Purpose of Review <p>Alzheimer’s disease (AD) refers to a progressive neurodegenerative disease which is associated with dementia, neuronal dysfunction and cognitive decline. One of the molecular regulators that has been identified in the etiology of AD is the microRNA-124 (miR-124). This review will explore the basis of miR-124 in AD pathogenesis, its possible use as a diagnostic biomarker, and the possible treatment of miR-124.</p> Recent Findings <p>The miR-124 is highly expressed in the central nervous system (CNS) and modulates various pathological pathways in AD, such as amyloid-β metabolism, tau phosphorylation, neuroinflammation, synaptic plasticity, and mitochondrial activity. Studies show that miR-124 is significantly decreased in AD brains that are associated with disease progression and severity.</p> <p>It encourages the compilation of amyloid-B by means of a transformed metabolism of amyloid precursor protein (APP) and aids in the creation of neurofibrillary tangles by means of hyperphosphorylation of tau. Conversely, miR-124 exerts neuroprotective effects by suppressing pro-inflammatory signalling, preserving mitochondrial integrity, and promoting neuronal survival.</p> Summary <p>The multifaceted role of miR-124 supports its two possible applications as a biomarker to diagnose AD at the earliest stages and as a therapeutic agent to avoid the irreversible neuronal loss in AD. Restoring miR-124 is one of the promising therapeutic interventions in the management of AD. This review provides a comprehensive overview of miR-124-mediated molecular pathways, its diagnostic value and its therapeutic potential on AD. </p>

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microRNA-124 in Alzheimer’s Disease: Bridging Neuro-regulation and Emerging Therapeutic Strategies

  • Snehashis Mandal,
  • Gaurav Singh,
  • Ayushreeya Banga,
  • Kousik Maparu,
  • Khadga Raj Aran

摘要

Purpose of Review

Alzheimer’s disease (AD) refers to a progressive neurodegenerative disease which is associated with dementia, neuronal dysfunction and cognitive decline. One of the molecular regulators that has been identified in the etiology of AD is the microRNA-124 (miR-124). This review will explore the basis of miR-124 in AD pathogenesis, its possible use as a diagnostic biomarker, and the possible treatment of miR-124.

Recent Findings

The miR-124 is highly expressed in the central nervous system (CNS) and modulates various pathological pathways in AD, such as amyloid-β metabolism, tau phosphorylation, neuroinflammation, synaptic plasticity, and mitochondrial activity. Studies show that miR-124 is significantly decreased in AD brains that are associated with disease progression and severity.

It encourages the compilation of amyloid-B by means of a transformed metabolism of amyloid precursor protein (APP) and aids in the creation of neurofibrillary tangles by means of hyperphosphorylation of tau. Conversely, miR-124 exerts neuroprotective effects by suppressing pro-inflammatory signalling, preserving mitochondrial integrity, and promoting neuronal survival.

Summary

The multifaceted role of miR-124 supports its two possible applications as a biomarker to diagnose AD at the earliest stages and as a therapeutic agent to avoid the irreversible neuronal loss in AD. Restoring miR-124 is one of the promising therapeutic interventions in the management of AD. This review provides a comprehensive overview of miR-124-mediated molecular pathways, its diagnostic value and its therapeutic potential on AD.