Evidence map›Paper›PMID 34590423›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2022

Apolipoprotein B is a novel marker for early tau pathology in Alzheimer's disease.

Cynthia Picard, Nathalie Nilsson, Anne Labonté, Daniel Auld, Pedro Rosa-Neto, Alzheimer's Disease Neuroimaging Initiative, Nicholas J Ashton, Henrik Zetterberg, Kaj Blennow, John C B Breitner and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 66 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

13 authors at 3 institutions in 3 countries.

Cynthia PicardDouglas Mental Health University Institute, Montréal, Québec, Canada.
Nathalie NilssonDouglas Mental Health University Institute, Montréal, Québec, Canada.
Anne LabontéDouglas Mental Health University Institute, Montréal, Québec, Canada.
Daniel AuldMcGill University, Montréal, Québec, Canada.
Pedro Rosa-NetoDouglas Mental Health University Institute, Montréal, Québec, Canada.
Alzheimer's Disease Neuroimaging InitiativeDouglas Mental Health University Institute, Montréal, Québec, Canada.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
John C B BreitnerDouglas Mental Health University Institute, Montréal, Québec, Canada.
Sylvia VilleneuveDouglas Mental Health University Institute, Montréal, Québec, Canada.
Judes PoirierDouglas Mental Health University Institute, Montréal, Québec, Canada.
PREVENT-AD research groupDouglas Mental Health University Institute, Montréal, Québec, Canada.
Douglas Mental Health University Institute · CASahlgrenska University Hospital · SEMcGill University · CA

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
CIHR PJT 153287NIA NIH HHS U01 AG024904
6 · The paper itself

Abstract

introductionWe examine the role of brain apolipoprotein B (apoB) as a putative marker of early tau pathology and cognitive decline.

methodsCerebrospinal fluid (CSF) samples from cognitively normal and Alzheimer's disease (AD) participants were collected to measure protein levels of apoB and AD biomarkers amyloid beta (Aβ), t-tau and p-tau, as well as synaptic markers GAP43, SYNAPTOTAGMIN-1, synaptosome associated protein 25 (SNAP-25), and NEUROGRANIN. CSF apoB levels were contrasted with positron emission tomography (PET) scan measures of Aβ (18F-NAV4694) and Tau (flortaucipir) along with cognitive assessment alterations over 6 to 8 years.

resultsCSF apoB levels were elevated in AD participants and correlated with t-tau, p-tau, and the four synaptic markers in pre-symptomatic individuals. In the latter, CSF apoB levels correlated with PET flortaucipir-binding in entorhinal, parahippocampal, and fusiform regions. Baseline CSF apoB levels were associated with longitudinal visuospatial cognitive decline. DISCUSSION: CSF apoB markedly associates with early tau dysregulation in asymptomatic subjects and identifies at-risk individuals predisposed to develop visuospatial cognitive decline over time.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAmyloid beta-PeptidesApolipoprotein B-100ApolipoproteinsApolipoproteins BBiomarkersHumansPositron-Emission Tomographytau ProteinsAmyloid beta-PeptidesAPOB protein, humanApolipoprotein B-100ApolipoproteinsApolipoproteins BBiomarkerstau ProteinsAlzheimer's diseaseapolipoprotein Bcerebrospinal fluidPET scansRBANSsynaptic markerstau pathology

Identifiers

PMID34590423
PMCPMC9293308
OpenAlexW3202870961

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.