Evidence map›Paper›PMID 28882786›Full record

ReviewFree radical biology & medicine2018

Exosomal biomarkers in Down syndrome and Alzheimer's disease.

Eric D Hamlett, Aurélie Ledreux, Huntington Potter, Heidi J Chial, David Patterson, Joaquin M Espinosa, Brianne M Bettcher, Ann-Charlotte Granholm

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 8% 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, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Extracellular Vesicles in Tauopathies: Mechanisms and Applications.International journal of molecular sciences · 2026
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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.

Eric D HamlettKnoebel Institute for Healthy Aging and the Department of Biological Sciences, University of Denver, Denver, CO, USA; Medical University of South Carolina, Charleston, SC, USA.
Aurélie LedreuxKnoebel Institute for Healthy Aging and the Department of Biological Sciences, University of Denver, Denver, CO, USA.
Huntington PotterRocky Mountain Alzheimer's Disease Center, University of Colorado Anschutz Medical Campus, Denver, CO, USA; Linda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Denver, CO, USA; Department of Neurology, University of Colorado Anschutz Medical Campus, Denver, CO, USA.
Heidi J ChialRocky Mountain Alzheimer's Disease Center, University of Colorado Anschutz Medical Campus, Denver, CO, USA; Linda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Denver, CO, USA; Department of Neurology, University of Colorado Anschutz Medical Campus, Denver, CO, USA.
David PattersonKnoebel Institute for Healthy Aging and the Department of Biological Sciences, University of Denver, Denver, CO, USA.
Joaquin M EspinosaLinda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Denver, CO, USA; Department of Pharmacology, University of Colorado Anschutz Medical Campus, Denver, CO, USA.
Brianne M BettcherRocky Mountain Alzheimer's Disease Center, University of Colorado Anschutz Medical Campus, Denver, CO, USA; Linda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Denver, CO, USA; Department of Neurology, University of Colorado Anschutz Medical Campus, Denver, CO, USA; Department of Neurosurgery, University of Colorado Anschutz Medical Campus, Denver, CO, USA.
Ann-Charlotte GranholmKnoebel Institute for Healthy Aging and the Department of Biological Sciences, University of Denver, Denver, CO, USA; Medical University of South Carolina, Charleston, SC, USA. Electronic address: Lotta.Granholm-Bentley@DU.edu.
University of Colorado Anschutz Medical Campus · USMedical University of South Carolina · USUniversity of Denver · US

Funding

Neuronal dysfunction caused by Abeta inhibition of MT motorsR01NS076291 · NINDS · UNIVERSITY OF SOUTH FLORIDA · PI POTTER, HUNTINGTON · 2011 to 2015
$1.6M
Abnormal Low Density Lipoprotein Receptor Localization and Function in ADR01AG037942 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI POTTER, HUNTINGTON · 2011 to 2015
$1.5M
Biological Correlates of Alzheimer in Down Syndrome.R21AG056974 · NIA · UNIVERSITY OF DENVER (COLORADO SEMINARY) · PI GRANHOLM-BENTLEY, ANN-CHARLOTTE ESTHER · 2017 to 2018
$414k
Resolving Factors in Alzheimers DiseaseR21AG048631 · NIA · UNIVERSITY OF DENVER (COLORADO SEMINARY) · PI GRANHOLM-BENTLEY, ANN-CHARLOTTE ESTHER, SCHULTZBERG, MARIANNE · 2015 to 2016
$357k
NIA NIH HHS R01 AG037942NIA NIH HHS R21 AG048631NIA NIH HHS R21 AG056974NINDS NIH HHS R01 NS076291
6 · The paper itself

Abstract

Every person with Down syndrome (DS) has the characteristic features of Alzheimer's disease (AD) neuropathology in their brain by the age of forty, and most go on to develop AD dementia. Since people with DS show highly variable levels of baseline function, it is often difficult to identify early signs of dementia in this population. The discovery of blood biomarkers predictive of dementia onset and/or progression in DS is critical for developing effective clinical diagnostics. Our recent studies show that neuron-derived exosomes, which are small extracellular vesicles secreted by most cells in the body, contain elevated levels of amyloid-beta peptides and phosphorylated-Tau that could indicate a preclinical AD phase in people with DS starting in childhood. We also found that the relative levels of these biomarkers were altered following dementia onset. Exosome release and signaling are dependent on cellular redox homeostasis as well as on inflammatory processes, and exosomes may be involved in the immune response, suggesting a dual role as both triggers of inflammation in the brain and propagators of inflammatory signals between brain regions. Based on recently reported connections between inflammatory processes and exosome release, the elevated neuroinflammatory state observed in people with DS may affect exosomal AD biomarkers. Herein, we discuss findings from studies of people with DS, people with DS and AD (DS-AD), and mouse models of DS showing new connections between neuroinflammatory pathways, oxidative stress, exosomes, and exosome-mediated signaling, which may inform future AD diagnostics, preventions, and treatments in the DS population as well as in the general population.

Indexed as

Alzheimer DiseaseBiomarkersDown SyndromeExosomesHumansBiomarkersAlzheimer's diseaseDown syndromeExosomesNeurodegenerationNeuroinflammationOxidative stress

Identifiers

PMID28882786
PMCPMC6135098
OpenAlexW2752766390

What Socratic 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 Socratic graph.