Evidence map›Paper›PMID 26462653›Full record

ReviewBrain research2017

Modeling ALS and FTD with iPSC-derived neurons.

Sebum Lee, Eric J Huang

Abstract readReview
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 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

40 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Early disruption of the CREB pathway drives dendritic morphological alterations in FTD/ALS cortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. BMP/TGF-β signaling as a modulator of neurodegeneration in ALS.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
    Article
  17. Article
  18. Review
  19. 3D Bioprinting of Neural Tissues.Advanced healthcare materials · 2021
    Review
  20. Epigenetics in blood-brain barrier disruption.Fluids and barriers of the CNS · 2021
    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

2 authors.

Sebum LeeDepartment of Pathology, University of California San Francisco, 505 Parnassus Avenue, San Francisco, CA 94143-0502, United States.
Eric J HuangDepartment of Pathology, University of California San Francisco, 505 Parnassus Avenue, San Francisco, CA 94143-0502, United States; Pathology Service 113B, San Francisco VA Medical Center, 505 Parnassus Avenue, San Francisco, CA 94143-0502, United States. Electronic address: eric.huang2@ucsf.edu.

Funding

Cellular and Animal Models of FUS Mutations in ALSR21OD011915 · OD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HUANG, ERIC J · 2012 to 2013
$421k
ER Stress-induced Neurodegeneration as Therapeutic Targets for ALSI01RX002133 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI HUANG, ERIC J · 2016 to 2019
–
Mechanism of FUS Mutations in the Pathogenesis of ALSI21BX001625 · VA · VETERANS AFFAIRS MED CTR SAN FRANCISCO · PI HUANG, ERIC J · 2013 to 2014
–
BLRD VA I21 BX001625NIH HHS R21 OD011915RRD VA I01 RX002133
6 · The paper itself

Abstract

Recent advances in genetics and neuropathology support the idea that amyotrophic lateral sclerosis (ALS) and frontotemporal lobar dementia (FTD) are two ends of a disease spectrum. Although several animal models have been developed to investigate the pathogenesis and disease progression in ALS and FTD, there are significant limitations that hamper our ability to connect these models with the neurodegenerative processes in human diseases. With the technical breakthrough in reprogramming biology, it is now possible to generate patient-specific induced pluripotent stem cells (iPSCs) and disease-relevant neuron subtypes. This review provides a comprehensive summary of studies that use iPSC-derived neurons to model ALS and FTD. We discuss the unique capabilities of iPSC-derived neurons that capture some key features of ALS and FTD, and underscore their potential roles in drug discovery. There are, however, several critical caveats that require improvements before iPSC-derived neurons can become highly effective disease models. This article is part of a Special Issue entitled SI: Exploiting human neurons.

Indexed as

Amyotrophic Lateral SclerosisAnimalsFrontotemporal DementiaHumansInduced Pluripotent Stem CellsNeuronsAmyotrophic lateral sclerosis (ALS)Frontotemporal dementia (FTD)Frontotemporal lobar degeneration (FTLD)Induced pluripotent stem cells (iPSCs)

Identifiers

PMID26462653
PMCPMC4833714

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.