Evidence map›Paper›PMID 30103319›Full record

ArticleJournal of Alzheimer's disease : JAD2018

Postsynaptic Proteome of Non-Demented Individuals with Alzheimer's Disease Neuropathology.

Olga Zolochevska, Nicole Bjorklund, Randall Woltjer, John E Wiktorowicz, Giulio Taglialatela

Open access · greenAbstract read
In one paragraph

Article 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 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. A brain-derived tau oligomer polymorph is associated with cognitive resilience to Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  8. Article
  9. Hippocampal Neural Stem Cell Exosomes Promote Brain Resilience against the Impact of Tau Oligomers.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Structural polymorphism and cytotoxicity of brain-derived β-amyloid extracts.Protein science : a publication of the Protein Society · 2023
    Review
  17. Article
  18. Review
  19. Review
  20. Article
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 2 institutions in 1 country.

Olga ZolochevskaDepartment of Neurology, University of Texas Medical Branch, Galveston, TX, USA.
Nicole BjorklundDepartment of Neurology, University of Texas Medical Branch, Galveston, TX, USA.
Randall WoltjerDepartment of Pathology, Oregon Health and Science University, Portland, OR, USA.
John E WiktorowiczDepartment of Biochemistry and Molecular Biology, Sealy Center for Molecular Medicine, University of Texas Medical Branch, Galveston, TX, USA.
Giulio TaglialatelaDepartment of Neurology, University of Texas Medical Branch, Galveston, TX, USA.
The University of Texas Medical Branch at Galveston · USOregon Health & Science University · US

Funding

Molecular Mechanisms of Environmental InjuryT32ES007254 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI AMEREDES, BILL T · 1990 to 2022
$6.6M
Mechanisms of resistance to cognitive decline in ADR01AG042890 · NIA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI TAGLIALATELA, GIULIO · 2013 to 2017
$1.5M
Epigenetic Modulation of Amyloid Beta-resistant Synapses in Non-demented Subjects with Alzheimer's NeuropathologyF31AG057217 · NIA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI CAIN, OLGA ZOLOCHEVSKA · 2017 to 2018
$50k
NIA NIH HHS F31 AG057217NIA NIH HHS R01 AG042890NIEHS NIH HHS T32 ES007254
6 · The paper itself

Abstract

Some individuals, here referred to as Non-Demented with Alzheimer's Neuropathology (NDAN), retain their cognitive function despite the presence of amyloid plaques and tau tangles typical of symptomatic Alzheimer's disease (AD). In NDAN, unlike AD, toxic amyloid-β oligomers do not localize to the postsynaptic densities (PSDs). Synaptic resistance to amyloid-β in NDAN may thus enable these individuals to remain cognitively intact despite the AD-like pathology. The mechanism(s) responsible for this resistance remains unresolved and understanding such protective biological processes could reveal novel targets for the development of effective treatments for AD. The present study uses a proteomic approach to compare the hippocampal postsynaptic densities of NDAN, AD, and healthy age-matched persons to identify protein signatures characteristic for these groups. Subcellular fractionation followed by 2D gel electrophoresis and mass spectrometry were used to analyze the PSDs. We describe fifteen proteins which comprise the unique proteomic signature of NDAN PSDs, thus setting them apart from control subjects and AD patients.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseElectrophoresis, Gel, Two-DimensionalFemaleHippocampusHumansMaleMass SpectrometryPost-Synaptic DensityProteomeProteomicsSubcellular FractionsProteomeAlzheimer’s diseasenon-demented with AD-like pathologypostsynaptic density proteomesynapse

Identifiers

PMID30103319
PMCPMC6130411
OpenAlexW2887785247

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.