Evidence map›Paper›PMID 31202913›Full record

ReviewNeurobiology of disease2019

Modeling Alzheimer's disease with human iPS cells: advancements, lessons, and applications.

Sofia Essayan-Perez, Bo Zhou, Amber M Nabet, Marius Wernig, Yu-Wen Alvin Huang

Abstract readReview
In one paragraph

Review in Neurobiology of disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Mental health dished up-the use of iPSC models in neuropsychiatric research.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Pooled it
  3. Article
  4. Article
  5. Review
  6. Review
  7. Potential role of chitinase-3-like protein 1 (CHI3L1/YKL-40) in neurodegeneration and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article
  8. Article
  9. Modeling Alzheimer's Disease Using Human Brain Organoids.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. 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

5 authors.

Sofia Essayan-PerezDepartment of Molecular and Cellular Physiology, Stanford University Medical School, Stanford, CA 94305, United States of America.
Bo ZhouDepartment of Molecular and Cellular Physiology, Stanford University Medical School, Stanford, CA 94305, United States of America; Institute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University Medical School, Stanford, CA 94305, United States of America.
Amber M NabetDepartment of Molecular and Cellular Physiology, Stanford University Medical School, Stanford, CA 94305, United States of America.
Marius WernigInstitute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University Medical School, Stanford, CA 94305, United States of America.
Yu-Wen Alvin HuangDepartment of Molecular and Cellular Physiology, Stanford University Medical School, Stanford, CA 94305, United States of America. Electronic address: alvinhuang@stanford.edu.

Funding

Training Program in Basic NeuroscienceT32MH020016 · NIMH · STANFORD UNIVERSITY · PI Justin L Gardner, Merritt C Maduke · 1997 to 2026
$16.2M
Probing Alzheimer synaptopathy in neurons derived from engineered human iPS cellsRF1AG048131 · NIA · STANFORD UNIVERSITY · PI SUDHOF, THOMAS C., WERNIG, MARIUS · 2014 to 2019
$5.4M
A molecular signaling pathway underlying differential predisposition of ApoE4 genotype to Alzheimer's diseaseK99AG054616 · NIA · STANFORD UNIVERSITY · PI HUANG, YU-WEN ALVIN · 2017 to 2018
$237k
NIA NIH HHS K99 AG054616NIA NIH HHS RF1 AG048131NIMH NIH HHS T32 MH020016
6 · The paper itself

Abstract

One in three people will develop Alzheimer's disease (AD) or another dementia and, despite intense research efforts, treatment options remain inadequate. Understanding the mechanisms of AD pathogenesis remains our principal hurdle to developing effective therapeutics to tackle this looming medical crisis. In light of recent discoveries from whole-genome sequencing and technical advances in humanized models, studying disease risk genes with induced human neural cells presents unprecedented advantages. Here, we first review the current knowledge of the proposed mechanisms underlying AD and focus on modern genetic insights to inform future studies. To highlight the utility of human pluripotent stem cell-based innovations, we then present an update on efforts in recapitulating the pathophysiology by induced neuronal, non-neuronal and a collection of brain cell types, departing from the neuron-centric convention. Lastly, we examine the translational potentials of such approaches, and provide our perspectives on the promise they offer to deepen our understanding of AD pathogenesis and to accelerate the development of intervention strategies for patients and risk carriers.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainCell DifferentiationHumansInduced Pluripotent Stem CellsNeuronstau ProteinsAmyloid beta-Peptidestau ProteinsAlzheimer’s disease (AD)Amyloid-β (Aβ)Apolipoprotein E (apoE)AstrocytesBlood-brain barrier (BBB)Genetic riskInduced pluripotent stem cell (iPSC)MicrogliaOligodendrocytesTau

Identifiers

PMID31202913
PMCPMC6689423

What OpenQuestion holds

Textmetadata
LicenceTDM
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.