Evidence map›Paper›PMID 38978706›Full record

ReviewFrontiers in cellular neuroscience2024

Brain organoid as a model to study the role of mitochondria in neurodevelopmental disorders: achievements and weaknesses.

Raquel Coronel, Enrique García-Moreno, Emilio Siendones, Maria J Barrero, Beatriz Martínez-Delgado, Carlos Santos-Ocaña, Isabel Liste, M V Cascajo-Almenara

Abstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. 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

8 authors.

Raquel CoronelNeural Regeneration Unit, Functional Unit for Research on Chronic Diseases (UFIEC), National Institute of Health Carlos III (ISCIII), Madrid, Spain.
Enrique García-MorenoAndalusian Centre for Developmental Biology, CIBERER, National Institute of Health Carlos III (ISCIII), Pablo de Olavide University-CSIC-JA, Seville, Spain.
Emilio SiendonesAndalusian Centre for Developmental Biology, CIBERER, National Institute of Health Carlos III (ISCIII), Pablo de Olavide University-CSIC-JA, Seville, Spain.
Maria J BarreroModels and Mechanisms Unit, Institute of Rare Diseases Research (IIER), Spanish National Institute of Health Carlos III (ISCIII), Madrid, Spain.
Beatriz Martínez-DelgadoMolecular Genetics Unit, Institute of Rare Diseases Research (IIER), CIBER of Rare Diseases (CIBERER), Institute of Health Carlos III (ISCIII), Madrid, Spain.
Carlos Santos-OcañaAndalusian Centre for Developmental Biology, CIBERER, National Institute of Health Carlos III (ISCIII), Pablo de Olavide University-CSIC-JA, Seville, Spain.
Isabel ListeNeural Regeneration Unit, Functional Unit for Research on Chronic Diseases (UFIEC), National Institute of Health Carlos III (ISCIII), Madrid, Spain.
M V Cascajo-AlmenaraAndalusian Centre for Developmental Biology, CIBERER, National Institute of Health Carlos III (ISCIII), Pablo de Olavide University-CSIC-JA, Seville, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial diseases are a group of severe pathologies that cause complex neurodegenerative disorders for which, in most cases, no therapy or treatment is available. These organelles are critical regulators of both neurogenesis and homeostasis of the neurological system. Consequently, mitochondrial damage or dysfunction can occur as a cause or consequence of neurodevelopmental or neurodegenerative diseases. As genetic knowledge of neurodevelopmental disorders advances, associations have been identified between genes that encode mitochondrial proteins and neurological symptoms, such as neuropathy, encephalomyopathy, ataxia, seizures, and developmental delays, among others. Understanding how mitochondrial dysfunction can alter these processes is essential in researching rare diseases. Three-dimensional (3D) cell cultures, which self-assemble to form specialized structures composed of different cell types, represent an accessible manner to model organogenesis and neurodevelopmental disorders. In particular, brain organoids are revolutionizing the study of mitochondrial-based neurological diseases since they are organ-specific and model-generated from a patient's cell, thereby overcoming some of the limitations of traditional animal and cell models. In this review, we have collected which neurological structures and functions recapitulate in the different types of reported brain organoids, focusing on those generated as models of mitochondrial diseases. In addition to advancements in the generation of brain organoids, techniques, and approaches for studying neuronal structures and physiology, drug screening and drug repositioning studies performed in brain organoids with mitochondrial damage and neurodevelopmental disorders have also been reviewed. This scope review will summarize the evidence on limitations in studying the function and dynamics of mitochondria in brain organoids.

Indexed as

3D culturesdrug repurposinghigh-throughput screeningmitochondrial diseasesneurodevelopmental disordersorganoidspheroids

Identifiers

PMID38978706
PMCPMC11228165

What OpenQuestion holds

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Registered trials

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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.