Evidence map›Paper›PMID 26657538›Full record

ReviewMolecular & cellular proteomics : MCP2016

Neurodegeneration and Alzheimer's disease (AD). What Can Proteomics Tell Us About the Alzheimer's Brain?

Guillermo Moya-Alvarado, Noga Gershoni-Emek, Eran Perlson, Francisca C Bronfman

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular & cellular proteomics : MCP, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.7field-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

62 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Targeted ErbB4 receptor activation ameliorates neuronal deficits via DOCK3 signaling in a transgenic mouse AD model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Neuroprotective and anti-inflammatory activity ofFrontiers in pharmacology · 2025
    Article
  11. Article
  12. Article
  13. Review
  14. Alzheimer's disease pathophysiology in the Retina.Progress in retinal and eye research · 2024
    Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Current neuropharmacology · 2024
    Article
  20. Review

2 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

4 authors at 2 institutions in 2 countries.

Guillermo Moya-AlvaradoFrom the ‡Millennium Nucleus of Regenerative Biology (MINREB) and CARE Center, Department of Physiology,Pontificia Universidad Católica de Chile, Santiago, Chile.;
Noga Gershoni-Emek§Sagol School of Neuroscience and Department of Physiology and Pharmacology, Sackler School of Medicine, Tel Aviv University, Israel.
Eran Perlson§Sagol School of Neuroscience and Department of Physiology and Pharmacology, Sackler School of Medicine, Tel Aviv University, Israel.
Francisca C BronfmanFrom the ‡Millennium Nucleus of Regenerative Biology (MINREB) and CARE Center, Department of Physiology,Pontificia Universidad Católica de Chile, Santiago, Chile.; fbronfman@bio.puc.cl.
Tel Aviv University · ILPontificia Universidad Católica de Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative diseases, such as Alzheimer's diseases (AD), are becoming more prevalent as the population ages. However, the mechanisms that lead to synapse destabilization and neuron death remain elusive. The advent of proteomics has allowed for high-throughput screening methods to search for biomarkers that could lead to early diagnosis and treatment and to identify alterations in the cellular proteome that could provide insight into disease etiology and possible treatment avenues. In this review, we have concentrated mainly on the findings that are related to how and whether proteomics studies have contributed to two aspects of AD research, the development of biomarkers for clinical diagnostics, and the recognition of proteins that can help elucidate the pathways leading to AD brain pathology. As a result of these studies, several candidate cerebrospinal fluid biomarkers are now available for further validation in different AD cohorts. Studies in AD brain and AD transgenic models support the notion that oxidative damage results in the alterations of metabolic enzymes and that mitochondrial dysfunction is central to AD neuropathology.

Indexed as

ProteomicsAlzheimer DiseaseAnimalsBiomarkersBrainHumansMiceMice, TransgenicNerve DegenerationNeuronsProteomeSynapsesBiomarkersProteome

Identifiers

PMID26657538
PMCPMC4739664
OpenAlexW2194075469

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.