ArticleBMC neuroscience2026
Milk-derived miR-126-3p-loaded small extracellular vesicles attenuate amyloid-β-induced cellular stress in a neuroblastoma cell model.
Article in BMC neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
- Integration of Transcriptional Signatures from Brain Tissue and Plasma Extracellular Vesicles of a Preclinical Tauopathy Mouse Model.International journal of molecular sciences · 2026Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer’s disease (AD) is characterized by progressive neurodegeneration driven by amyloid-β (Aβ)–associated oxidative stress, mitochondrial dysfunction, and dysregulated inflammatory signaling. Although microRNAs (miRNAs) represent promising regulators of these interconnected pathways, their therapeutic application is limited by instability and inefficient cellular delivery. In this study, the cytoprotective potential of milk-derived small extracellular vesicles (sEVs) loaded with miR-126-3p was evaluated in an Aβ-induced SH-SY5Y neuroblastoma cell model. sEVs were isolated and characterized according to MISEV guidelines, loaded with synthetic miR-126-3p, and administered to Aβ-induced cells. miR-126-3p–enriched sEVs significantly attenuated Aβ-induced oxidative stress, as evidenced by normalization of ROS, LDH, GPX1, MDA, and SOD levels, while naïve sEVs exerted only partial effects. At the transcriptional level, miR-126-3p delivery restored stress-responsive gene expression patterns by reducing ICAM1 and TNF-α expression and normalizing BDNF levels, reflecting modulation of neuron-intrinsic inflammatory signaling rather than tissue-level neuroinflammation. Markers of cytoskeletal and mitochondrial stress, including intracellular NfL, cytochrome c, 8-OHdG, TFAM, PINK1, and DNM1L, were also significantly reduced following miR-126-3p–loaded sEV treatment, indicating improved cellular homeostasis under amyloid stress. Furthermore, intracellular tau-related markers and Aβ1–40 accumulation were attenuated, consistent with suppression of Aβ-triggered pathological signaling cascades. Collectively, these findings demonstrate that sEV-mediated miR-126-3p delivery confers robust cytoprotective effects at the cellular level in a neuroblastoma model. While extrapolation to in vivo neurodegeneration requires caution, the results highlight milk-derived sEVs as a biocompatible and scalable platform for miRNA-based modulation of AD-relevant cellular stress pathways.
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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.