitive ability
cognitive decline
csf amyloid-beta
CSF biomarkers
Dementia
Dementia disorders
differential-diagnosis
Disease Progression
Female
Follow-Up Studies
Humans
Klinisk medicin
Lewy bodies
Lewy body dementia
Lewy Body Disease - cerebrospinal fluid
Lewy Body Disease - physiopathology
Life Sciences
Male
Medical and Health Sciences
Medicin och hälsovetenskap
Mental Status and Dementia Tests
mini-mental-state
Movement disorders
Neurodegenerative diseases
Neurologi
Neurology
Neurons and Cognition
Neurosciences
Neurosciences & Neurology
Neurovetenskaper
Parkinson's disease
parkinsons-disease
pathology
Peptide Fragments - cerebrospinal fluid
Prognosis
Tau protein
tau Proteins - cerebrospinal fluid
Threonine
Vitamin E
β-Amyloid
CSF biomarkers
cognitive decline
Lewy body dementia
Online AccessGet full text

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Abstract ABSTRACT Introduction Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta 1‐42, total tau, and tau phosphorylated at threonine 181 reflect Alzheimer's disease neuropathology antemortem. In PD, low CSF amyloid beta 1‐42 predict long‐term cognitive decline, but little is known about these biomarkers as predictors for cognitive decline in Lewy body dementia. The aim of this study was to assess whether Alzheimer's disease CSF biomarkers predict cognitive decline in Lewy body dementia. Methods From a large European dementia with Lewy bodies multicenter study, we analyzed baseline Alzheimer's disease CSF biomarkers and serial MMSE (baseline and 1‐ and 2‐year follow‐up) in 100 patients with Lewy body dementia. Linear mixed‐effects analyses, adjusted for sex, age, baseline MMSE, and education, were performed to model the association between CSF biomarkers and rate of cognitive decline measured with MMSE. An Alzheimer's disease CSF profile was defined as pathological amyloid beta 1‐42 plus pathological total tau or phosphorylated tau. Results The Alzheimer's disease CSF profile, and pathological levels of amyloid beta 1‐42, were associated with a more rapid decline in MMSE (2.2 [P < 0.05] and 2.9 points difference [P < 0.01], respectively). Higher total tau values showed a trend toward association without statistical significance (2.0 points difference; P = 0.064), whereas phosphorylated tau was not associated with decline. Conclusions Reduced levels of CSF amyloid beta 1‐42 were associated with more rapid cognitive decline in Lewy body dementia patients. Future prospective studies should include larger samples, centralized CSF analyses, longer follow‐up, and biomarker‐pathology correlation. © 2016 International Parkinson and Movement Disorder Society
AbstractList Introduction Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta 1-42, total tau, and tau phosphorylated at threonine 181 reflect Alzheimer's disease neuropathology antemortem. In PD, low CSF amyloid beta 1-42 predict long-term cognitive decline, but little is known about these biomarkers as predictors for cognitive decline in Lewy body dementia. The aim of this study was to assess whether Alzheimer's disease CSF biomarkers predict cognitive decline in Lewy body dementia. Methods From a large European dementia with Lewy bodies multicenter study, we analyzed baseline Alzheimer's disease CSF biomarkers and serial MMSE (baseline and 1- and 2-year follow-up) in 100 patients with Lewy body dementia. Linear mixed-effects analyses, adjusted for sex, age, baseline MMSE, and education, were performed to model the association between CSF biomarkers and rate of cognitive decline measured with MMSE. An Alzheimer's disease CSF profile was defined as pathological amyloid beta 1-42 plus pathological total tau or phosphorylated tau. Results The Alzheimer's disease CSF profile, and pathological levels of amyloid beta 1-42, were associated with a more rapid decline in MMSE (2.2 [P < 0.05] and 2.9 points difference [P < 0.01], respectively). Higher total tau values showed a trend toward association without statistical significance (2.0 points difference; P = 0.064), whereas phosphorylated tau was not associated with decline. Conclusions Reduced levels of CSF amyloid beta 1-42 were associated with more rapid cognitive decline in Lewy body dementia patients. Future prospective studies should include larger samples, centralized CSF analyses, longer follow-up, and biomarker-pathology correlation. copyright 2016 International Parkinson and Movement Disorder Society
