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Background <p>microRNA-4284 is associated with various diseases, but its role in Alzheimer’s disease remains unclear. This study explores the therapeutic potential of miR-4284 inhibition by targeting the APBA1 and the JAK/STAT3 pathways in AD models.</p> Results <p>miR-4284 expression was analyzed in Aβ-treated SH-SY5Y cells and 5xFAD mice. Luciferase assays identified APBA1 as a direct target of miR-4284. Apoptosis, inflammation, and neuronal survival were assessed using qPCR, western blotting analysis, FACS, and immunohistochemistry. The Morris water maze test evaluated cognitive function, while western blotting analysis examined the JAK/STAT3 pathway. miR-4284 was upregulated in AD models. Its inhibition increased APBA1 expression, reduced Aβ accumulation, suppressed apoptosis and inflammation, and enhanced neuronal survival and cognitive function, correlating with JAK/STAT3 activation.</p> Conclusions <p>miR-4284 inhibition confers neuroprotection by modulating APBA1 and JAK/STAT3 signaling, suggesting its potential as a therapeutic target for AD.</p>

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Inhibition of miR-4284 could reduce apoptosis and neuroinflammation by targeting APBA1/JAK1/STAT3 signaling in Alzheimer’s disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月31日

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  • Jiyun Choi,
  • Jinsu Hwang,
  • Dohee Kim,
  • Eunjae Jang,
  • Geupil Jang,
  • Hyong-Ho Cho,
  • Byeong C. Kim,
  • Han-Seong Jeong,
  • Sujeong Jang

摘要

Background

microRNA-4284 is associated with various diseases, but its role in Alzheimer’s disease remains unclear. This study explores the therapeutic potential of miR-4284 inhibition by targeting the APBA1 and the JAK/STAT3 pathways in AD models.

Results

miR-4284 expression was analyzed in Aβ-treated SH-SY5Y cells and 5xFAD mice. Luciferase assays identified APBA1 as a direct target of miR-4284. Apoptosis, inflammation, and neuronal survival were assessed using qPCR, western blotting analysis, FACS, and immunohistochemistry. The Morris water maze test evaluated cognitive function, while western blotting analysis examined the JAK/STAT3 pathway. miR-4284 was upregulated in AD models. Its inhibition increased APBA1 expression, reduced Aβ accumulation, suppressed apoptosis and inflammation, and enhanced neuronal survival and cognitive function, correlating with JAK/STAT3 activation.

Conclusions

miR-4284 inhibition confers neuroprotection by modulating APBA1 and JAK/STAT3 signaling, suggesting its potential as a therapeutic target for AD.