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<p>Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. This study investigated the roles of HOMER1, ATAD1, and miR-361 in AD pathogenesis using microarray (GSE106241, GSE157239; n = 60) and RT-PCR (n = 100; 50 AD patients, 50 controls from Northwest Iran) analyses. Decreased expression of HOMER1 and ATAD1, key regulators of glutamatergic synapses, and miR-361, a potential regulator of both, was observed in AD brain tissue (GSE106241, categorized into seven Braak stages), suggesting a link between their dysregulation, impaired synaptic function, and increased neuroinflammation. However, blood-based RT-PCR showed no significant difference in HOMER1 or ATAD1. miR-361 was significantly lower in AD patients (adjusted p &lt; 0.043). These findings, limited by sample size and lacking a formal power analysis, require further investigation to validate their potential as peripheral biomarkers for AD. Future studies with larger sample sizes are warranted.</p>

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miR-361-5p contributes to the pathogenesis of Alzheimer’s disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月23日

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  • Abbas Jalaiei,
  • Jalal Gharesouran,
  • Shahram Arsang-Jang,
  • Mahnaz Talebi,
  • Maryam Rezazadeh,
  • Soudeh Ghafouri-Fard

摘要

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder. This study investigated the roles of HOMER1, ATAD1, and miR-361 in AD pathogenesis using microarray (GSE106241, GSE157239; n = 60) and RT-PCR (n = 100; 50 AD patients, 50 controls from Northwest Iran) analyses. Decreased expression of HOMER1 and ATAD1, key regulators of glutamatergic synapses, and miR-361, a potential regulator of both, was observed in AD brain tissue (GSE106241, categorized into seven Braak stages), suggesting a link between their dysregulation, impaired synaptic function, and increased neuroinflammation. However, blood-based RT-PCR showed no significant difference in HOMER1 or ATAD1. miR-361 was significantly lower in AD patients (adjusted p < 0.043). These findings, limited by sample size and lacking a formal power analysis, require further investigation to validate their potential as peripheral biomarkers for AD. Future studies with larger sample sizes are warranted.