SynthesisJournal of translational medicine2024
Mitochondrial dysfunction gene expression, DNA methylation, and inflammatory cytokines interaction activate Alzheimer's disease: a multi-omics Mendelian randomization study.
Synthesis in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Alzheimer's Disease as a Multi-Layer Network Disorder: A Systems Biology Framework Integrating Multi-Omics Mechanisms.Biomedicines · 2026Review
- Mitochondrial-Epigenetic Crosstalk in Autism Spectrum Disorder: Linking Cellular Stress to Synaptic Dysfunction and Treatment Resistance.Molecular neurobiology · 2026Review
- Article
- Identifying therapeutic target genes for rheumatoid arthritis-associated interstitial lung disease by systematic druggable genome-wide Mendelian randomization analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Aberrant methylation of mitochondrial genes as a link between oxidative phosphorylation dysregulation and the pathogenesis of hypospadias: a multiomics and clinical sample study.Translational andrology and urology · 2026Article
- Tet2 deficiency orchestrates Alzheimer's pathogenesis through oxidative mtDNA-driven cGAS-STING activation.Journal of neuroinflammation · 2026Article
- The complement cascade in Alzheimer's disease: modern implications of an ancient immune protagonist.Molecular neurodegeneration · 2025Review
- Systematic Review: Proteomics-Driven Multi-Omics Integration for Alzheimer's Disease Pathology and Precision Medicine.Neurology international · 2025Review
- Exploration and validation of biomarkers for Alzheimer's disease based on GEO database.IBRO neuroscience reports · 2025Article
- Association of DRD4 promoter-associated methylation with mild cognitive impairment in Han and Uygur populations.European journal of medical research · 2025Article
- Article
- Exploring biomarkers for noise-induced hearing loss through mitochondrial DNA methylation analysis.Frontiers in pharmacology · 2025Article
- New Bitongling Ameliorates Joint Tissue Damage in Collagen-Induced Arthritis Mice by Suppressing Mapt Expression: A Genome-Wide Sequencing Study.Journal of inflammation research · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundMitochondrial dysfunction (MD) is increasingly recognized as a key pathophysiological contributor in Alzheimer disease (AD). As differential MD genes expression may serve as either a causative factor or a consequence in AD, and expression of these genes could be influenced by epigenetic modifications or interact with inflammatory cytokines, hence, the precise role of MD in AD remains uncertain.
methodsMeta-analysis of brain transcriptome datasets was conducted to pinpoint differentially expressed genes (DEGs) associated with MD in AD. We utilized three-step SMR to analyze the AD genome-wide association study summaries with expression quantitative trait loci (eQTLs) and DNA methylation QTLs from the blood and brain tissues, respectively. Through SMR and colocalization analysis, we further explored the interactions between brain eQTLs and inflammatory cytokines.
resultsFive datasets were meta-analyzed to prioritize 825 DEGs in AD from 1339 MD-related genes. Among these, seven genes from blood samples such as NDUFS8 and SPG7 and thirty-two genes from brain tissue including CLU and MAPT were identified as candidate AD-causal MD genes and regulated by methylation level. Furthermore, we revealed 13 MD gene expression-inflammatory pathway pairs involving LDLR, ACE and PTPMT1 along with interleukin-17C, interleukin-18 and hepatocyte growth factor.
conclusionsThis study highlighted that the AD-causal MD genes could be regulated by epigenetic changes and interact with inflammatory cytokines, providing evidence for AD prevention and intervention.
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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 Socratic graph.