Evidence map›Paper›PMID 25766620›Full record

ReviewExperimental & molecular medicine2015

Stem cell therapy for Alzheimer's disease and related disorders: current status and future perspectives.

Leslie M Tong, Helen Fong, Yadong Huang

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Experimental & molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
–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

39 citing papers in PubMed.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Review
  6. Stem Cell Interventions in the Treatment of Alzheimer's Disease.Current stem cell research & therapy · 2025
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
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  16. 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

3 authors.

Leslie M Tong1] Gladstone Institute of Neurological Disease, University of California, San Francisco, CA, USA [2] Biomedical Sciences Graduate Program, University of California, San Francisco, CA, USA.
Helen Fong1] Gladstone Institute of Neurological Disease, University of California, San Francisco, CA, USA [2] Department of Neurology, University of California, San Francisco, CA, USA.
Yadong Huang1] Gladstone Institute of Neurological Disease, University of California, San Francisco, CA, USA [2] Biomedical Sciences Graduate Program, University of California, San Francisco, CA, USA [3] Department of Neurology, University of California, San Francisco, CA, USA [4] Department of Pathology, University of California, San Francisco, CA, USA.

Funding

PrPSc SPECIFIC INTERACTION WITH NOVEL PrP-Fc FUSION PROTEINSP50AG023501 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MILLER, BRUCE L · 2004 to 2018
$27.1M
PREDOCTORAL TRAINING IN DEVELOPMENTAL BIOLOGYT32HD007470 · NICHD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Todd Nystul · 1994 to 2026
$7.7M
Investigating Common Molecular Pathogenic Pathways in Frontotemporal Dementia Patients iPSC-Derived NeuronsR01NS057553 · NINDS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Fen-Biao Gao · 2008 to 2026
$4.5M
Frontotemporal Dementia Induced Pluripotent Stem Cell ConsortiumR01NS079725 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI GAO, FEN-BIAO, HUANG, YADONG · 2013 to 2016
$3.1M
Studying Alzheimer's Disease Using Human iPS CellsRF1AG048030 · NIA · J. DAVID GLADSTONE INSTITUTES · PI HUANG, YADONG · 2014 to 2014
$2.4M
Optogenetic Study of ApoE4-Related Alzheimers DiseaseRF1AG047655 · NIA · J. DAVID GLADSTONE INSTITUTES · PI HUANG, YADONG, KREITZER, ANATOL · 2014 to 2014
$2.1M
NIA NIH HHS AG023501NIA NIH HHS AG047655NIA NIH HHS AG048030NIA NIH HHS P50 AG023501NIA NIH HHS RF1 AG047655NIA NIH HHS RF1 AG048030NICHD NIH HHS T32 HD007470NINDS NIH HHS NS079725NINDS NIH HHS R01 NS057553NINDS NIH HHS R01 NS079725
6 · The paper itself

Abstract

Underlying cognitive declines in Alzheimer's disease (AD) are the result of neuron and neuronal process losses due to a wide range of factors. To date, all efforts to develop therapies that target specific AD-related pathways have failed in late-stage human trials. As a result, an emerging consensus in the field is that treatment of AD patients with currently available drug candidates might come too late, likely as a result of significant neuronal loss in the brain. In this regard, cell-replacement therapies, such as human embryonic stem cell- or induced pluripotent stem cell-derived neural cells, hold potential for treating AD patients. With the advent of stem cell technologies and the ability to transform these cells into different types of central nervous system neurons and glial cells, some success in stem cell therapy has been reported in animal models of AD. However, many more steps remain before stem cell therapies will be clinically feasible for AD and related disorders in humans. In this review, we will discuss current research advances in AD pathogenesis and stem cell technologies; additionally, the potential challenges and strategies for using cell-based therapies for AD and related disorders will be discussed.

Indexed as

Stem Cell TransplantationAlzheimer DiseaseAnimalsCell- and Tissue-Based TherapyDisease Models, AnimalHumansResearch

Identifiers

PMID25766620
PMCPMC4351411

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.