Evidence map›Paper›PMID 32157747›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2020

Endothelial-derived plasma exosome proteins in Alzheimer's disease angiopathy.

Erin L Abner, Fanny M Elahi, Gregory A Jicha, Maja Mustapic, Omar Al-Janabi, Joel H Kramer, Dimitrios Kapogiannis, Edward J Goetzl

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 34 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

8 authors at 3 institutions in 1 country.

Erin L AbnerSanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA.
Fanny M ElahiDepartment of Neurology, Memory and Aging Center, University of California, San Francisco, San Francisco, CA, USA.
Gregory A JichaSanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA.
Maja MustapicCellular and Molecular Neurosciences Section, Laboratory of Neurosciences, National Institute on Aging, Baltimore, MD, USA.
Omar Al-JanabiSanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA.
Joel H KramerDepartment of Neurology, Memory and Aging Center, University of California, San Francisco, San Francisco, CA, USA.
Dimitrios KapogiannisCellular and Molecular Neurosciences Section, Laboratory of Neurosciences, National Institute on Aging, Baltimore, MD, USA.
Edward J GoetzlDepartment of Medicine, University of California, San Francisco, San Francisco, CA, USA.
University of California, San Francisco · USUniversity of Kentucky · USNational Institute on Aging · US

Funding

TDP-43 Loss-of-Function: Biology to BiomarkersP01AG019724 · NIA · UNIVERSITY OF PENNSYLVANIA · PI Jennifer Merrilees · 2002 to 2026
$67.2M
Research Education ComponentP30AG062422 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Serggio Carlo Lanata · 2019 to 2026
$36.9M
Studies in Dementia and Neurodegenerative DiseasesZIAAG000975 · NIA · NATIONAL INSTITUTE ON AGING · PI KAPOGIANNIS, DIMITRIOS · 2009 to 2025
$31.5M
UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
South Texas Alzheimer's Disease Research CenterP30AG066546 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Sudha Seshadri · 2021 to 2026
$24.0M
University of Kentucky Alzheimer's Disease Research CenterP30AG072946 · NIA · UNIVERSITY OF KENTUCKY · PI LINDA J VAN ELDIK · 2021 to 2026
$23.5M
University of Kentucky Alzheimer's Disease Core Center - Biomarker CoreP30AG028383 · NIA · UNIVERSITY OF KENTUCKY · PI SCHMITT, FREDERICK · 2006 to 2020
$23.3M
Temporal Trends, Novel Imaging and Molecular Characterization of Preclinical and Clinical Alzheimer's Disease in the Framingham CohortsR01AG054076 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI DECARLI, CHARLES, SESHADRI, SUDHA · 2016 to 2020
$12.3M
Multidisciplinary Research Fellowship in Alzheimer’s disease and Related DementiasT32AG023481 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BRUCE L MILLER, HOWARD J ROSEN · 2005 to 2026
$7.4M
Novel imaging and endothelial biomarkers of small vessel cerebrovascular diseaseUH3NS100608 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DECARLI, CHARLES, KRAMER, JOEL H · 2018 to 2020
$3.5M
Effects of chronic inflammation on brain structure and functionR01AG048234 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KRAMER, JOEL H · 2015 to 2019
$3.2M
Novel imaging and endothelial biomarkers of small vessel cerebrovascular diseaseUH2NS100608 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DECARLI, CHARLES, KRAMER, JOEL H · 2016 to 2017
$2.1M
NIA NIH HHS K24 AG045333NIA NIH HHS P01 AG019724NIA NIH HHS P30 AG010129NIA NIH HHS P30 AG028383NIA NIH HHS P30 AG062422NIA NIH HHS P30 AG066546NIA NIH HHS P30 AG072946NIA NIH HHS R01 AG042419NIA NIH HHS R01 AG048234NIA NIH HHS R01 AG054076NIA NIH HHS T32 AG023481NINDS NIH HHS UH2 NS100608NINDS NIH HHS UH3 NS100608
6 · The paper itself

Abstract

Small cerebral vascular disease (SCeVD) demonstrated by white matter hyperintensity (WMH) on MRI contributes to the development of dementia in Alzheimer's disease (AD), but it has not been possible to correlate onset, severity, or protein components of SCeVD with characteristics of WMH in living patients. Plasma endothelial-derived exosomes (EDEs) were enriched by two-step immunoabsorption from four groups of participants with no clinical evidence of cerebrovascular disease: cognitively normal (CN) without WMH (CN without SCeVD, n = 20), CN with SCeVD (n = 22), preclinical AD (pAD) + mild cognitive impairment (MCI) without SCeVD (pAD/MCI without SCeVD, n = 22), and pAD/MCI with SCeVD (n = 16) for ELISA quantification of cargo proteins. Exosome marker CD81-normalized EDE levels of the cerebrovascular-selective biomarkers large neutral amino acid transporter 1 (LAT-1), glucose transporter type 1 (Glut-1), and permeability-glycoprotein (p-GP, ABCB1) were similarly significantly higher in the CN with SCeVD and pAD/MCI with SCeVD groups than their corresponding control groups without SCeVD. CD81-normalized EDE levels of Aβ40 and Aβ42 were significantly higher in the pAD/MCI with SCeVD group but not in the CN with SCeVD group relative to controls without SCeVD. Levels of normal cellular prion protein (PrPc), a receptor for amyloid peptides, and phospho-181T-tau were higher in both CN and pAD/MCI with SCeVD groups than in the corresponding controls. High EDE levels of Aβ40, Aβ42, and phospho-181T-tau in patients with WMH suggesting SCeVD appear at the pre-clinical or MCI stage of AD and therapeutic lowering of neurotoxic peptide levels may delay progression of AD angiopathy.

Indexed as

AgedAlzheimer DiseaseAmyloid beta-PeptidesBiomarkersCase-Control StudiesCerebral Small Vessel DiseasesCognitive DysfunctionDisease ProgressionEndothelial CellsExosomesFemaleHumansMaleProspective Studiestau ProteinsWhite MatterAmyloid beta-PeptidesBiomarkerstau Proteinsamyloidprion cellular proteinP-tau proteinsmall cerebral vascular disease

Identifiers

PMID32157747
PMCPMC7233139
OpenAlexW3011881118

What OpenQuestion holds

Textmetadata
LicenceTDM
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.