Evidence map›Paper›PMID 32760239›Full record

ReviewFrontiers in neuroscience2020

Mitochondrial Dysfunction, Neurogenesis, and Epigenetics: Putative Implications for Amyotrophic Lateral Sclerosis Neurodegeneration and Treatment.

Michele Longoni Calió, Elisandra Henriques, Amanda Siena, Clélia Rejane Antonio Bertoncini, Joana Gil-Mohapel, Tatiana Rosado Rosenstock

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.6field-weighted citation impact, top 5% 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

44 citing papers in PubMed, 61 citations in OpenAlex.

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  13. Mitochondrial Inherited Disorders and their Correlation with Neurodegenerative Diseases.Endocrine, metabolic & immune disorders drug targets · 2024
    Review
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  17. Role of neuroinflammation in neurodegeneration development.Signal transduction and targeted therapy · 2023
    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

6 authors at 3 institutions in 2 countries.

Michele Longoni CalióDepartment of Physiology, Federal University of São Paulo, São Paulo, Brazil.
Elisandra HenriquesDepartment of Physiological Science, Santa Casa de São Paulo School of Medical Science, São Paulo, Brazil.
Amanda SienaDepartment of Physiological Science, Santa Casa de São Paulo School of Medical Science, São Paulo, Brazil.
Clélia Rejane Antonio BertonciniCEDEME, Center of Development of Experimental Models for Medicine and Biology, Federal University of São Paulo, São Paulo, Brazil.
Joana Gil-MohapelDivision of Medical Sciences, Faculty of Medicine, University of Victoria and Island Medical Program, University of British Columbia, Victoria, BC, Canada.
Tatiana Rosado RosenstockDepartment of Physiological Science, Santa Casa de São Paulo School of Medical Science, São Paulo, Brazil.
Faculdade de Ciências Médicas da Santa Casa de São Paulo · BRUniversidade Federal de São Paulo · BRUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive and devastating multifactorial neurodegenerative disorder. Although the pathogenesis of ALS is still not completely understood, numerous studies suggest that mitochondrial deregulation may be implicated in its onset and progression. Interestingly, mitochondrial deregulation has also been associated with changes in neural stem cells (NSC) proliferation, differentiation, and migration. In this review, we highlight the importance of mitochondrial function for neurogenesis, and how both processes are correlated and may contribute to the pathogenesis of ALS; we have focused primarily on preclinical data from animal models of ALS, since to date no studies have evaluated this link using human samples. As there is currently no cure and no effective therapy to counteract ALS, we have also discussed how improving neurogenic function by epigenetic modulation could benefit ALS. In support of this hypothesis, changes in histone deacetylation can alter mitochondrial function, which in turn might ameliorate cellular proliferation as well as neuronal differentiation and migration. We propose that modulation of epigenetics, mitochondrial function, and neurogenesis might provide new hope for ALS patients, and studies exploring these new territories are warranted in the near future.

Indexed as

amyotrophic lateral sclerosisepigeneticsmitochondrianeural stem cellsneurogenesis

Identifiers

PMID32760239
PMCPMC7373761
OpenAlexW3036708798

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.