Introduction Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta 1-42, total tau, and tau phosphorylated at threonine 181 reflect Alzheimer's disease neuropathology antemortem. In PD, low CSF amyloid beta 1-42 predict long-term cognitive decline, but little is known about these biomarkers as predictors for cognitive decline in Lewy body dementia. The aim of this study was to assess whether Alzheimer's disease CSF biomarkers predict cognitive decline in Lewy body dementia. Methods From a large European dementia with Lewy bodies multicenter study, we analyzed baseline Alzheimer's disease CSF biomarkers and serial MMSE (baseline and 1- and 2-year follow-up) in 100 patients with Lewy body dementia. Linear mixed-effects analyses, adjusted for sex, age, baseline MMSE, and education, were performed to model the association between CSF biomarkers and rate of cognitive decline measured with MMSE. An Alzheimer's disease CSF profile was defined as pathological amyloid beta 1-42 plus pathological total tau or phosphorylated tau. Results The Alzheimer's disease CSF profile, and pathological levels of amyloid beta 1-42, were associated with a more rapid decline in MMSE (2.2 [P < 0.05] and 2.9 points difference [P < 0.01], respectively). Higher total tau values showed a trend toward association without statistical significance (2.0 points difference; P = 0.064), whereas phosphorylated tau was not associated with decline. Conclusions Reduced levels of CSF amyloid beta 1-42 were associated with more rapid cognitive decline in Lewy body dementia patients. Future prospective studies should include larger samples, centralized CSF analyses, longer follow-up, and biomarker-pathology correlation. © 2016 International Parkinson and Movement Disorder Society
Introduction: Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta 1-42, total tau, and tau phosphorylated at threonine 181 reflect Alzheimer's disease neuropathology antemortem. In PD, low CSF amyloid beta 1-42 predict long-term cognitive decline, but little is known about these biomarkers as predictors for cognitive decline in Lewy body dementia. The aim of this study was to assess whether Alzheimer's disease CSF biomarkers predict cognitive decline in Lewy body dementia. Methods: From a large European dementia with Lewy bodies multicenter study, we analyzed baseline Alzheimer's disease CSF biomarkers and serial MMSE (baseline and 1- and 2-year follow-up) in 100 patients with Lewy body dementia. Linear mixed-effects analyses, adjusted for sex, age, baseline MMSE, and education, were performed to model the association between CSF biomarkers and rate of cognitive decline measured with MMSE. An Alzheimer's disease CSF profile was defined as pathological amyloid beta 1-42 plus pathological total tau or phosphorylated tau. Results: The Alzheimer's disease CSF profile, and pathological levels of amyloid beta 1-42, were associated with a more rapid decline in MMSE (2.2 [P < 0.05] and 2.9 points difference [P < 0.01], respectively). Higher total tau values showed a trend toward association without statistical significance (2.0 points difference; P = 0.064), whereas phosphorylated tau was not associated with decline. Conclusions: Reduced levels of CSF amyloid beta 1-42 were associated with more rapid cognitive decline in Lewy body dementia patients. Future prospective studies should include larger samples, centralized CSF analyses, longer follow-up, and biomarker-pathology correlation.
ABSTRACT Introduction Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta 1‐42, total tau, and tau phosphorylated at threonine 181 reflect Alzheimer's disease neuropathology antemortem. In PD, low CSF amyloid beta 1‐42 predict long‐term cognitive decline, but little is known about these biomarkers as predictors for cognitive decline in Lewy body dementia. The aim of this study was to assess whether Alzheimer's disease CSF biomarkers predict cognitive decline in Lewy body dementia. Methods From a large European dementia with Lewy bodies multicenter study, we analyzed baseline Alzheimer's disease CSF biomarkers and serial MMSE (baseline and 1‐ and 2‐year follow‐up) in 100 patients with Lewy body dementia. Linear mixed‐effects analyses, adjusted for sex, age, baseline MMSE, and education, were performed to model the association between CSF biomarkers and rate of cognitive decline measured with MMSE. An Alzheimer's disease CSF profile was defined as pathological amyloid beta 1‐42 plus pathological total tau or phosphorylated tau. Results The Alzheimer's disease CSF profile, and pathological levels of amyloid beta 1‐42, were associated with a more rapid decline in MMSE (2.2 [P < 0.05] and 2.9 points difference [P < 0.01], respectively). Higher total tau values showed a trend toward association without statistical significance (2.0 points difference; P = 0.064), whereas phosphorylated tau was not associated with decline. Conclusions Reduced levels of CSF amyloid beta 1‐42 were associated with more rapid cognitive decline in Lewy body dementia patients. Future prospective studies should include larger samples, centralized CSF analyses, longer follow‐up, and biomarker‐pathology correlation. © 2016 International Parkinson and Movement Disorder Society
Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta 1-42, total tau, and tau phosphorylated at threonine 181 reflect Alzheimer's disease neuropathology antemortem. In PD, low CSF amyloid beta 1-42 predict long-term cognitive decline, but little is known about these biomarkers as predictors for cognitive decline in Lewy body dementia. The aim of this study was to assess whether Alzheimer's disease CSF biomarkers predict cognitive decline in Lewy body dementia. From a large European dementia with Lewy bodies multicenter study, we analyzed baseline Alzheimer's disease CSF biomarkers and serial MMSE (baseline and 1- and 2-year follow-up) in 100 patients with Lewy body dementia. Linear mixed-effects analyses, adjusted for sex, age, baseline MMSE, and education, were performed to model the association between CSF biomarkers and rate of cognitive decline measured with MMSE. An Alzheimer's disease CSF profile was defined as pathological amyloid beta 1-42 plus pathological total tau or phosphorylated tau. The Alzheimer's disease CSF profile, and pathological levels of amyloid beta 1-42, were associated with a more rapid decline in MMSE (2.2 [P < 0.05] and 2.9 points difference [P < 0.01], respectively). Higher total tau values showed a trend toward association without statistical significance (2.0 points difference; P = 0.064), whereas phosphorylated tau was not associated with decline. Reduced levels of CSF amyloid beta 1-42 were associated with more rapid cognitive decline in Lewy body dementia patients. Future prospective studies should include larger samples, centralized CSF analyses, longer follow-up, and biomarker-pathology correlation. © 2016 International Parkinson and Movement Disorder Society.
IntroductionAlzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta 1-42, total tau, and tau phosphorylated at threonine 181 reflect Alzheimer's disease neuropathology antemortem. In PD, low CSF amyloid beta 1-42 predict long-term cognitive decline, but little is known about these biomarkers as predictors for cognitive decline in Lewy body dementia. The aim of this study was to assess whether Alzheimer's disease CSF biomarkers predict cognitive decline in Lewy body dementia. MethodsFrom a large European dementia with Lewy bodies multicenter study, we analyzed baseline Alzheimer's disease CSF biomarkers and serial MMSE (baseline and 1- and 2-year follow-up) in 100 patients with Lewy body dementia. Linear mixed-effects analyses, adjusted for sex, age, baseline MMSE, and education, were performed to model the association between CSF biomarkers and rate of cognitive decline measured with MMSE. An Alzheimer's disease CSF profile was defined as pathological amyloid beta 1-42 plus pathological total tau or phosphorylated tau. ResultsThe Alzheimer's disease CSF profile, and pathological levels of amyloid beta 1-42, were associated with a more rapid decline in MMSE (2.2 [P < 0.05] and 2.9 points difference [P < 0.01], respectively). Higher total tau values showed a trend toward association without statistical significance (2.0 points difference; P = 0.064), whereas phosphorylated tau was not associated with decline. ConclusionsReduced levels of CSF amyloid beta 1-42 were associated with more rapid cognitive decline in Lewy body dementia patients. Future prospective studies should include larger samples, centralized CSF analyses, longer follow-up, and biomarker-pathology correlation. (c) 2016 International Parkinson and Movement Disorder Society
Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta 1-42, total tau, and tau phosphorylated at threonine 181 reflect Alzheimer's disease neuropathology antemortem. In PD, low CSF amyloid beta 1-42 predict long-term cognitive decline, but little is known about these biomarkers as predictors for cognitive decline in Lewy body dementia. The aim of this study was to assess whether Alzheimer's disease CSF biomarkers predict cognitive decline in Lewy body dementia.INTRODUCTIONAlzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta 1-42, total tau, and tau phosphorylated at threonine 181 reflect Alzheimer's disease neuropathology antemortem. In PD, low CSF amyloid beta 1-42 predict long-term cognitive decline, but little is known about these biomarkers as predictors for cognitive decline in Lewy body dementia. The aim of this study was to assess whether Alzheimer's disease CSF biomarkers predict cognitive decline in Lewy body dementia.From a large European dementia with Lewy bodies multicenter study, we analyzed baseline Alzheimer's disease CSF biomarkers and serial MMSE (baseline and 1- and 2-year follow-up) in 100 patients with Lewy body dementia. Linear mixed-effects analyses, adjusted for sex, age, baseline MMSE, and education, were performed to model the association between CSF biomarkers and rate of cognitive decline measured with MMSE. An Alzheimer's disease CSF profile was defined as pathological amyloid beta 1-42 plus pathological total tau or phosphorylated tau.METHODSFrom a large European dementia with Lewy bodies multicenter study, we analyzed baseline Alzheimer's disease CSF biomarkers and serial MMSE (baseline and 1- and 2-year follow-up) in 