Wasim Muhammad, Guo Junhao, Wang Zhendong, Parveen Rabia, Chen Riling, Wang Yajun, Ma Guoda
Maternal and Children's Health Research Institute, Shunde Women and Children's Hospital, Guangdong Medical University, Foshan, China.
Institute of Pediatric, Shunde Women and Children Hospital, Guangdong Medical University, Foshan, China.
J Alzheimers Dis Rep. 2025 Jun 25;9:25424823251352166. doi: 10.1177/25424823251352166. eCollection 2025 Jan-Dec.
Alzheimer's disease (AD) is a neurodegenerative disorder driven by amyloid-β accumulation, tau pathology, and synaptic dysfunction. Recent studies highlight miR-137, a brain-enriched microRNA, as a pivotal regulator of AD pathogenesis. This review synthesizes evidence that miR-137 modulates amyloid-β production, tau phosphorylation, synaptic plasticity, and neuroinflammation, while also preserving mitochondrial function and mitigating oxidative stress. Notably, circulating miR-137 levels correlate with AD progression, offering promise as a non-invasive diagnostic biomarker. Beyond diagnostics, miR-137's ability to target multiple AD-related pathways positions it as a novel therapeutic candidate for neuroprotection. Hence, miR-137 serves as both a biomarker and therapeutic target, offering promising strategies to slow AD progression and improve outcomes. Our bioinformatic analyses further identify miR-137-regulated genes and disrupted networks, underscoring its central role in AD. By bridging molecular mechanisms and clinical potential, miR-137-based strategies could transform AD management, addressing both pathological hallmarks and cognitive decline. Hence, this review article consolidates evidence of miR-137's multifaceted functions in AD, encouraging further investigation into its molecular mechanisms and translational potential to address this pathogenic condition.
阿尔茨海默病（AD）是一种由淀粉样β蛋白积累、tau蛋白病变和突触功能障碍驱动的神经退行性疾病。最近的研究强调了miR-137，一种在大脑中富集的微小RNA，是AD发病机制的关键调节因子。这篇综述综合了证据表明，miR-137调节淀粉样β蛋白的产生、tau蛋白磷酸化、突触可塑性和神经炎症，同时还能维持线粒体功能并减轻氧化应激。值得注意的是，循环miR-137水平与AD进展相关，有望成为一种非侵入性诊断生物标志物。除了诊断之外，miR-137靶向多个AD相关途径的能力使其成为神经保护的新型治疗候选物。因此，miR-137既是一种生物标志物又是治疗靶点，为减缓AD进展和改善预后提供了有前景的策略。我们的生物信息学分析进一步确定了miR-137调节的基因和破坏的网络，强调了其在AD中的核心作用。通过连接分子机制和临床潜力，基于miR-137的策略可以改变AD的管理，解决病理特征和认知衰退问题。因此，这篇综述文章巩固了miR-137在AD中多方面功能的证据，鼓励进一步研究其分子机制和转化潜力以应对这种致病状况。
