Evidence map›Paper›PMID 26718979›Full record

ArticleThe American journal of pathology2016

Synaptic Amyloid-β Oligomers Precede p-Tau and Differentiate High Pathology Control Cases.

Tina Bilousova, Carol A Miller, Wayne W Poon, Harry V Vinters, Maria Corrada, Claudia Kawas, Eric Y Hayden, David B Teplow, Charles Glabe, Ricardo Albay and 3 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing 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

78 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
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  9. Rapidly reversible persistent long-term potentiation inhibition by patient-derived brain tau and amyloid ß proteins.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
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  10. Review
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  19. Tau and Amyloid β Protein in Patient-Derived Aqueous Brain Extracts Act Concomitantly to Disrupt Long-Term PotentiationThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  20. Cross-Platform Synaptic Network Analysis of Human Entorhinal Cortex Identifies TWF2 as a Modulator of Dendritic Spine Length.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article

18 more citing papers are in PubMed but not listed here.

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 5 institutions in 1 country.

Tina BilousovaUniversity of California Los Angeles School of Nursing, Los Angeles, California; Mary S. Easton Center for Alzheimer's Research at the University of California Los Angeles, Los Angeles, California.
Carol A MillerDepartments of Pathology, Neurology, and the Program in Neuroscience, University of Southern California Keck School of Medicine, Los Angeles, California.
Wayne W PoonInstitute for Memory Impairments and Neurological Disorders, University of California Irvine, Irvine, California.
Harry V VintersDepartment of Neurology, University of California Los Angeles School of Medicine, Los Angeles, California; Department of Pathology and Laboratory Medicine, University of California Los Angeles School of Medicine, Los Angeles, California.
Maria CorradaInstitute for Memory Impairments and Neurological Disorders, University of California Irvine, Irvine, California; Department of Neurology, University of California Irvine, Irvine, California.
Claudia KawasInstitute for Memory Impairments and Neurological Disorders, University of California Irvine, Irvine, California; Department of Neurology, University of California Irvine, Irvine, California; Department of Neurobiology & Behavior, University of California Irvine, Irvine, California.
Eric Y HaydenMary S. Easton Center for Alzheimer's Research at the University of California Los Angeles, Los Angeles, California; Department of Neurology, University of California Los Angeles School of Medicine, Los Angeles, California.
David B TeplowMary S. Easton Center for Alzheimer's Research at the University of California Los Angeles, Los Angeles, California; Department of Neurology, University of California Los Angeles School of Medicine, Los Angeles, California.
Charles GlabeDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California.
Ricardo AlbayDepartment of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California.
Gregory M ColeMary S. Easton Center for Alzheimer's Research at the University of California Los Angeles, Los Angeles, California; Department of Neurology, University of California Los Angeles School of Medicine, Los Angeles, California; Department of Medicine, University of California Los Angeles School of Medicine, Los Angeles, California; Geriatric Research, Education and Clinical Center, VA Greater Los Angeles Healthcare System, Los Angeles, California.
Edmond TengMary S. Easton Center for Alzheimer's Research at the University of California Los Angeles, Los Angeles, California; Department of Neurology, University of California Los Angeles School of Medicine, Los Angeles, California; Geriatric Research, Education and Clinical Center, VA Greater Los Angeles Healthcare System, Los Angeles, California.
Karen H GylysUniversity of California Los Angeles School of Nursing, Los Angeles, California; Mary S. Easton Center for Alzheimer's Research at the University of California Los Angeles, Los Angeles, California. Electronic address: kgylys@sonnet.ucla.edu.
University of California, Irvine · USUniversity of California, Los Angeles · USFoundation for Psychocultural Research · USGeriatric Research Education and Clinical Center · USUniversity of Southern California · US

