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miR-137: A therapeutic candidate or a key molecular regulator in Alzheimer's disease?
Muhammad Wasim1, Junhao Guo2, Zhendong Wang1
1Maternal and Children's Health Research Institute, Shunde Women and Children's Hospital, Guangdong Medical University, Foshan, China.
Abstract:
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.
Insights
MicroRNA-137 (miR-137) is a key regulator in Alzheimer's disease (AD), impacting amyloid-β and tau pathologies. This review explores miR-137's potential as both a diagnostic biomarker and a therapeutic target for AD.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Alzheimer's disease (AD) is characterized by amyloid-β plaques, tau tangles, and synaptic loss.
- MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene expression and are implicated in neurodegenerative diseases.
- miR-137, a brain-specific miRNA, has emerged as a significant factor in AD pathogenesis.
Purpose of the Study:
- To review the multifaceted roles of miR-137 in Alzheimer's disease.
- To explore miR-137's potential as a diagnostic biomarker and therapeutic target for AD.
- To consolidate evidence on miR-137's molecular mechanisms and translational potential in AD.
Main Methods:
- Literature review and synthesis of existing research on miR-137 in AD.
- Bioinformatic analysis to identify miR-137-regulated genes and networks in AD.
- Analysis of studies investigating circulating miR-137 levels in AD patients.
Main Results:
- miR-137 influences key AD pathologies including amyloid-β production, tau phosphorylation, synaptic plasticity, neuroinflammation, mitochondrial function, and oxidative stress.
- Circulating miR-137 levels show correlation with AD progression, suggesting diagnostic utility.
- Bioinformatic analyses reveal disrupted gene networks regulated by miR-137 in AD.
Conclusions:
- miR-137 is a critical regulator in Alzheimer's disease, affecting multiple pathological pathways.
- miR-137 holds significant promise as a non-invasive biomarker for AD diagnosis and a therapeutic target for neuroprotection.
- Further research into miR-137's mechanisms and therapeutic applications could revolutionize AD management.
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