Evidence map›Paper›PMID 28502044›Full record

ArticleMolecular neurobiology2018

Hippocampal Proteomic Analysis Reveals Distinct Pathway Deregulation Profiles at Early and Late Stages in a Rat Model of Alzheimer's-Like Amyloid Pathology.

Sonia Do Carmo, Gogce Crynen, Tiffany Paradis, Jon Reed, M Florencia Iulita, Adriana Ducatenzeiler, Fiona Crawford, A Claudio Cuello

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Amyloid-Directed Antibodies: Past, Present, and Future.Journal of Alzheimer's disease : JAD · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Article
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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

8 authors at 2 institutions in 2 countries.

Sonia Do CarmoDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QC, Canada.
Gogce CrynenRoskamp Institute, Sarasota, FL, USA.
Tiffany ParadisDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QC, Canada.
Jon ReedRoskamp Institute, Sarasota, FL, USA.
M Florencia IulitaDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QC, Canada.
Adriana DucatenzeilerDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QC, Canada.
Fiona CrawfordRoskamp Institute, Sarasota, FL, USA.
A Claudio CuelloDepartment of Pharmacology and Therapeutics, McGill University, Montreal, QC, Canada. claudio.cuello@mcgill.ca.
McGill University · CARoskamp Institute · US

Funding

Canadian Institutes of Health Research MOP-102752
6 · The paper itself

Abstract

The cerebral accumulation and cytotoxicity of amyloid beta (Aβ) is central to Alzheimer's pathogenesis. However, little is known about how the amyloid pathology affects the global expression of brain proteins at different disease stages. In order to identify genotype and time-dependent significant changes in protein expression, we employed quantitative proteomics analysis of hippocampal tissue from the McGill-R-Thy1-APP rat model of Alzheimer-like amyloid pathology. McGill transgenic rats were compared to wild-type rats at early and late pathology stages, i.e., when intraneuronal Aβ amyloid burden is conspicuous and when extracellular amyloid plaques are abundant with more pronounced cognitive deficits. After correction for multiple testing, the expression levels of 64 proteins were found to be considerably different in transgenic versus wild-type rats at the pre-plaque stage (3 months), and 86 proteins in the post-plaque group (12 months), with only 9 differentially regulated proteins common to the 2 time-points. This minimal overlap supports the hypothesis that different molecular pathways are affected in the hippocampus at early and late stages of the amyloid pathology throughout its continuum. At early stages, disturbances in pathways related to cellular responses to stress, protein homeostasis, and neuronal structure are predominant, while disturbances in metabolic energy generation dominate at later stages. These results shed new light on the molecular pathways affected by the early accumulation of Aβ and how the evolving amyloid pathology impacts other complex metabolic pathways.

Indexed as

ProteomicsAdenosine TriphosphateAlzheimer DiseaseAmyloidAmyloid beta-Protein PrecursorAnimalsBrainDisease Models, AnimalEnergy MetabolismHippocampusHumansNF-E2-Related Factor 2Oxidative StressPlaque, AmyloidRats, TransgenicReproducibility of ResultsAdenosine TriphosphateAmyloidAmyloid beta-Protein PrecursorNfe2l2 protein, ratNF-E2-Related Factor 2Alzheimer’s diseaseAmyloid pathologyCellular stressEnergy metabolismHippocampusProteomicsTransgenic rat

Identifiers

PMID28502044
OpenAlexW2613982973

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.