100 patients with Lewy body dementia. Linear mixed-effects analyses, adjusted for sex, age, baseline MMSE, and education, were performed to model the association between CSF biomarkers and rate of cognitive decline measured with MMSE. An Alzheimer's disease CSF profile was defined as pathological amyloid beta 1-42 plus pathological total tau or phosphorylated tau.The Alzheimer's disease CSF profile, and pathological levels of amyloid beta 1-42, were associated with a more rapid decline in MMSE (2.2 [P < 0.05] and 2.9 points difference [P < 0.01], respectively). Higher total tau values showed a trend toward association without statistical significance (2.0 points difference; P = 0.064), whereas phosphorylated tau was not associated with decline.RESULTSThe Alzheimer's disease CSF profile, and pathological levels of amyloid beta 1-42, were associated with a more rapid decline in MMSE (2.2 [P < 0.05] and 2.9 points difference [P < 0.01], respectively). Higher total tau values showed a trend toward association without statistical significance (2.0 points difference; P = 0.064), whereas phosphorylated tau was not associated with decline.Reduced levels of CSF amyloid beta 1-42 were associated with more rapid cognitive decline in Lewy body dementia patients. Future prospective studies should include larger samples, centralized CSF analyses, longer follow-up, and biomarker-pathology correlation. © 2016 International Parkinson and Movement Disorder Society.CONCLUSIONSReduced levels of CSF amyloid beta 1-42 were associated with more rapid cognitive decline in Lewy body dementia patients. Future prospective studies should include larger samples, centralized CSF analyses, longer follow-up, and biomarker-pathology correlation. © 2016 International Parkinson and Movement Disorder Society.
Author van Steenoven, Inger
Blanc, Frédéric
Auestad, Bjørn
Aarsland, Dag
Zetterberg, Henrik
Mollenhauer, Brit
Boada, Mercè
Abdelnour, Carla
Londos, Elisabet
Kramberger, Milica G.
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  organization: Alzheimer Center, Department of Neurology, VU Medical Center, Amsterdam, The Netherlands
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  surname: Londos
  fullname: Londos, Elisabet
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  surname: Blanc
  fullname: Blanc, Frédéric
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  givenname: Henrik
  surname: Zetterberg
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  organization: Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden
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  givenname: Brit
  surname: Mollenhauer
  fullname: Mollenhauer, Brit
  organization: Paracelsus-Elena-Klinik, Kassel and University Medical Center, Department of Neurosurgery and Institute of Neuropathology, Göttingen, Germany
– sequence: 9
  givenname: Mercè
  surname: Boada
  fullname: Boada, Mercè
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ContentType Journal Article
Copyright 2016 International Parkinson and Movement Disorder Society
2016 International Parkinson and Movement Disorder Society.
Distributed under a Creative Commons Attribution 4.0 International License
Copyright_xml – notice: 2016 International Parkinson and Movement Disorder Society
– notice: 2016 International Parkinson and Movement Disorder Society.
– notice: Distributed under a Creative Commons Attribution 4.0 International License
CorporateAuthor on behalf of the European DLB Consortium
European DLB Consortium
MultiPark: Multidisciplinary research focused on Parkinson's disease
Lunds universitet
Profile areas and other strong research environments
Department of Clinical Sciences, Malmö
Lund University
Strategiska forskningsområden (SFO)
Faculty of Medicine
Strategic research areas (SRA)
Clinical Memory Research
Klinisk minnesforskning
Medicinska fakulteten
Profilområden och andra starka forskningsmiljöer
Institutionen för kliniska vetenskaper, Malmö
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– name: Strategic research areas (SRA)
– name: Lunds universitet
– name: Klinisk minnesforskning
– name: Profilområden och andra starka forskningsmiljöer
– name: Lund University
– name: Profile areas and other strong research environments
– name: MultiPark: Multidisciplinary research focused on Parkinson's disease
– name: Department of Clinical Sciences, Malmö
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Issue 8
Keywords CSF biomarkers
cognitive decline
Lewy body dementia
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
2016 International Parkinson and Movement Disorder Society.
Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0
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This article was published online on 14 June 2016. After online publication, the Acknowledgments were revised. This notice is included in the online and print versions to indicate that both have been corrected on 27 June 2016.
