Evidence map›Paper›PMID 31306137›Full record

ArticleJournal of Alzheimer's disease : JAD2019

Highly Elevated Cerebrospinal Fluid Total Tau Level Reflects Higher Likelihood of Non-Amnestic Subtype of Alzheimer's Disease.

Jagan A Pillai, Aaron Bonner-Jackson, Lynn M Bekris, Jiri Safar, Jim Bena, James B Leverenz

Abstract 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 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 54 citations in OpenAlex.

  1. Operationalizing Alzheimer's disease trials in the era of targeted therapies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  17. Tau as a Biomarker of Neurodegeneration.International journal of molecular sciences · 2022
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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

6 authors at 3 institutions in 1 country.

Jagan A PillaiLou Ruvo Center for Brain Health, Cleveland Clinic, Cleveland, OH, USA.
Aaron Bonner-JacksonLou Ruvo Center for Brain Health, Cleveland Clinic, Cleveland, OH, USA.
Lynn M BekrisDepartment of Genomic Medicine Institute, Cleveland Clinic, Cleveland, OH, USA.
Jiri SafarDepartment of Pathology, Cleveland, OH, USA.
Jim BenaDepartment of Quantitative Health Sciences, Cleveland Clinic, Cleveland, OH, USA.
James B LeverenzLou Ruvo Center for Brain Health, Cleveland Clinic, Cleveland, OH, USA.
Cleveland Clinic · USLou Ruvo Brain Institute · USUniversity Hospitals of Cleveland · US

Funding

Characterization of Rapidly Progressive Alzheimer's DiseaseRF1AG058267 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HAINES, JONATHAN L, SAFAR, JIRI G. · 2017 to 2017
$4.0M
Inflammatory Networks Mediating Cognitive Decline In Preclinical Alzheimers DiseaseK23AG055685 · NIA · CLEVELAND CLINIC LERNER COM-CWRU · PI PILLAI, JAGAN AYYAPPAN · 2017 to 2021
$916k
NIA NIH HHS K23 AG055685NIA NIH HHS RF1 AG058267
6 · The paper itself

Abstract

backgroundCerebrospinal fluid (CSF) levels of total tau (t-tau) protein are thought to reflect the intensity of the neuronal damage in neurodegeneration, including Alzheimer's disease (AD). The recent link of CSF t-tau to rapidly progressive AD raises the question among other AD clinical variants regarding CSF t-tau. We investigated the clinical phenotypes of AD patients with varying CSF t-tau levels.

objectiveWe tested the hypothesis that highly elevated CSF t-tau level would have a higher likelihood of presenting with atypical non-amnestic variants of AD.

methodsRetrospective comparative case study of 97 patients evaluated in a memory clinic with clinical presentation and CSF biomarkers consistent with AD. We compared the age, sex, education, APOEɛ4 status, Montreal Cognitive Assessment (MoCA) score, clinical phenotype, and MRI volumetric measures by CSF t-tau quartile at baseline. Multivariable logistic regression models were used to evaluate if CSF t-tau levels predict non-amnestic presentations controlling for covariates.

resultsNon-amnestic AD had a higher median CSF t-tau level compared to amnestic-AD (p = 0.014). Each 50 pg/ml increase in CSF t-tau was associated with an increase in the odds of having a non-amnestic presentation (7.4%) and aphasia (10.6 %) as the initial presenting symptom even after taking into account; age, sex, education, APOEɛ4, MoCA, and CSF Aβ42. Logopenic AD had higher t-tau and p-tau levels compared to other variants.

conclusionsHighly elevated CSF t-tau levels could indicate more cortical involvement presenting with early non-amnestic symptoms in atypical AD subtypes, particularly in the logopenic variant.

Indexed as

Mental Status and Dementia TestsAgedAlzheimer DiseaseBiomarkersCerebral CortexCohort StudiesCross-Sectional StudiesFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedRetrospective Studiestau ProteinsBiomarkersMAPT protein, humantau ProteinsAlzheimer’s diseaseatypical variantbiomarkerscerebrospinal fluidcortical atrophyhippocampal atrophymild cognitive impairmenttau

Identifiers

PMID31306137
PMCPMC7086408
OpenAlexW2962225906

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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.