Evidence map›Paper›PMID 30086796›Full record

ArticleAlzheimer's research & therapy2018

Greater tau load and reduced cortical thickness in APOE ε4-negative Alzheimer's disease: a cohort study.

Niklas Mattsson, Rik Ossenkoppele, Ruben Smith, Olof Strandberg, Tomas Ohlsson, Jonas Jögi, Sebastian Palmqvist, Erik Stomrud, Oskar Hansson

Open access · goldAbstract read
In one paragraph

Article in Alzheimer's research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
5.1field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.

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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

9 authors at 4 institutions in 2 countries.

Niklas MattssonClinical Memory Research Unit, Department of Clinical Sciences, Faculty of Medicine, Lund University, Lund, Sweden. Niklas.mattsson@med.lu.se.
Rik OssenkoppeleClinical Memory Research Unit, Department of Clinical Sciences, Faculty of Medicine, Lund University, Lund, Sweden.
Ruben SmithClinical Memory Research Unit, Department of Clinical Sciences, Faculty of Medicine, Lund University, Lund, Sweden.
Olof StrandbergClinical Memory Research Unit, Department of Clinical Sciences, Faculty of Medicine, Lund University, Lund, Sweden.
Tomas OhlssonDepartment of Radiation Physics, Skåne University Hospital, Lund, Sweden.
Jonas JögiDepartment of Clinical Physiology and Nuclear Medicine, Skåne University Hospital, Lund, Sweden.
Sebastian PalmqvistClinical Memory Research Unit, Department of Clinical Sciences, Faculty of Medicine, Lund University, Lund, Sweden.
Erik StomrudClinical Memory Research Unit, Department of Clinical Sciences, Faculty of Medicine, Lund University, Lund, Sweden.
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences, Faculty of Medicine, Lund University, Lund, Sweden.
Lund University · SESkåne University Hospital · SEAmsterdam Neuroscience · NLAmsterdam UMC Location VUmc · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease is characterized by aggregated β-amyloid and tau proteins, but the clinical presentations and patterns of brain atrophy vary substantially. A part of this heterogeneity may be linked to the risk allele APOE ε4. The spread of tau pathology is related to atrophy and cognitive decline, but little data exist on the effects of APOE ε4 on tau. The objective of this preliminary study was therefore to test if tau load and brain structure differ by APOE ε4 in Alzheimer's disease.

methodsSixty-five β-amyloid-positive patients at the prodromal and dementia stages of Alzheimer's disease were enrolled, including APOE ε4-positive (n = 46) and APOE ε4-negative (n = 19) patients.

resultsCompared with their APOE ε4-positive counterparts, APOE ε4-negative patients had greater tau load and reduced cortical thickness, with the most pronounced effects for both in the parietal cortex. Relative to the overall cortical tau load, APOE ε4-positive patients had greater tau load in the entorhinal cortex. APOE ε4-positive patients also had slightly greater cortical β-amyloid load. There was an interaction between APOE ε4 and

conclusionsAPOE genotype may be associated with differences in pathways in Alzheimer's disease, potentially through differential development and spread of tau, as well as through effects on cognitive outcomes involving non-tau-related mechanisms.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesApolipoprotein E4CarbolinesCerebral CortexCohort StudiesFemaleFluorodeoxyglucose F18HumansImaging, Three-DimensionalMagnetic Resonance ImagingMaleMental Status and Dementia TestsMiddle Aged7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indoleAmyloid beta-PeptidesApolipoprotein E4CarbolinesFluorodeoxyglucose F18tau ProteinsAlzheimer’s diseaseAPOEAtrophyCognitionTau

Identifiers

PMID30086796
PMCPMC6081879
OpenAlexW2887364468

What OpenQuestion holds

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LicenceCC BY
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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.