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