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Association of Longitudinal Changes in Cerebrospinal Fluid Total Tau and Phosphorylated Tau 181 and Brain Atrophy With Disease Progression in Patients With Alzheimer Disease

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dc.contributor.author Llibre Guerra, Jorge J.
dc.contributor.author Li, H
dc.contributor.author Schindler, Suzanne E.
dc.contributor.author Gordon, Brian A.
dc.contributor.author Fagan, Anne M.
dc.contributor.author Morris, John C.
dc.contributor.author Benzinger, Tammie L.S.
dc.contributor.author Hassenstab, Jason
dc.contributor.author Wang, Guoqiao
dc.contributor.author Allegri, Ricardo Francisco
dc.contributor.author Berman, Sarah B.
dc.contributor.author Chhatwal, Jasmeer P.
dc.contributor.author Farlow, Martin R.
dc.contributor.author Holtzman, David M.
dc.contributor.author Jucker, Mathias
dc.contributor.author Levin, Johannes
dc.contributor.author Noble, James M.
dc.contributor.author Salloway, Stephen
dc.contributor.author Schofield, Peter R.
dc.contributor.author Karch, Celeste M.
dc.contributor.author Fox, Nick C.
dc.contributor.author Xiong, Chengjie
dc.contributor.author Bateman, Randall J.
dc.contributor.author McDade, Eric
dc.date.accessioned 2019-12-20T17:31:31Z
dc.date.available 2019-12-20T17:31:31Z
dc.date.issued 2019-12-02
dc.identifier.citation Llibre Guerra JJ, Li Y, Schindler SE, et al. Association of Longitudinal Changes in Cerebrospinal Fluid Total Tau and Phosphorylated Tau 181 and Brain Atrophy With Disease Progression in Patients With Alzheimer Disease. JAMA Netw Open. 2019;2(12):e1917126. doi:10.1001/jamanetworkopen.2019.17126 en_US
dc.identifier.uri https://repositorio.fleni.org.ar/handle/123456789/142
dc.identifier.uri https://doi.org/10.1001/jamanetworkopen.2019.17126
dc.description.abstract The amyloid/tau/neurodegeneration (A/T/N) framework uses cerebrospinal fluid (CSF) levels of total tau (tTau) as a marker of neurodegeneration and CSF levels of phosphorylated tau 181 (pTau181) as a marker of tau tangles. However, it is unclear whether CSF levels of tTau and pTau181 have similar or different trajectories over the course of Alzheimer disease. OBJECTIVES To examine the rates of change in CSF levels of tTau and pTau181 across the Alzheimer disease course and how the rates of change are associated with brain atrophy as measured by magnetic resonance imaging. DESIGN, SETTING, AND PARTICIPANTS This cohort study was set in tertiary research clinics. Each participants a member of a pedigree with a known mutation for dominantly inherited Alzheimer disease. Participants were divided into 3 groups on the basis of the presence of a mutation and their Clinical Dementia Rating score. Data analysis was performed in June 2019. MAIN OUTCOMES AND MEASURES Rates of change of CSF tTau and pTau181 levels and their association with the rate of change of brain volume. RESULTS Data from 465 participants (283 mutation carriers and 182 noncarriers) were analyzed. The mean (SD) age of the cohort was 37.8 (11.3) years, and 262 (56.3%) were women. The mean (SD) follow-up durationwas 2.7 (1.5) years. Two or more longitudinal CSF and magnetic resonance imaging assessmentswere available for 160 and 247 participants, respectively. Sixty-five percent of mutation carriers (183) did not have symptoms at baseline (Clinical Dementia Rating score, 0). For mutation carriers, the annual rates of change for CSF tTau and pTau181 became significantly different from 0 approximately 10 years before the estimated year of onset (mean [SE] rates of change, 5.5 [2.8] for tTau [P = .05] and 0.7 [0.3] for pTau 181 [P = .04]) and 15 years before onset (mean [SE] rates of change, 5.4 [3.9] for tTau [P = .17] and 1.1 [0.5] for pTau181 [P = .03]), respectively. The rate of change of pTau181 was positive and increased at the early stages of the disease, showing