Evidence map›Paper›PMID 31133789›Full record

ArticleFrontiers in neuroscience2019

Neuron-Derived Exosome Proteins May Contribute to Progression From Repetitive Mild Traumatic Brain Injuries to Chronic Traumatic Encephalopathy.

Edward J Goetzl, Aurélie Ledreux, Ann-Charlotte Granholm, Fanny M Elahi, Laura Goetzl, Jade Hiramoto, Dimitrios Kapogiannis

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

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  7. RPS3-Enriched Extracellular Vesicles Mediate Liver-Spinal Cord Inter-Organ Communication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Synaptogyrin-3 plays a critical role in addiction-related dopamine dysfunction and behavioral maladaptations.Proceedings of the National Academy of Sciences of the United States of America · 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

7 authors at 5 institutions in 1 country.

Edward J GoetzlDepartment of Medicine, University of California, San Francisco, San Francisco, CA, United States.
Aurélie LedreuxKnoebel Institute for Healthy Aging, University of Denver, Denver, CO, United States.
Ann-Charlotte GranholmKnoebel Institute for Healthy Aging, University of Denver, Denver, CO, United States.
Fanny M ElahiDepartment of Neurology, Memory and Aging Center, University of California, San Francisco, San Francisco, CA, United States.
Laura GoetzlDepartment of Obstetrics, Gynecology and Reproductive Sciences, Health Sciences Center at Houston, University of Texas, Houston, TX, United States.
Jade HiramotoDivision of Vascular Surgery, Department of Surgery, University of California, San Francisco, San Francisco, CA, United States.
Dimitrios KapogiannisLaboratory of Neurosciences, Intramural Research Program, National Institute on Aging, Baltimore, MD, United States.
University of California, San Francisco · USUniversity of Denver · USNational Institute on Aging · USThe University of Texas Health Science Center at Houston · USUniversity Memory and Aging Center · US

Funding

Studies in Dementia and Neurodegenerative DiseasesZIAAG000975 · NIA · NATIONAL INSTITUTE ON AGING · PI KAPOGIANNIS, DIMITRIOS · 2009 to 2025
$31.5M
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
Biological Correlates of Alzheimer in Down Syndrome.R21AG056974 · NIA · UNIVERSITY OF DENVER (COLORADO SEMINARY) · PI GRANHOLM-BENTLEY, ANN-CHARLOTTE ESTHER · 2017 to 2018
$414k
NIA NIH HHS R21 AG056974NIA NIH HHS T32 AG023481
6 · The paper itself

Abstract

The recent recognition that Alzheimer disease-like pathology may be found in chronic traumatic encephalopathy (CTE) even after acute mild traumatic brain injury (mTBI) has increased the urgency of elucidating mechanisms, identifying biomarkers predictive of high risk of development of CTE, and establishing biomarker profiles indicative of impactful effects of treatments. Of the many proteins that are loaded into neuron-derived exosomes (NDEs) from damaged neurons after acute TBI, the levels of prion cellular protein (PRPc), coagulation factor XIII (XIIIa), synaptogyrin-3, IL-6, and aquaporins remain elevated for months. Prolonged heightened expression of aquaporins and IL-6 may account for the persistent central nervous system edema and inflammation of CTE. PRPc, XIIIa and synaptogyrin-3 bind and concentrate neurotoxic forms of oligomeric amyloid β peptides or P-tau for delivery into neurons at or distant from the site of trauma. Our progression factor hypothesis of CTE asserts that physiological neuronal proteins, such as PRPc, XIIIa, synaptogyrin-3, IL-6 and aquaporins, that increase in concentration in neurons and NDEs for months after acute TBI, are etiological contributors to CTE by either direct actions or by recruiting neurotoxic forms of Aβ peptides or P-tau. Such progression factors also may be useful new targets for development of drugs to prevent CTE.

Indexed as

Alzheimer diseaseamyloidcellular prion proteinphospho-tausynaptogyrin-3

Identifiers

PMID31133789
PMCPMC6517542
OpenAlexW2943039400

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.