ArticleMolecular biology reports2025
Single-cell sequencing reveals that AK5 inhibits apoptosis in AD oligodendrocytes by regulating the AMPK signaling pathway.
Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The iron-energy metabolism axis in Alzheimer's pathogenesis: from mechanisms to interventions.Cell death discovery · 2026Review
- Environmental Stressors and Neuroinflammation: Linking Climate Change to Alzheimer's Disease.Current issues in molecular biology · 2025Review
- Decoding neuroinflammation in Alzheimer's disease: a multi-omics and AI-driven perspective for precision medicine.Frontiers in immunology · 2025Review
- Construction of a Prognostic Model of Prostate Cancer Based on Immune and Metabolic Genes and Experimental Validation of the Gene AK5.Oncology research · 2025Article
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8 authors.
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Abstract
backgroundNeuroinflammation and abnormal energy metabolism have been shown to significantly contribute to the progression of Alzheimer's disease (AD). Adenylate kinase 5 (AK5), an enzyme predominantly expressed in the brain regulates ATP metabolism, has an unclear role in energy metabolism and neuroinflammation in AD.
methodsThe AD datasets were derived from the GEO public database to analyze the expression levels of AK5 in AD and normal samples and to assess the relationship between AK5 expression and the clinical characteristics of AD patients. Functional enrichment analysis was employed to investigate the effects of changes in AK5 expression on energy metabolism and immunoinflammation in AD, as well as the underlying mechanisms. Moreover, the influence of AK5 expression variations on oligodendrocyte development was assessed, and the predicted outcomes were validated through cellular experiments.
resultsBioinformatic analysis revealed that AK5 was lowly expressed in AD olfactory lobe tissues, accompanied by increased immunoinflammation and apoptosis. Increased expression of AK5 was associated with the activation of AMPK signaling, enhanced oxidative phosphorylation, and overall stimulation of energy metabolism. In oligodendrocytes treated with Aβ1-42, overexpression of AK5 resulted in elevated levels of P-AMPK, SIRT1, and BCL-2 proteins, while reducing the levels of BAX, CASPASE-3, and NF-κB proteins. This modulation activated AMPK signaling, thereby inhibiting neuroinflammation and apoptosis. In contrast, low levels of AK5 expression during early differentiation triggered inflammatory responses and increased apoptosis in oligodendrocytes.
conclusionAK5 inhibits AD oligodendrocyte apoptosis by activating the AMPK signaling pathway.
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