ArticleInternational journal of molecular sciences2023
An Exploration of the Coherent Effects between METTL3 and NDUFA10 on Alzheimer's Disease.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Neuromodulatory role and therapeutic potential of N 6 -methyladenosine RNA methylation in neurodegenerative diseases.Neural regeneration research · 2026Article
- Decoding causal m6A: a bioinformatics roadmap for psychiatric disorders.Briefings in bioinformatics · 2026Review
- Linking Personality Traits to Mediterranean Diet Adherence and Exploring Gene-Diet Interactions in Neuroticism.Nutrients · 2025Article
- Decreased METTL3 in atrial myocytes promotes atrial fibrillation.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025Article
- Identification and validation of pyroptosis-related genes in Alzheimer's disease based on multi-transcriptome and machine learning.Frontiers in aging neuroscience · 2025Article
- Effects of mFrontiers in aging neuroscience · 2025Article
- Special Issue "Bioinformatics Study in Human Diseases: Integration of Omics Data for Personalized Medicine".International journal of molecular sciences · 2024Article
- RNA methylation in neurodevelopment and related diseases.Acta biochimica et biophysica Sinica · 2024Review
- The features analysis of hemoglobin expression on visual information transmission pathway in early stage of Alzheimer's disease.Scientific reports · 2024Article
- Longitudinal Neuropathological Consequences of Extracranial Radiation Therapy in Mice.International journal of molecular sciences · 2024Article
- Sensitivity of substrate translocation in chaperone-mediated autophagy to Alzheimer's disease progression.Aging · 2024Article
- CAV3 alleviates diabetic cardiomyopathy via inhibiting NDUFA10-mediated mitochondrial dysfunction.Journal of translational medicine · 2024Article
- Emerging Roles for DNA 6mA and RNA m6A Methylation in Mammalian Genome.International journal of molecular sciences · 2023Review
- The coherence between PSMC6 and α-ring in the 26S proteasome is associated with Alzheimer's disease.Frontiers in molecular neuroscience · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder characterized primarily by a decline in cognitive function. However, the etiopathogenesis of AD is unclear. N6-methyladenosine (m6A) is abundant in the brain, and it is interesting to explore the relationship between m6A and AD causes. In this paper, the gene expression of METTL3 and NDUFA10 were found to correlate with the Mini-mental State Examination (MMSE), which is a clinical indicator of the degree of dementia. METTL3 is involved in post-transcriptional methylation and the formation of m6A. NDUFA10 encodes the protein with NADH dehydrogenase activity and oxidoreductase activity in the mitochondrial electron transport chain. The following three characteristics were observed in this paper: 1. The lower the expression level of NDUFA10, the smaller the MMSE, and the higher the degree of dementia. 2. If the expression level of METTL3 dropped below its threshold, the patient would have a risk of AD with a probability close to 100%, suggesting a basic necessity for m6A to protect mRNA. 3. The lower the expression levels of both METTL3 and NDUFA10, the more likely the patient would suffer from AD, implying the coherence between METTL3 and NDUFA10. Regarding the above discovery, the following hypothesis is presented: METTL3 expression level is downregulated, then the m6A modification level of NDUFA10 mRNA is also decreased, thereby reducing the expression level of NDUFA10-encoded protein. Furthermore, the abnormal expression of NDUFA10 contributes to the assembly disorder of mitochondrial complex I and affects the process of the electron respiratory chain, with the consequent development of AD. In addition, to confirm the above conclusions, the AI Ant Colony Algorithm was improved to be more suitable for discovering the characteristics of AD data, and the SVM diagnostic model was applied to mine the coherent effects on AD between METTL3 and NDUFA10. In conclusion, our findings suggest that dysregulated m6A leads to altered expression of its target genes, thereby affecting AD's development.
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