Relevant conflicts of interest/financial disclosures
Funding agencies
This research has been partially funded by JNPD.
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References Vanderstichele H, De Vreese K, Blennow K, et al. Analytical performance and clinical utility of the INNOTEST® PHOSPHO-TAU (181P) assay for discrimination between Alzheimer's disease and dementia with Lewy bodies. Clin Chem Lab Med 2006;44:1472-1480.
Lebedev AV, Westman E, Beyer M, et al. Multivariate classification of patients with Alzheimer's and dementia with Lewy bodies using high-dimensional cortical thickness measurements: an MRI surface-based morphometric study. J Neurol 2013;260:1104-1115.
Wang CS, Pai MC, Chen PL, Hou NT, Chien PF, Huang YC. Montreal Cognitive Assessment and Mini-Mental State Examination performance in patients with mild-to-moderate dementia with Lewy bodies, Alzheimer's disease, and normal participants in Taiwan. Int Psychogeriatr 2013;25:1839-1848.
Hansson O, Hall S, Öhrfelt A, et al. Levels of cerebrospinal fluid α-synuclein oligomers are increased in Parkinson's disease with dementia and dementia with Lewy bodies compared to Alzheimer's disease. Alzheimers Res Ther 2014;6:1-6.
Alves G, Brønnick K, Aarsland D, et al. CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's disease: the Norwegian ParkWest study. J Neurol Neurosurg Psychiatry 2010;81:1080-1086.
Liu C, Cholerton B, Shi M, et al. CSF tau and tau/Aβ 42 predict cognitive decline in Parkinson's disease. Parkinsonism Relat Disord 2015;21:271-276.
McKeith I, Ballard C, Perry R, et al. Prospective validation of consensus criteria for the diagnosis of dementia with Lewy bodies. Neurology 2000;54:1050-1058.
R Foundation for Statistical Computing. R: A language and environment for statistical computing [computer program]. Vienna, Austria: R Foundation for Statistical Computing; 2014.
Wennström M, Hall S, Nägga K, Londos E, Minthon L, Hansson O. Cerebrospinal fluid levels of IL-6 are decreased and correlate with cognitive status in DLB patients. Alzheimers Res Ther 2015;7:1-8.
Boström F, Hansson O, Blennow K, et al. Cerebrospinal fluid total tau is associated with shorter survival in dementia with Lewy bodies. Dement Geriatr Cogn Disord 2009;28:314-319.
Schoonenboom N, Reesink F, Verwey N, et al. Cerebrospinal fluid markers for differential dementia diagnosis in a large memory clinic cohort. Neurology 2012;78:47-54.
Wang ZY, Han ZM, Liu QF, Tang W, Ye K, Yao YY. Use of CSF α-synuclein in the differential diagnosis between Alzheimer's disease and other neurodegenerative disorders. Int Psychogeriatr 2015;27:1429-1438.
Clinton LK, Blurton-Jones M, Myczek K, Trojanowski JQ, LaFerla FM. Synergistic interactions between Aβ, tau, and α-synuclein: acceleration of neuropathology and cognitive decline. J Neurosci 2010;30:7281-7289.
Mollenhauer B, Parnetti L, Rektorova I, et al. Biological confounders for the values of cerebrospinal fluid proteins in Parkinson's disease and related disorders. J Neurochem 2015 Oct 10. doi: 10.1111/jnc.13390. [Epub ahead of print]
McKeith I, Dickson D, Lowe J, et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology 2005;65:1863-1872.
Folstein MF, Folstein SE, McHugh PR. "Mini-mental state": a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975;12:189-198.
Gomperts SN. Imaging the role of amyloid in PD dementia and dementia with Lewy bodies. Curr Neurol Neurosci Rep 2014;14:472.
Howlett DR, Whitfield D, Johnson M, et al. Regional Multiple Pathology Scores are associated with cognitive decline in Lewy body dementias. Brain Pathol 2015;25:401-408.
Zetterberg H. Cerebrospinal fluid biomarkers for Alzheimer's disease: current limitations and recent developments. Curr Opin Psychiatry 2015;28:402-409.
Ballard C, O'Brien J, Morris CM, Barber R, Swann A, Neil D, McKeith I. The progression of cognitive impairment in dementia with Lewy bodies, vascular dementia and Alzheimer's disease. Int J Geriatr Psychiatry 2011;16:499-503.
