Evidence map›Paper›PMID 32466216›Full record

ReviewInternational journal of molecular sciences2020

Mitochondrial Dysfunctions: A Red Thread across Neurodegenerative Diseases.

Serena Stanga, Anna Caretto, Marina Boido, Alessandro Vercelli

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
–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

61 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  9. Diabetic retinopathy and Alzheimer's disease: Convergence of the unfolded protein response in neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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1 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

4 authors.

Serena StangaDepartment of Neuroscience Rita Levi Montalcini, University of Turin, 10126 Turin, Italy.ORCID 0000-0003-1454-0713
Anna CarettoDepartment of Neuroscience Rita Levi Montalcini, University of Turin, 10126 Turin, Italy.
Marina BoidoDepartment of Neuroscience Rita Levi Montalcini, University of Turin, 10126 Turin, Italy.ORCID 0000-0003-1211-1552
Alessandro VercelliDepartment of Neuroscience Rita Levi Montalcini, University of Turin, 10126 Turin, Italy.

Funding

Fondazione CRT RF 2017.2052Ministero dell'Istruzione, dell'Università e della Ricerca "Dipartimenti di Eccellenza 2018-2022" to Department of Neuroscience "Rita Levi Montalcini
6 · The paper itself

Abstract

Mitochondria play a central role in a plethora of processes related to the maintenance of cellular homeostasis and genomic integrity. They contribute to preserving the optimal functioning of cells and protecting them from potential DNA damage which could result in mutations and disease. However, perturbations of the system due to senescence or environmental factors induce alterations of the physiological balance and lead to the impairment of mitochondrial functions. After the description of the crucial roles of mitochondria for cell survival and activity, the core of this review focuses on the "mitochondrial switch" which occurs at the onset of neuronal degeneration. We dissect the pathways related to mitochondrial dysfunctions which are shared among the most frequent or disabling neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's, Amyotrophic Lateral Sclerosis, and Spinal Muscular Atrophy. Can mitochondrial dysfunctions (affecting their morphology and activities) represent the early event eliciting the shift towards pathological neurobiological processes? Can mitochondria represent a common target against neurodegeneration? We also review here the drugs that target mitochondria in neurodegenerative diseases.

Indexed as

Alzheimer DiseaseAmyotrophic Lateral SclerosisAnimalsAntioxidantsHumansMitochondriaMuscular Atrophy, SpinalNeuroprotective AgentsOrganelle BiogenesisParkinson DiseaseAntioxidantsNeuroprotective Agentscellular homeostasismitochondriamitochondria biogenesis and dynamicsmitochondria targeting drugsmotor neuron diseasesneurodegenerationneurodegenerative diseasesoxidative stress

Identifiers

PMID32466216
PMCPMC7279270

What OpenQuestion holds

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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.