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
VASCULAR RISK AND COGNITIVE STATUS IN A LATINO POPULATIONP50AG005142 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI BRASKIE, MEREDITH NICOLE · 1985 to 2019
$41.0M
Virology CoreP30AI028697 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KITCHEN, SCOTT G · 1991 to 2018
$39.9M
UC Irvine Alzheimer's Disease Research Center Induced Pluripotent Stem Cell CoreP50AG016573 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI LAFERLA, FRANK M · 2000 to 2019
$37.0M
Diversity Supplement to R01AG021055; Clinical, Imaging, and Pathological Studies in the Oldest Old: The 90+ StudyR01AG021055 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI CORRADA, MARIA, KAWAS, CLAUDIA H. · 2002 to 2024
$36.9M
TISSUE REPOSITORY COREP01AG000538 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI TENNER, ANDREA JOAN · 1985 to 2018
$24.8M
UCLA OLDER AMERICANS INDEPENDENCE CENTERP30AG028748 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MOORE, ALISON AHERN · 2006 to 2017
$9.8M
STRUCTURAL/KINETIC ANALYSIS OF ABETA FIBRILLOGENESISR01NS038328 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TEPLOW, DAVID B. · 1999 to 2014
$4.0M
THE AGING BRAIN-- OXIDANT STRESSR01AG018879 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI MILLER, CAROL A · 2001 to 2005
$1.6M
Physical Biochemistry and Biology of Amyloid Beta-ProteinR01AG041295 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TEPLOW, DAVID B. · 2011 to 2015
$1.6M
ApoE and Cholesterol Effects on Amyloid-beta in Synaptic Terminals in ADR01AG027465 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GYLYS, KAREN H · 2008 to 2012
$1.4M
NCATS NIH HHS UL1 TR000124NCATS NIH HHS UL1TR000124NCI NIH HHS CA16042NCI NIH HHS P30 CA016042NIAID NIH HHS AI 28697NIAID NIH HHS P30 AI028697NIA NIH HHS AG041295NIA NIH HHS AG18879NIA NIH HHS AG27465NIA NIH HHS AG34628NIA NIH HHS K08 AG034628NIA NIH HHS P01 AG000538NIA NIH HHS P30 AG028748NIA NIH HHS P50 AG005142NIA NIH HHS P50 AG016573NIA NIH HHS P50 AG05142NIA NIH HHS P50 AG16573NIA NIH HHS P50 AG16970NIA NIH HHS R01 AG018879NIA NIH HHS R01 AG021055NIA NIH HHS R01 AG027465NIA NIH HHS R01 AG041295NIA NIH HHS R01AG21055NIA NIH HHS R21 AG051946NIA NIH HHS R56 AG027465NINDS NIH HHS NS038328NINDS NIH HHS R01 NS038328
6 · The paper itself

Abstract

Amyloid-β (Aβ) and hyperphosphorylated tau (p-tau) aggregates form the two discrete pathologies of Alzheimer disease (AD), and oligomeric assemblies of each protein are localized to synapses. To determine the sequence by which pathology appears in synapses, Aβ and p-tau were quantified across AD disease stages in parietal cortex. Nondemented cases with high levels of AD-related pathology were included to determine factors that confer protection from clinical symptoms. Flow cytometric analysis of synaptosome preparations was used to quantify Aβ and p-tau in large populations of individual synaptic terminals. Soluble Aβ oligomers were assayed by a single antibody sandwich enzyme-linked immunosorbent assay. Total in situ Aβ was elevated in patients with early- and late-stage AD dementia, but not in high pathology nondemented controls compared with age-matched normal controls. However, soluble Aβ oligomers were highest in early AD synapses, and this assay distinguished early AD cases from high pathology controls. Overall, synapse-associated p-tau did not increase until late-stage disease in human and transgenic rat cortex, and p-tau was elevated in individual Aβ-positive synaptosomes in early AD. These results suggest that soluble oligomers in surviving neocortical synaptic terminals are associated with dementia onset and suggest an amyloid cascade hypothesis in which oligomeric Aβ drives phosphorylated tau accumulation and synaptic spread. These results indicate that antiamyloid therapies will be less effective once p-tau pathology is developed.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryHumansMaleMicroscopy, ConfocalPhosphorylationRatsRats, TransgenicAmyloid beta-Peptidestau Proteins

Identifiers

PMID26718979
PMCPMC4715217
OpenAlexW2202388976

What OpenQuestion holds

Textmetadata
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.