Wang HF, Yu JT, Tang SW, et al. Efficacy and safety of cholinesterase inhibitors and memantine in cognitive impairment in Parkinson's disease, Parkinson's disease dementia, and dementia with Lewy bodies: systematic review with meta-analysis and trial sequential analysis. J Neurol Neurosurg Psychiatry 2015;86:135-143.
Kaerst L, Kuhlmann A, Wedekind D, Stoeck K, Lange P, Zerr I. Using cerebrospinal fluid marker profiles in clinical diagnosis of dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. J Alzheimers Dis 2014;38:63-73.
Terrelonge M, Jr., Marder KS, Weintraub D, Alcalay RN. CSF β-amyloid 1-42 predicts progression to cognitive impairment in newly diagnosed Parkinson disease. J Mol Neurosci 2016;58:88-92.
Vranová HP, Hényková E, Kaiserová M, et al. Tau protein, beta-amyloid1-42 and clusterin CSF levels in the differential diagnosis of Parkinsonian syndrome with dementia. J Neurol Sci 2014;343:120-124.
Walker Z, Possin KL, Boeve BF, Aarsland D. Lewy body dementias. Lancet 2015;386:1683-1697.
Mollenhauer B, Trenkwalder C, von Ahsen N, et al. Beta-amlyoid 1-42 and tau-protein in cerebrospinal fluid of patients with Parkinson's disease dementia. Dement Geriatr Cogn Disord 2006;22:200-208.
Slaets S, Le Bastard N, Theuns J, et al. Amyloid pathology influences aβ1-42 cerebrospinal fluid levels in dementia with lewy bodies. J Alzheimers Dis 2013 ;35:137-146.
Biundo R, Weis L, Bostantjopoulou S, et al. MMSE and MoCA in Parkinson's disease and dementia with Lewy bodies: a multicenter 1-year follow-up study. J Neural Transm (Vienna) 2016;123:431-438.
Portelius E, Mattsson N, Andreasson U, Blennow K, Zetterberg H. Novel Aβ isoforms in Alzheimer's disease-their role in diagnosis and treatment. Curr Pharm Des 2011;17:2594-2602.
Kraybill ML, Larson EB, Tsuang D, et al. Cognitive differences in dementia patients with autopsy-verified AD, Lewy body pathology, or both. Neurology 2005;64:2069-2073.
Hall S, Surova Y, Öhrfelt A, Zetterberg H, Lindqvist D, Hansson O. CSF biomarkers and clinical progression of Parkinson disease. Neurology 2015;84:57-63.
Siderowf A, Xie SX, Hurtig H, et al. CSF amyloid {beta} 1-42 predicts cognitive decline in Parkinson disease. Neurology 2010;75:1055-1061.
Parnetti L, Farotti L, Eusebi P, et al. Differential role of CSF alpha-synuclein species, tau, and Aβ42 in Parkinson's disease. Front Aging Neurosci 2014;6:53.
Duits FH, Teunissen CE, Bouwman FH, et al. The cerebrospinal fluid "Alzheimer profile": easily said, but what does it mean? Alzheimers Dement 2014;10:713-723.
Brunnström H, Hansson O, Zetterberg H, Londos E, Englund E. Correlations of CSF tau and amyloid levels with Alzheimer pathology in neuropathologically verified dementia with Lewy bodies. Int J Geriatr Psychiatry 2013;28:738-744.
Buongiorno M, Compta Y, Martí MJ. Amyloid-β and τ biomarkers in Parkinson's disease-dementia. J Neurol Sci 2011;310:25-30.
Kandiah N, Zhang A, Cenina AR, Au WL, Nadkarni N, Tan LC. Montreal Cognitive Assessment for the screening and prediction of cognitive decline in early Parkinson's disease. Parkinsonism Relat Disord 2014;20:1145-1148.
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30991465 - Mov Disord. 2019 Apr;34(4):593
References_xml – reference: Zetterberg H. Cerebrospinal fluid biomarkers for Alzheimer's disease: current limitations and recent developments. Curr Opin Psychiatry 2015;28:402-409.
– reference: Kandiah N, Zhang A, Cenina AR, Au WL, Nadkarni N, Tan LC. Montreal Cognitive Assessment for the screening and prediction of cognitive decline in early Parkinson's disease. Parkinsonism Relat Disord 2014;20:1145-1148.
