Evidence map›Paper›PMID 29025866›Full record

Trial reportFASEB journal : official publication of the Federation of American Societies for Experimental Biology2018

Declining levels of functionally specialized synaptic proteins in plasma neuronal exosomes with progression of Alzheimer's disease.

Edward J Goetzl, Erin L Abner, Gregory A Jicha, Dimitrios Kapogiannis, Janice B Schwartz

Open access · greenAbstract readClinical TrialMulticenter Study
PubMed Full text at PMC Publisher
In one paragraph

Trial report in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed, 2 pooled it
6.7field-weighted citation impact, top 2% 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

138 citing papers in PubMed, 2 syntheses or guidelines pooled it, 224 citations in OpenAlex.

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  9. Differences in blood levels of neuroligin-derived peptides in a cohort for early detection of Alzheimer's disease.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026
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78 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

5 authors at 3 institutions in 1 country.

Edward J GoetzlDepartment of Medicine, University of California, San Francisco, San Francisco, California, 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.
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.
University of Kentucky · USUniversity of San Francisco · USNational Institute on Aging · 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 WILCOCK, DONNA M · 2006 to 2020
$23.3M
NIA NIH HHS P30 AG028383
6 · The paper itself

Abstract

Interactions of the presynaptic proteins, neuronal pentraxin 2 (NPTX2) and neurexin 2α (NRXN2α), with their respective postsynaptic functional partners, GluA4-containing glutamate (AMPA4) receptor and neuroligin 1 (NLGN1), enhance excitatory synaptic activity in some areas of the hippocampus and cerebral cortex. As early damage of such excitatory circuits in the brain tissues of participants with Alzheimer's disease (AD) correlates with cognitive losses, plasma neuron-derived exosome (NDE) levels of these 2 pairs of specialized synaptic proteins were quantified to assess their biomarker characteristics. The NDE contents of all 4 proteins were decreased significantly in AD dementia ( n = 46), and diminished levels of AMPA4 and NLGN1 correlated with the extent of cognitive loss. In a preclinical period, 6-11 yr before the onset of dementia, the NDE levels of all but NPTX2 were significantly lower than those of matched controls, and levels of all proteins declined significantly with the development of dementia. Reductions in NDE levels of these specialized excitatory synaptic proteins may therefore be indicative of the extent of cognitive loss and may reflect progression of the severity of AD.-Goetzl, E. J., Abner, E. L., Jicha, G. A., Kapogiannis, D., Schwartz, J. B. Declining levels of functionally specialized synaptic proteins in plasma neuronal exosomes with progression of Alzheimer's disease.

Indexed as

AgedAlzheimer DiseaseCell Adhesion Molecules, NeuronalC-Reactive ProteinExosomesFemaleHumansMaleNerve Tissue ProteinsNeuronsPentraxinsReceptors, AMPASynaptic MembranesCell Adhesion Molecules, NeuronalC-Reactive Proteinglutamate receptor ionotropic, AMPA 4Nerve Tissue Proteinsneuroligin 1NRXN2 protein, humanPentraxinsReceptors, AMPAbiomarkersdementianeurodegeneration

Identifiers

PMID29025866
PMCPMC5888398
OpenAlexW2761598264

What Socratic 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 Socratic graph.