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<p>AD is a progressive neurodegenerative disease characterized by oxidative stress (OS), mitochondrial dysfunction, and synaptic dysfunction. Long non-coding RNAs (lncRNAs) play a crucial role in gene expression at transcriptional and post-transcriptional levels. Among them, NEAT1 is a structural component of nuclear paraspeckles that maintains transcriptional stability and coordinates stress responses. NEAT1 serves as a molecular scaffold that interacts with RNA-binding proteins to regulate pre-mRNA splicing, transcriptional repression, and cellular homeostasis. NEAT1 expression is elevated in AD and is associated with neuroinflammation, synaptic plasticity alterations, and neuronal apoptosis. It epigenetically regulates targets including CAV2, TGFB2, TGFBR1, and FZD3, suggesting context-dependent protective and pathogenic roles in AD progression. This multifaceted nature highlights NEAT1 as a potential noninvasive biomarker and therapeutic target. This review summarizes the structure and function of NEAT1, its regulatory role in the pathophysiology of AD, and new therapeutic approaches to regulate its expression.</p>

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Role of LncRNA NEAT1 in Alzheimer’s Disease: Pathophysiological Insights and Therapeutic Approaches

  • 期刊论文

  • 发表日期：

    2026年3月21日

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  • Shreya,
  • Gursimran Singh,
  • Garry Hunjan,
  • Khadga Raj Aran

摘要

AD is a progressive neurodegenerative disease characterized by oxidative stress (OS), mitochondrial dysfunction, and synaptic dysfunction. Long non-coding RNAs (lncRNAs) play a crucial role in gene expression at transcriptional and post-transcriptional levels. Among them, NEAT1 is a structural component of nuclear paraspeckles that maintains transcriptional stability and coordinates stress responses. NEAT1 serves as a molecular scaffold that interacts with RNA-binding proteins to regulate pre-mRNA splicing, transcriptional repression, and cellular homeostasis. NEAT1 expression is elevated in AD and is associated with neuroinflammation, synaptic plasticity alterations, and neuronal apoptosis. It epigenetically regulates targets including CAV2, TGFB2, TGFBR1, and FZD3, suggesting context-dependent protective and pathogenic roles in AD progression. This multifaceted nature highlights NEAT1 as a potential noninvasive biomarker and therapeutic target. This review summarizes the structure and function of NEAT1, its regulatory role in the pathophysiology of AD, and new therapeutic approaches to regulate its expression.