– reference: Mollenhauer B, Parnetti L, Rektorova I, et al. Biological confounders for the values of cerebrospinal fluid proteins in Parkinson's disease and related disorders. J Neurochem 2015 Oct 10. doi: 10.1111/jnc.13390. [Epub ahead of print]
– reference: Wang CS, Pai MC, Chen PL, Hou NT, Chien PF, Huang YC. Montreal Cognitive Assessment and Mini-Mental State Examination performance in patients with mild-to-moderate dementia with Lewy bodies, Alzheimer's disease, and normal participants in Taiwan. Int Psychogeriatr 2013;25:1839-1848.
– reference: Ballard C, O'Brien J, Morris CM, Barber R, Swann A, Neil D, McKeith I. The progression of cognitive impairment in dementia with Lewy bodies, vascular dementia and Alzheimer's disease. Int J Geriatr Psychiatry 2011;16:499-503.
– reference: Biundo R, Weis L, Bostantjopoulou S, et al. MMSE and MoCA in Parkinson's disease and dementia with Lewy bodies: a multicenter 1-year follow-up study. J Neural Transm (Vienna) 2016;123:431-438.
– reference: Walker Z, Possin KL, Boeve BF, Aarsland D. Lewy body dementias. Lancet 2015;386:1683-1697.
– reference: Brunnström H, Hansson O, Zetterberg H, Londos E, Englund E. Correlations of CSF tau and amyloid levels with Alzheimer pathology in neuropathologically verified dementia with Lewy bodies. Int J Geriatr Psychiatry 2013;28:738-744.
– reference: Boström F, Hansson O, Blennow K, et al. Cerebrospinal fluid total tau is associated with shorter survival in dementia with Lewy bodies. Dement Geriatr Cogn Disord 2009;28:314-319.
– reference: Portelius E, Mattsson N, Andreasson U, Blennow K, Zetterberg H. Novel Aβ isoforms in Alzheimer's disease-their role in diagnosis and treatment. Curr Pharm Des 2011;17:2594-2602.
– reference: Slaets S, Le Bastard N, Theuns J, et al. Amyloid pathology influences aβ1-42 cerebrospinal fluid levels in dementia with lewy bodies. J Alzheimers Dis 2013 ;35:137-146.
– reference: Mollenhauer B, Trenkwalder C, von Ahsen N, et al. Beta-amlyoid 1-42 and tau-protein in cerebrospinal fluid of patients with Parkinson's disease dementia. Dement Geriatr Cogn Disord 2006;22:200-208.
– reference: Wang ZY, Han ZM, Liu QF, Tang W, Ye K, Yao YY. Use of CSF α-synuclein in the differential diagnosis between Alzheimer's disease and other neurodegenerative disorders. Int Psychogeriatr 2015;27:1429-1438.
– reference: Folstein MF, Folstein SE, McHugh PR. "Mini-mental state": a practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res 1975;12:189-198.
– reference: Gomperts SN. Imaging the role of amyloid in PD dementia and dementia with Lewy bodies. Curr Neurol Neurosci Rep 2014;14:472.
– reference: Vanderstichele H, De Vreese K, Blennow K, et al. Analytical performance and clinical utility of the INNOTEST® PHOSPHO-TAU (181P) assay for discrimination between Alzheimer's disease and dementia with Lewy bodies. Clin Chem Lab Med 2006;44:1472-1480.
– reference: Siderowf A, Xie SX, Hurtig H, et al. CSF amyloid {beta} 1-42 predicts cognitive decline in Parkinson disease. Neurology 2010;75:1055-1061.
– reference: Kraybill ML, Larson EB, Tsuang D, et al. Cognitive differences in dementia patients with autopsy-verified AD, Lewy body pathology, or both. Neurology 2005;64:2069-2073.
– reference: Wang HF, Yu JT, Tang SW, et al. Efficacy and safety of cholinesterase inhibitors and memantine in cognitive impairment in Parkinson's disease, Parkinson's disease dementia, and dementia with Lewy bodies: systematic review with meta-analysis and trial sequential analysis. J Neurol Neurosurg Psychiatry 2015;86:135-143.
– reference: McKeith I, Dickson D, Lowe J, et al. Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium. Neurology 2005;65:1863-1872.
– reference: Howlett DR, Whitfield D, Johnson M, et al. Regional Multiple Pathology Scores are associated with cognitive decline in Lewy body dementias. Brain Pathol 2015;25:401-408.
– reference: Liu C, Cholerton B, Shi M, et al. CSF tau and tau/Aβ 42 predict cognitive decline in Parkinson's disease. Parkinsonism Relat Disord 2015;21:271-276.
