Evidence map›Paper›PMID 26459988›Full record

ReviewBrain research2017

Induced pluripotent stem cells as a discovery tool for Alzheimer׳s disease.

Sarah E Sullivan, Tracy L Young-Pearse

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Brain research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. The complete genome of the KOLF2.1J reference iPSC line.bioRxiv : the preprint server for biology · 2026
    Article
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  14. Article
  15. The Role of P2X7 Receptor in Alzheimer's Disease.Frontiers in molecular neuroscience · 2020
    Review
  16. Article
  17. Review
  18. 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

2 authors.

Sarah E SullivanBrigham and Women׳s Hospital and Harvard Medical School, USA.
Tracy L Young-PearseBrigham and Women׳s Hospital and Harvard Medical School, USA. Electronic address: tyoung@rics.bwh.harvard.edu.

Funding

Pathway discovery, validation and compound identification for Alzheimer's disease - SupplementU01AG046152 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BENNETT, DAVID ALAN, DE JAGER, PHILIP L · 2013 to 2017
$13.6M
Genes and developmental signaling pathways in neuropsychiatric disordersR01MH101148 · NIMH · BRIGHAM AND WOMEN'S HOSPITAL · PI YOUNG-PEARSE, TRACY L · 2014 to 2018
$2.5M
Detection of cell type specific effects of pathway manipulation in neural cellsR33AG049864 · NIA · BRIGHAM AND WOMEN'S HOSPITAL · PI YOUNG-PEARSE, TRACY L · 2014 to 2016
$1.3M
NIA NIH HHS R33 AG049864NIA NIH HHS U01 AG046152NIMH NIH HHS R01 MH101148
6 · The paper itself

Abstract

The ability to accurately and systematically evaluate the cellular mechanisms underlying human neurodegenerative disorders such as Alzheimer׳s disease (AD) should lead to advancements in therapeutics. Recent developments in human induced pluripotent stem cells (iPSCs) have afforded the opportunity to use human neurons and glia to study cellular changes involved in neurological diseases. iPSCs have the potential to be differentiated into AD-relevant cell types, including forebrain neurons, astrocytes, and microglia. This permits the evaluation of individual cell types in isolation or in concert, thus modeling the interdependence of cell types within the brain. When discussing the potential of modeling AD with iPSCs, it is important to remember that the umbrella diagnosis of "Alzheimer׳s disease" represents a disease that is heterogeneous in terms of age of onset, underlying causes, and at times precise pathology. The ability of iPSCs to be derived from an array of AD patients allows for a closer examination of the mechanism of disease progression in particular subsets of subjects, who may have different mutations and allelic variants affecting their risk for disease. Disease mechanisms can be probed both by the genetic manipulation of iPSCs and by modifications to the cellular environment by chemical treatment. These studies may lead not only to the refinement of known pathways implicated in AD, but also to the identification of novel pathways heretofore unaffiliated with disease pathology. In this review, we describe the potential of iPSC models to transform our understanding of AD and to lead to valuable advancements in therapeutics. This article is part of a Special Issue entitled SI: Exploiting human neurons.

Indexed as

Alzheimer DiseaseAnimalsHumansInduced Pluripotent Stem CellsAlzheimer׳s diseaseAβInduced pluripotent stem celliPSStem cellTau

Identifiers

PMID26459988
PMCPMC4833689

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.