ReviewFrontiers in aging neuroscience2018
Modulation of Mitochondrial Dynamics in Neurodegenerative Diseases: An Insight Into Prion Diseases.
Review in Frontiers in aging neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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.
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.
Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- Review
- Conformational Rearrangement of Fission DSPs.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Extremely low-frequency electromagnetic field (ELF-EMF) enhances mitochondrial energy production in NARP cybrids.Scientific reports · 2025Article
- Accumulation of Prion Triggers the Enhanced Glycolysis via Activation of AMKP Pathway in Prion-Infected Rodent and Cell Models.Molecular neurobiology · 2024Article
- Extremely Low-Frequency Electromagnetic Field (ELF-EMF) Increases Mitochondrial Electron Transport Chain Activities and Ameliorates Depressive Behaviors in Mice.International journal of molecular sciences · 2024Article
- Adenosine diphosphate released from stressed cells triggers mitochondrial transfer to achieve tissue homeostasis.PLoS biology · 2024Article
- Messenger RNA transport on lysosomal vesicles maintains axonal mitochondrial homeostasis and prevents axonal degeneration.Nature neuroscience · 2024Article
- Molecular insights into codon usage analysis of mitochondrial fission and fusion gene: relevance to neurodegenerative diseases.Annals of medicine and surgery (2012) · 2024Article
- PHB2 Alleviates Neurotoxicity of Prion Peptide PrPInternational journal of molecular sciences · 2023Article
- Redox mechanisms and their pathological role in prion diseases: The road to ruin.PLoS pathogens · 2023Review
- In-depth analysis of the Sirtuin 5-regulated mouse brain malonylome and succinylome using library-free data-independent acquisitions.Proteomics · 2023Article
- Emerging Promise of Therapeutic Approaches Targeting Mitochondria in Neurodegenerative Disorders.Current neuropharmacology · 2023Review
- How cytoskeletal proteins regulate mitochondrial energetics in cell physiology and diseases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Alterations in hippocampal mitochondrial dynamics are associated with neurodegeneration and recognition memory decline in old male mice.Biogerontology · 2022Article
- ER-mitochondria communication is involved in NLRP3 inflammasome activation under stress conditions in the innate immune system.Cellular and molecular life sciences : CMLS · 2022Article
- Regulation by Different Types of Chaperones of Amyloid Transformation of Proteins Involved in the Development of Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- PINK1-parkin-mediated neuronal mitophagy deficiency in prion disease.Cell death & disease · 2022Article
- Loss of prion protein control of glucose metabolism promotes neurodegeneration in model of prion diseases.PLoS pathogens · 2021Article
- GRP78 Overexpression Triggers PINK1-IPBiomedicines · 2021Article
- Regulation of neuronal bioenergetics as a therapeutic strategy in neurodegenerative diseases.Neural regeneration research · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction is a common and prominent feature of prion diseases and other neurodegenerative disorders. Mitochondria are dynamic organelles that constantly fuse with one another and subsequently break apart. Defective or superfluous mitochondria are usually eliminated by a form of autophagy, referred to as mitophagy, to maintain mitochondrial homeostasis. Mitochondrial dynamics are tightly regulated by processes including fusion and fission. Dysfunction of mitochondrial dynamics can lead to the accumulation of abnormal mitochondria and contribute to cellular damage. Neurons are among the cell types that consume the most energy, have a highly complex morphology, and are particularly dependent on mitochondrial functions and dynamics. In this review article, we summarize the molecular mechanisms underlying the mitochondrial dynamics and the regulation of mitophagy and discuss the dysfunction of these processes in the progression of prion diseases and other neurodegenerative disorders. We have also provided an overview of mitochondrial dynamics as a therapeutic target for neurodegenerative diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.