– reference: Kaerst L, Kuhlmann A, Wedekind D, Stoeck K, Lange P, Zerr I. Using cerebrospinal fluid marker profiles in clinical diagnosis of dementia with Lewy bodies, Parkinson's disease, and Alzheimer's disease. J Alzheimers Dis 2014;38:63-73.
– reference: Wennström M, Hall S, Nägga K, Londos E, Minthon L, Hansson O. Cerebrospinal fluid levels of IL-6 are decreased and correlate with cognitive status in DLB patients. Alzheimers Res Ther 2015;7:1-8.
– reference: Parnetti L, Farotti L, Eusebi P, et al. Differential role of CSF alpha-synuclein species, tau, and Aβ42 in Parkinson's disease. Front Aging Neurosci 2014;6:53.
– reference: Clinton LK, Blurton-Jones M, Myczek K, Trojanowski JQ, LaFerla FM. Synergistic interactions between Aβ, tau, and α-synuclein: acceleration of neuropathology and cognitive decline. J Neurosci 2010;30:7281-7289.
– reference: Terrelonge M, Jr., Marder KS, Weintraub D, Alcalay RN. CSF β-amyloid 1-42 predicts progression to cognitive impairment in newly diagnosed Parkinson disease. J Mol Neurosci 2016;58:88-92.
– reference: Alves G, Brønnick K, Aarsland D, et al. CSF amyloid-β and tau proteins, and cognitive performance, in early and untreated Parkinson's disease: the Norwegian ParkWest study. J Neurol Neurosurg Psychiatry 2010;81:1080-1086.
– reference: Duits FH, Teunissen CE, Bouwman FH, et al. The cerebrospinal fluid "Alzheimer profile": easily said, but what does it mean? Alzheimers Dement 2014;10:713-723.
– reference: McKeith I, Ballard C, Perry R, et al. Prospective validation of consensus criteria for the diagnosis of dementia with Lewy bodies. Neurology 2000;54:1050-1058.
– reference: Hall S, Surova Y, Öhrfelt A, Zetterberg H, Lindqvist D, Hansson O. CSF biomarkers and clinical progression of Parkinson disease. Neurology 2015;84:57-63.
– reference: Vranová HP, Hényková E, Kaiserová M, et al. Tau protein, beta-amyloid1-42 and clusterin CSF levels in the differential diagnosis of Parkinsonian syndrome with dementia. J Neurol Sci 2014;343:120-124.
– reference: Lebedev AV, Westman E, Beyer M, et al. Multivariate classification of patients with Alzheimer's and dementia with Lewy bodies using high-dimensional cortical thickness measurements: an MRI surface-based morphometric study. J Neurol 2013;260:1104-1115.
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Snippet ABSTRACT Introduction Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers...
Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta 1-42, total...
Introduction Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta...
IntroductionAlzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta...
Introduction: Alzheimer's disease pathologies are common in dementia with Lewy bodies, but their clinical relevance is not clear. CSF biomarkers amyloid beta...
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StartPage 1203
SubjectTerms a-beta
Aged
Aged, 80 and over
alpha-synuclein
Alzheimer Disease - cerebrospinal fluid
Alzheimer Disease - physiopathology
Alzheimer's disease
Amyloid beta-Peptides - cerebrospinal fluid
Biomarkers
bodies
Cerebrospinal fluid
Clinical Medicine
Cognitive ability
cognitive decline
csf amyloid-beta
CSF biomarkers
Dementia
Dementia disorders
differential-diagnosis
Disease Progression
Female
Follow-Up Studies
Humans
Klinisk medicin
Lewy bodies
Lewy body dementia
Lewy Body Disease - cerebrospinal fluid
Lewy Body Disease - physiopathology
Life Sciences
Male
Medical and Health Sciences
Medicin och hälsovetenskap
Mental Status and Dementia Tests
mini-mental-state
Movement disorders
Neurodegenerative diseases
Neurologi
Neurology
Neurons and Cognition
Neurosciences
Neurosciences & Neurology
Neurovetenskaper
Parkinson's disease
parkinsons-disease
pathology
Peptide Fragments - cerebrospinal fluid
Prognosis
Tau protein
tau Proteins - cerebrospinal fluid
Threonine
Vitamin E
β-Amyloid
Title Alzheimer's disease cerebrospinal fluid biomarkers predict cognitive decline in lewy body dementia
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Volume 31
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