Evidence map›Paper›PMID 27601437›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016

Decreased synaptic proteins in neuronal exosomes of frontotemporal dementia and Alzheimer's disease.

Edward J Goetzl, Dimitrios Kapogiannis, Janice B Schwartz, Iryna V Lobach, Laura Goetzl, Erin L Abner, Gregory A Jicha, Anna M Karydas, Adam Boxer, Bruce L Miller

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

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 245 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
245citing papers in PubMed, 7 pooled it
17.3field-weighted citation impact, top 1% 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

245 citing papers in PubMed, 7 syntheses or guidelines pooled it, 401 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Pooled it
  5. Pooled it
  6. Pooled it
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  8. Trial
  9. Article
  10. Increased circulating TREM2Brain, behavior, & immunity - health · 2026
    Article
  11. Review
  12. Review
  13. Article
  14. Neuronal Calcium Signaling and Cytoskeletal Dynamics in Neurodegeneration.International journal of molecular sciences · 2026
    Review
  15. Extracellular Vesicles in Tauopathies: Mechanisms and Applications.International journal of molecular sciences · 2026
    Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review

185 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

10 authors at 7 institutions in 1 country.

Edward J GoetzlDepartment of Medicine, University of California, San Francisco, San Francisco, California, USA; edward.goetzl@ucsf.edu.
Dimitrios KapogiannisLaboratory of Neurosciences, National Institute on Aging, Baltimore, Maryland, USA.
Janice B SchwartzDepartment of Medicine, University of California, San Francisco, San Francisco, California, USA.
Iryna V LobachClinical Translational Science Institute, University of California, San Francisco, San Francisco, California, USA.
Laura GoetzlDepartment of Obstetrics, Gynecology, and Reproductive Sciences, Temple University, Philadelphia, Pennsylvania, USA.
Erin L AbnerSanders-Brown Center on Aging, University of Kentucky, Lexington, Kentucky, USA.
Gregory A JichaSanders-Brown Center on Aging, University of Kentucky, Lexington, Kentucky, USA.
Anna M KarydasMemory and Aging Center, Department of Neurology, University of California, San Francisco, San Francisco, California, USA.
Adam BoxerMemory and Aging Center, Department of Neurology, University of California, San Francisco, San Francisco, California, USA.
Bruce L MillerMemory and Aging Center, Department of Neurology, University of California, San Francisco, San Francisco, California, USA.
Jewish Home · USUniversity of California, San Francisco · USUniversity of Kentucky · USNational Institute on Aging · USSouthern California Clinical and Translational Science Institute · USTemple University · 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
University of Kentucky Alzheimer's Disease Core Center - Biomarker CoreP30AG028383 · NIA · UNIVERSITY OF KENTUCKY · PI SCHMITT, FREDERICK · 2006 to 2020
$23.3M
The Four Repeat Tauopathy Neuroimaging InitiativeR01AG038791 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BOXER, ADAM L. · 2010 to 2020
$18.1M
Training - The Frontotemporal Lobar Degeneration Clinical Research ConsortiumU54NS092089 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BOXER, ADAM L. · 2014 to 2018
$6.4M
NIA NIH HHS P30 AG028383NIA NIH HHS R01 AG038791NINDS NIH HHS U54 NS092089
6 · The paper itself

Abstract

Synaptic dysfunction occurs early in senile dementias, presumably as a result of decreased levels of functional synaptic proteins as found in autopsied brains of patients with Alzheimer's disease (AD) or frontotemporal dementia (FTD). Plasma neuronal-derived exosomes (NDEs) were recovered by precipitation and immunoabsorption from 12 patients with AD, 16 with FTD, and 28 controls in a cross-sectional study, and from 9 patients with AD, 10 with FTD, and 19 controls in a longitudinal study. Six synaptic proteins in NDE extracts were quantified by ELISAs and normalized for exosome amounts. NDE levels of synaptophysin, synaptopodin, synaptotagmin-2, and neurogranin were significantly lower in patients with FTD and AD than in controls, but those of growth-associated protein 43 and synapsin 1 were reduced only in patients with AD. Functionally relevant phosphorylation of synapsin 1 serine 9 was reduced in patients with FTD and AD, although total synapsin 1 protein was higher in FTD than in controls. NDE levels of synaptotagmin, synaptophysin, and neurogranin were decreased years before dementia in patients with FTD and AD. NDE levels of synaptopodin, synaptotagmin, and synaptophysin, but not of amyloid β-peptide 42 or P-T181-tau, were correlated significantly with cognition assessed by mini-mental state examination or AD assessment scale-cognitive subscale. NDE synaptic proteins may be useful preclinical indices and progression measures in senile dementias.-Goetzl, E. J., Kapogiannis, D., Schwartz, J. B., Lobach, I. V., Goetzl, L., Abner, E. L., Jicha, G. A., Karydas, A. M., Boxer, A., Miller, B. L. Decreased synaptic proteins in neuronal exosomes of frontotemporal dementia and Alzheimer's disease.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBiomarkersCognitionCross-Sectional StudiesExosomesFrontotemporal DementiaHumansLongitudinal StudiesSynapsestau ProteinsAmyloid beta-PeptidesBiomarkerstau Proteinsbiomarkerscognitionneurotransmissionproteinopathy

Identifiers

PMID27601437
PMCPMC5102122
OpenAlexW2511373877

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.