Evidence map›Paper›PMID 31444473›Full record

ReviewMolecular psychiatry2020

Three-dimensional modeling of human neurodegeneration: brain organoids coming of age.

Karl Grenier, Jennifer Kao, Phedias Diamandis

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 2 pooled it
5.6field-weighted citation impact, top 3% 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

79 citing papers in PubMed, 2 syntheses or guidelines pooled it, 117 citations in OpenAlex.

  1. Pooled it
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  8. Dual Targeting of Tau Kinases and Autophagy by Abemaciclib Independent of CDK4/6 Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  17. 3DMaterials today. Bio · 2025
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19 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Karl GrenierDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Jennifer KaoDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, M5S 1A8, Canada.
Phedias DiamandisDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, M5S 1A8, Canada. p.diamandis@mail.utoronto.ca.ORCID http://orcid.org/0000-0001-5291-9068
University Health Network · CAUniversity of Toronto · CA

Funding

CIHR
6 · The paper itself

Abstract

The prevalence of dementia and other neurodegenerative diseases is rapidly increasing in aging nations. These relentless and progressive diseases remain largely without disease-modifying treatments despite decades of research and investments. It is becoming clear that traditional two-dimensional culture and animal model systems, while providing valuable insights on the major pathophysiological pathways associated with these diseases, have not translated well to patients' bedside. Fortunately, the advent of induced-pluripotent stem cells and three-dimensional cell culture now provide tools that are revolutionizing the study of human diseases by permitting analysis of patient-derived human tissue with non-invasive procedures. Specifically, brain organoids, self-organizing neural structures that can mimic human fetal brain development, have now been harnessed to develop alternative models of Alzheimer's disease, Parkinson's disease, motor neuron disease, and Frontotemporal dementia by recapitulating important neuropathological hallmarks found in these disorders. Despite these early breakthroughs, several limitations need to be vetted in brain organoid models in order to more faithfully match human tissue qualities, including relative tissue immaturity, lack of vascularization and incomplete cellular diversity found in this culture system. Here, we review current brain organoid protocols, the pathophysiology of neurodegenerative disorders, and early studies with brain organoid neurodegeneration models. We then discuss the multiple engineering and conceptual challenges surrounding their use and provide possible solutions and exciting avenues to be pursued. Altogether, we believe that brain organoids models, improved with classical and emerging molecular and analytic tools, have the potential to unravel the opaque pathophysiological mechanisms of neurodegeneration and devise novel treatments for an array of neurodegenerative disorders.

Indexed as

Alzheimer DiseaseAnimalsBrainCell Culture TechniquesDisease Models, AnimalHumansInduced Pluripotent Stem CellsModels, BiologicalNeurodegenerative DiseasesOrganoidsParkinson Disease

Identifiers

PMID31444473
OpenAlexW2969563383

What OpenQuestion holds

Textmetadata
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.