What question did this study set out to answer?

The central aim is to investigate the effects of miRNA-25802 on mitochondrial damage, oxidative stress, and neuroinflammation in Alzheimer's disease.

April 24, 2026Open Access

Delivery of miR-25802 via Small Vesicles Protects Against Mitochondrial Injury, Oxidative Stress, and Neuroinflammation in Alzheimer’s Disease

Puntos clave

The central aim is to investigate the effects of miRNA-25802 on mitochondrial damage, oxidative stress, and neuroinflammation in Alzheimer's disease.
Evaluated neuroblastoma cells under various conditions including control, amyloid beta-induced, and treatment with miR-25802-loaded small extracellular vesicles.
Analyzed oxidative stress using reactive oxygen species, malondialdehyde, and other biochemical markers.
Assessed neuroinflammation and mitochondrial function through cytokine levels and protein expression.
miR-25802 demonstrated protective effects by reducing oxidative stress and neuroinflammation in treated cells.
The study found decreased levels of inflammatory markers and improved mitochondrial function following treatment with sEV-miR25802.
Regulatory effects of miR-25802 were shown to mitigate tau hyperphosphorylation and amyloid beta accumulation.

Resumen

Abstract Mitochondrial dysfunction, oxidative stress, and neuroinflammation play a critical role in the occurrence and progression of Alzheimer's disease (AD). MicroRNAs (miRNAs) have been studied recently as potential therapeutic approaches for AD. In this study, we examined the function and underlying mechanism of microRNA-25802 (miR-25802), a newly discovered miRNA in an AD model. In order to evaluate the levels of oxidative stress, mitochondrial damage and neuroinflammation in neuroblastoma cells, four experimental groups were created: control group (neuroblastoma cells, SH-SY5Y), amyloid beta (Aβ)-induced neuroblastoma cells (SY5Y-Aβ), small extracellular vesicles (sEVs)-only group and miR-25802–loaded small extracellular vesicles (sEV-miR25802) administered group. Neuroinflammation, oxidative stress, mitochondrial damage, tau hyperphosphorylation, and Aβ accumulation were evaluated in Aβ-induced neuroblastoma cells. Oxidative stress was analyzed by measuring reactive oxygen species (ROS), malondialdehyde (MDA), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase 1 (GPX1). Inflammatory markers such as tumor necrosis factor-alpha (TNF-α), intercellular adhesion molecule 1 (ICAM1), and brain-derived neurotrophic factor (BDNF) mRNA levels, a neurotrophic factor, were evaluated by RT-qPCR. Neurofilament light chain (NfL), vascular endothelial growth factor-A (VEGF-A), macrophage migration inhibitory factor (MIF), monocyte chemoattractant protein-1 (MCP-1) and cytochrome c (Cyt-c), mitochondrial transcription factor A (TFAM), PTEN-induced kinase 1 (PINK1) and dynamin-1-like protein (DNM1L) protein levels were determined by ELISA. Mechanistically, sEV-miR25802 were shown to provide anti-inflammatory and neuroprotective effects by regulating neuroinflammation, mitochondrial dysfunction, and oxidative stress. These findings reveal the regulatory role of miR-25802 on neuroinflammation, mitochondrial damage, and oxidative stress and suggest that it may be a potential therapeutic target for AD. Graphical Abstract

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