Evidence map›Paper›PMID 30372675›Full record

Trial reportJournal of Alzheimer's disease : JAD2018

Growth Hormone-Releasing Hormone Modulation of Neuronal Exosome Biomarkers in Mild Cognitive Impairment.

Charisse N Winston, Edward J Goetzl, Laura D Baker, Michael V Vitiello, Robert A Rissman

Open access · greenAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 4 pooled it
1.4field-weighted citation impact, top 18% 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

39 citing papers in PubMed, 4 syntheses or guidelines pooled it, 53 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Measurement of α-synuclein as protein cargo in plasma extracellular vesicles.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  14. Evolving Role of Exosomes in Plastic and Reconstructive Surgery and Dermatology.Plastic and reconstructive surgery. Global open · 2024
    Article
  15. Article
  16. Extracellular vesicles in Alzheimer's disease.Arquivos de neuro-psiquiatria · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. Extracellular vesicles, the emerging mirrors of brain physiopathology.International journal of biological sciences · 2023
    Review
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

5 authors at 4 institutions in 1 country.

Charisse N Winston
Edward J Goetzl
Laura D Baker
Michael V Vitiello
Robert A Rissman
University of California, San Diego · USBehavioral Tech Research, Inc. · USJewish Home · USWake Forest University · US

Funding

VIRUS-INDUCED BRAIN PATHOLOGYP50AG005131 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BREWER, JAMES B · 1985 to 2018
$55.4M
UCSD Shiley-Marcos Alzheimer's Disease Research Center P30P30AG062429 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Steven Dyal Edland · 2019 to 2026
$34.9M
Wake Forest Alzheimer's Disease Core CenterP30AG049638 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BATEMAN, JAMES R., CRAFT, SUZANNE · 2016 to 2020
$12.2M
B-Synuclein as a Treatment for Lewy Body DiseaseR01AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISSMAN, ROBERT · 2001 to 2021
$5.2M
Proinflammatory Endophenotype to predict NSAID treatment response Alzheimer's trialsR01AG051848 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI LYKETSOS, CONSTANTINE G, O'BRYANT, SID E · 2016 to 2020
$3.7M
a-synuclein clearance strategies for the treatment of Lewy body disease.R37AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MASLIAH, ELIEZER · 2006 to 2014
$2.7M
GHRH: COGNITION IN AGING AND MILD COGNITIVE IMPAIRMENTR01AG025515 · NIA · UNIVERSITY OF WASHINGTON · PI VITIELLO, MICHAEL V. · 2005 to 2009
$2.5M
Proteomic characterization of exosomes from AD patientsR56AG057459 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI RISSMAN, ROBERT, YATES III, JOHN R · 2017 to 2017
$844k
Biogenesis of Exosomes, Secretion, and Trafficking in Alzheimer's DiseaseR56AG057469 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HOOK, VIVIAN Y. H, IKEZU, TSUNEYA · 2017 to 2017
$833k
Pathogenicity of neuronally-derived tau in exosomesR21AG051839 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISSMAN, ROBERT · 2016 to 2017
$426k
Neuronal exosomes to identify biomarkers and pathology of deployment-related TBII01BX004312 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI RISBROUGH, VICTORIA B, RISSMAN, ROBERT · 2019 to 2022
–
Validation Studies of CRF Receptor 1 as a Target for ADI01BX003040 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI RISSMAN, ROBERT · 2016 to 2020
–
BLRD VA I01 BX003040BLRD VA I01 BX004312NIA NIH HHS P30 AG049638NIA NIH HHS P30 AG062429NIA NIH HHS P50 AG005131NIA NIH HHS R01 AG018440NIA NIH HHS R01 AG025515NIA NIH HHS R01 AG051848NIA NIH HHS R21 AG051839NIA NIH HHS R37 AG018440NIA NIH HHS R56 AG057459NIA NIH HHS R56 AG057469
6 · The paper itself

Abstract

Age-related changes in cognition are linked to decreased expression of somatotropins, GHRH and IGF-1. Mild cognitive impairment (MCI) and Alzheimer's disease (AD) are heterogeneous conditions. The loss of GHRH signaling in the brain may be mechanistically involved in AD pathogenesis. The consequent need to identify AD at an early and perhaps more treatable stage has fueled research into blood-based, exosome biomarkers. Plasma exosomes from participants enrolled in a randomized, double-blind, placebo-controlled 20-week trial of GHRH administration, were isolated, precipitated, and enriched by immuno-absorption with anti-L1CAM antibody (neural adhesion protein) from adults with MCI and age-matched, cognitively normal controls (CNC). Extracted protein cargo from neuronally-derived exosomes (NDEs) were assessed by ELISAs for protein levels implicated in AD neuropathology and for synaptic proteins altered by AD. Plasma NDE concentrations of Aβ1-42 were significantly increased while plasma NDE concentrations of NRGN, synaptophysin, synaptotagmin, and synaptopodin were significantly decreased in patients with MCI, independent of GHRH treatment. Plasma NDE concentrations of ptau-S396 and GAP43 were not affected by cognitive status (CNC versus MCI) or by GHRH treatment. Aβ1-42, neurogranin (NRGN), synaptophysin, synaptotagmin, and synaptopodin demonstrated the highest diagnostic accuracy for distinguishing between CNC and MCI patients, while synaptophysin and synaptotagmin demonstrated moderate accuracy in distinguishing between placebo-treated and GHRH-treated, MCI patients.

Indexed as

AgedAmyloid beta-PeptidesBiomarkersCognitive DysfunctionDouble-Blind MethodExosomesFemaleGrowth Hormone-Releasing HormoneHumansMaleMiddle AgedNeuropsychological TestsPeptide FragmentsSynaptophysinSynaptotagminsAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersGrowth Hormone-Releasing HormonePeptide FragmentsSynaptophysinSynaptotagminsAmyloidbiomarkerGHRHgrowth hormonemild cognitive impairmentneuronal exosomessynapsetau

Identifiers

PMID30372675
PMCPMC6487872
OpenAlexW2897962727

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.