Evidence map›Paper›PMID 37108421›Full record

ReviewInternational journal of molecular sciences2023

Recent Development in the Understanding of Molecular and Cellular Mechanisms Underlying the Etiopathogenesis of Alzheimer's Disease.

Atefeh Afsar, Maria Del Carmen Chacon Castro, Adedamola Saidi Soladogun, Li Zhang

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.6field-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

25 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  5. Article
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  9. Article
  10. Altered Heme and Redox Homeostasis Underpin Late-onset Alzheimer's Disease.International journal of biological sciences · 2025
    Article
  11. Article
  12. Neurotrophic Effects ofInternational journal of molecular sciences · 2024
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
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  19. Review
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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

4 authors at 1 institution in 1 country.

Atefeh AfsarDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Maria Del Carmen Chacon CastroDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0000-0001-7743-8789
Adedamola Saidi SoladogunDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.
Li ZhangDepartment of Biological Sciences, The University of Texas at Dallas, Richardson, TX 75080, USA.ORCID 0000-0001-9242-0763
The University of Texas at Dallas · US

Funding

The Cecil H. and Ida Green Distinguished Chair fund. N/A
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder that leads to dementia and patient death. AD is characterized by intracellular neurofibrillary tangles, extracellular amyloid beta (Aβ) plaque deposition, and neurodegeneration. Diverse alterations have been associated with AD progression, including genetic mutations, neuroinflammation, blood-brain barrier (BBB) impairment, mitochondrial dysfunction, oxidative stress, and metal ion imbalance.Additionally, recent studies have shown an association between altered heme metabolism and AD. Unfortunately, decades of research and drug development have not produced any effective treatments for AD. Therefore, understanding the cellular and molecular mechanisms underlying AD pathology and identifying potential therapeutic targets are crucial for AD drug development. This review discusses the most common alterations associated with AD and promising therapeutic targets for AD drug discovery. Furthermore, it highlights the role of heme in AD development and summarizes mathematical models of AD, including a stochastic mathematical model of AD and mathematical models of the effect of Aβ on AD. We also summarize the potential treatment strategies that these models can offer in clinical trials.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesHumansNeurofibrillary TanglesOxidative StressAmyloid beta-PeptidesAlzheimer’s diseaseamyloid β-proteinhemeheme oxygenasetau proteins

Identifiers

PMID37108421
PMCPMC10138573
OpenAlexW4365514154

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.