Evidence map›Paper›PMID 34359972›Full record

ArticleCells2021

Induced Pluripotent Stem Cell-Derived Neural Precursors Improve Memory, Synaptic and Pathological Abnormalities in a Mouse Model of Alzheimer's Disease.

Enrique Armijo, George Edwards, Andrea Flores, Jorge Vera, Mohammad Shahnawaz, Fabio Moda, Cesar Gonzalez, Magdalena Sanhueza, Claudio Soto

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Proposed Mechanisms of Cell Therapy for Alzheimer's Disease.International journal of molecular sciences · 2024
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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

9 authors at 4 institutions in 2 countries.

Enrique ArmijoMitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, Mc Govern Medical School, University of Texas, Houston, TX 77030, USA.
George EdwardsMitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, Mc Govern Medical School, University of Texas, Houston, TX 77030, USA.
Andrea FloresMitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, Mc Govern Medical School, University of Texas, Houston, TX 77030, USA.
Jorge VeraDepartment of Biology, Faculty of Sciences, University of Chile, Santiago 7800024, Chile.
Mohammad ShahnawazMitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, Mc Govern Medical School, University of Texas, Houston, TX 77030, USA.
Fabio ModaMitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, Mc Govern Medical School, University of Texas, Houston, TX 77030, USA.ORCID 0000-0002-2820-9880
Cesar GonzalezMitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, Mc Govern Medical School, University of Texas, Houston, TX 77030, USA.
Magdalena SanhuezaDepartment of Biology, Faculty of Sciences, University of Chile, Santiago 7800024, Chile.ORCID 0000-0001-8073-0385
Claudio SotoMitchell Center for Alzheimer's Disease and Related Brain Disorders, Department of Neurology, Mc Govern Medical School, University of Texas, Houston, TX 77030, USA.
Universidad de Los Andes, Chile · CLUniversity of Chile · CLFondazione IRCCS Istituto Neurologico Carlo Besta · ITSan Sebastián University · CL

Funding

Alzheimer's Association Zenith awardCynthia and George Mitchell Foundation Mitchell Center
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common type of dementia in the elderly population. The disease is characterized by progressive memory loss, cerebral atrophy, extensive neuronal loss, synaptic alterations, brain inflammation, extracellular accumulation of amyloid-β (Aβ) plaques, and intracellular accumulation of hyper-phosphorylated tau (p-tau) protein. Many recent clinical trials have failed to show therapeutic benefit, likely because at the time in which patients exhibit clinical symptoms the brain is irreversibly damaged. In recent years, induced pluripotent stem cells (iPSCs) have been suggested as a promising cell therapy to recover brain functionality in neurodegenerative diseases such as AD. To evaluate the potential benefits of iPSCs on AD progression, we stereotaxically injected mouse iPSC-derived neural precursors (iPSC-NPCs) into the hippocampus of aged triple transgenic (3xTg-AD) mice harboring extensive pathological abnormalities typical of AD. Interestingly, iPSC-NPCs transplanted mice showed improved memory, synaptic plasticity, and reduced AD brain pathology, including a reduction of amyloid and tangles deposits. Our findings suggest that iPSC-NPCs might be a useful therapy that could produce benefit at the advanced clinical and pathological stages of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAnimals, Genetically ModifiedDisease Models, AnimalEncephalitisHippocampusInduced Pluripotent Stem CellsMiceNeuronal PlasticityAmyloid beta-PeptidesAlzheimer’s diseaseamyloid-betaclinical symptomsinflammationstem cellstautherapy

Identifiers

PMID34359972
PMCPMC8303262
OpenAlexW3183798285

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.