a positive rate of change starting at 15 estimated years before onset until 5 estimated years before onset (mean [SE], 0.4 [0.3]), followed by a positive but decreasing rate of change at year 0 (mean [SE], 0.1 [0.3]) and then negative rates of change at 5 years (mean [SE], −0.3 [0.4]) and 10 years (mean [SE], −0.6 [0.6]) after symptom onset. In individuals without symptoms (Clinical Dementia Rating score, 0), the rates of change of CSF tTau and pTau181 were negatively associated with brain atrophy (high rates of change in CSF measures were associated with low rates of change in brain volume in asymptomatic stages). After symptom onset (Clinical Dementia Rating score, >0), an increased rate of brain atrophy was not associated with rates of change of levels of both CSF tTau and pTau181. en_US
dc.description.uri https://doi.org/10.1001/jamanetworkopen.2019.17126
dc.language.iso eng en_US
dc.publisher American Medical Association en_US
dc.rights info:eu-repo/semantics/openAccess
dc.rights.uri https://creativecommons.org/licenses/by/2.5/ar/
dc.subject Alzheimer Disease en_US
dc.subject Enfermedad de Alzheimer en_US
dc.subject Líquido Cefalorraquídeo en_US
dc.subject Cerebrospinal Fluid en_US
dc.title Association of Longitudinal Changes in Cerebrospinal Fluid Total Tau and Phosphorylated Tau 181 and Brain Atrophy With Disease Progression in Patients With Alzheimer Disease en_US
dc.type info:eu-repo/semantics/publishedVersion
dc.type info:eu-repo/semantics/article en_US
dc.description.fil Fil: Llibre Guerra, Jorge J.Washington University in St Louis ; Estados Unidos.
dc.description.fil Fil: Li, H. Washington University in St Louis ; Estados Unidos.
dc.description.fil Fil: Schindler, Suzanne E.Washington University in St Louis. ; Estados Unidos.
dc.description.fil Fil: Gordon, Brian A. Washington University in St Louis.; Estados Unidos.
dc.description.fil Fil: Fagan, Anne M. Washington University in St Louis ; Estados Unidos.
dc.description.fil Fil: Morris, John C.Washington University in St Louis ; Estados Unidos.
dc.description.fil Fil: Benzinger, Tammie L.S.Washington University in St Louis ; Estados Unidos.
dc.description.fil Fil: Hassenstab, Jason.Washington University in St Louis ; Estados Unidos.
dc.description.fil Fil: Wang, Guoquiao. University of Tübingen ; Alemania.
dc.description.fil Fil: Allegri, Ricardo Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.
dc.description.fil Fil: Berman, Sarah B. Washington University in St Louis; Estados Unidos.
dc.description.fil Fil: Chhatwal, Jasmeer P. Harvard Medical School; Estados Unidos.
dc.description.fil Fil: Farlow, Martin R.Indiana University; Estados Unidos.
dc.description.fil Fil: Holtzman, David M.Washington University in St Louis; Estados Unidos
dc.description.fil Fil: Jucker, Mathias. University of Tübingen; Alemania.
dc.description.fil Fil: Levin, Johannes. Ludwig-Maximilians-University; Alemania.
dc.description.fil Fil: Noble, James M. Columbia University Medical Center; Estados Unidos.
dc.description.fil Fil: Salloway, Stephen. Brown University; Estados Unidos
dc.description.fil Fil: Karch, Celeste M. Washington University in St Louis; Estados Unidos.
dc.description.fil Fil: Fox, Nick C.University College London; Reino Unido.
dc.description.fil Fil: Xiong, Chengjie. Washington University in St Louis; Estados Unidos.
dc.description.fil Fil: Bateman, Randall J.Washington University in St Louis; Estados Unidos.
dc.description.fil Fil: McDade, Eric. Washington University in St Louis; Estados Unidos.
dc.relation.ispartofVOLUME 2
dc.relation.ispartofNUMBER 12
dc.relation.ispartofPAGINATION e1917126.
dc.relation.ispartofCOUNTRY Estados Unidos
dc.relation.ispartofCITY Chicago
dc.relation.ispartofTITLE JAMA Network Open
dc.relation.ispartofISSN 2574-3805
dc.type.snrd info:ar-repo/semantics/artículo es_ES


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