ReviewMolecular neurobiology2021
Obscure Involvement of MYC in Neurodegenerative Diseases and Neuronal Repair.
Review in Molecular neurobiology, 2021. 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
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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.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Betulinic Acid Promotes Motor Function Recovery After Spinal Cord Injury by Inhibiting Apoptosis Through Myc/NF-κB Signaling Pathway.Neurochemical research · 2026Article
- dMyc suppresses CTG-induced cytotoxicity in the Drosophila model of DM1 by reducing autophagy and cell death.Cell death discovery · 2026Article
- Neurological Effects ofNutrients · 2026Article
- Decoding thebioRxiv : the preprint server for biology · 2026Article
- c-Myc: an emerging participant in heart failure.Frontiers in cardiovascular medicine · 2026Review
- Pyruvate kinase M2 in Alzheimer's disease: from dysregulation to therapeutic inhibition.Brain communications · 2026Review
- A Transcriptomic Roadmap of Parkinson's Disease Progression at Single Cell Resolution.medRxiv : the preprint server for health sciences · 2025Article
- Effects of E2F1 Point Acetylation at Lysine 117 or 125 on Neuronal Apoptosis After Ischemic Injury.Neurochemical research · 2025Article
- Review
- Transcriptomic analysis reinforces the implication of spatacsin in neuroinflammation and neurodevelopment.Scientific reports · 2025Article
- c-Myc and FOXO3a-The Everlasting Decision Between Neural Regeneration and Degeneration.International journal of molecular sciences · 2024Review
- Identification of molecular targets of Hypericum perforatum in blood for major depressive disorder: a machine-learning pharmacological study.Chinese medicine · 2024Article
- Comparison of Neurogenesis Promotion Effects between Cinnamoylquinic Acids in Neural Stem Cells from Adult Mice Brains.ACS chemical neuroscience · 2024Article
- Bioinformatics approaches for studying molecular sex differences in complex diseases.Briefings in bioinformatics · 2024Review
- Altered glia-neuron communication in Alzheimer's Disease affects WNT, p53, and NFkB Signaling determined by snRNA-seq.Cell communication and signaling : CCS · 2024Article
- Altered Glia-Neuron Communication in Alzheimer's Disease Affects WNT, p53, and NFkB Signaling Determined by snRNA-seq.bioRxiv : the preprint server for biology · 2024Article
- Acetylation of c-Myc at Lysine 148 Protects Neurons After Ischemia.Neuromolecular medicine · 2024Article
- Article
- Targeting MYC at the intersection between cancer metabolism and oncoimmunology.Frontiers in immunology · 2024Review
- Isoform-Directed Control of c-Myc Functions: Understanding the Balance from Proliferation to Growth Arrest.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
MYC is well known as a potent oncogene involved in regulating cell cycle and metabolism. Augmented MYC expression leads to cell cycle dysregulation, intense cell proliferation, and carcinogenesis. Surprisingly, its increased expression in neurons does not induce their proliferation, but leads to neuronal cell death and consequent development of a neurodegenerative phenotype. Interestingly, while cancer and neurodegenerative diseases such as Alzheimer's disease are placed at the opposite sides of cell division spectrum, both start with cell cycle dysregulation and stimulation of proliferation. It seems that MYC action directed toward neuron cell proliferation and neural tissue repair collides with evolutional loss of regenerative capacity of CNS neurons in order to strengthen synaptic structure, to protect our cognitive abilities and therefore character. Accordingly, there are abundant mechanisms that block its expression and action specifically in the brain. Moreover, while MYC expression in brain neurons during neurodegenerative processes is related to their death, there are obvious evidences that MYC action after physical injury is beneficial in case of peripheral nerve recovery. MYC might be a useful tool to repair brain cells upon development of neurodegenerative disease or CNS trauma, including stroke and traumatic brain and spinal cord injury, as even imperfect axonal growth and regeneration strategies will likely be of profound benefit. Understanding complex control of MYC action in the brain might have important therapeutic significance, but also it may contribute to the comprehension of development of neurodegenerative diseases.
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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.