Evidence map›Paper›PMID 33495355›Full record

ReviewBiology open2021

Molecular mechanisms of neurodegeneration in the entorhinal cortex that underlie its selective vulnerability during the pathogenesis of Alzheimer's disease.

Olayemi Joseph Olajide, Marcus E Suvanto, Clifton Andrew Chapman

Open access · goldAbstract readReview
In one paragraph

Review in Biology open, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Locus coeruleus-entorhinal cortex tract integrity is linked to plasma tau and glial fibrillary acidic protein.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Non-coding RNA-mediated gene regulation in Alzheimer's disease pathogenesis: molecular insights and emerging innovations.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2025
    Review
  13. Article
  14. Serotonergic Regulation in Alzheimer's Disease.International journal of molecular sciences · 2025
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  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

3 authors at 2 institutions in 2 countries.

Olayemi Joseph OlajideDivision of Neurobiology, Department of Anatomy, University of Ilorin, Ilorin, Nigeria, PMB 1515 olajide.oj@unilorin.edu.ng joseph.olajide@concordia.ca andrew.chapman@concordia.ca.ORCID 0000-0002-9259-2837
Marcus E SuvantoCenter for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montréal, Québec, Canada H4B 1R6.
Clifton Andrew ChapmanCenter for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montréal, Québec, Canada H4B 1R6 olajide.oj@unilorin.edu.ng joseph.olajide@concordia.ca andrew.chapman@concordia.ca.ORCID 0000-0002-1876-0898
Concordia University · CAUniversity of Ilorin · NG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The entorhinal cortex (EC) is a vital component of the medial temporal lobe, and its contributions to cognitive processes and memory formation are supported through its extensive interconnections with the hippocampal formation. During the pathogenesis of Alzheimer's disease (AD), many of the earliest degenerative changes are seen within the EC. Neurodegeneration in the EC and hippocampus during AD has been clearly linked to impairments in memory and cognitive function, and a growing body of evidence indicates that molecular and functional neurodegeneration within the EC may play a primary role in cognitive decline in the early phases of AD. Defining the mechanisms underlying molecular neurodegeneration in the EC is crucial to determining its contributions to the pathogenesis of AD. Surprisingly few studies have focused on understanding the mechanisms of molecular neurodegeneration and selective vulnerability within the EC. However, there have been advancements indicating that early dysregulation of cellular and molecular signaling pathways in the EC involve neurodegenerative cascades including oxidative stress, neuroinflammation, glia activation, stress kinases activation, and neuronal loss. Dysfunction within the EC can impact the function of the hippocampus, which relies on entorhinal inputs, and further degeneration within the hippocampus can compound this effect, leading to severe cognitive disruption. This review assesses the molecular and cellular mechanisms underlying early degeneration in the EC during AD. These mechanisms may underlie the selective vulnerability of neuronal subpopulations in this brain region to the disease development and contribute both directly and indirectly to cognitive loss.This paper has an associated Future Leader to Watch interview with the first author of the article.

Indexed as

Disease SusceptibilityAlzheimer DiseaseAmyloid beta-PeptidesAnimalsApoptosisDisease Models, AnimalEntorhinal CortexHumansNerve DegenerationNeurogliaNeuroinflammatory DiseasesOxidative StressReceptors, N-Methyl-D-Aspartatetau ProteinsAmyloid beta-PeptidesReceptors, N-Methyl-D-Aspartatetau ProteinsAlzheimer's diseaseAmyloid beta proteinApoptosisEntorhinal cortexExcitotoxicityGlia activationInflammationOxidative stressTau

Identifiers

PMID33495355
PMCPMC7860115
OpenAlexW3122042328

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.