@article{REAL224859,
           month = {June},
           title = {The Inflammasome-miR Axis in Alzheimer?s Disease and Chronic Pain: Molecular Mechanisms and Therapeutic Opportunities},
          author = {Ga{\'a}l Botond and Tak{\'a}cs Roland and Matta Csaba and Juh{\'a}sz Kriszti{\'a}n and F{\"u}lesdi B{\'e}la and Szekanecz Zolt{\'a}n and Benk{\H o} Szilvia and Ducza L{\'a}szl{\'o}},
            year = {2025},
         journal = {AGING AND DISEASE},
        keywords = {Alzheimer?s disease;  Chronic pain , Neuroinflammation , Inflammasome , MicroRNA , Spinal cord , Glia},
             url = {https://real.mtak.hu/224859/},
        abstract = {Alzheimer?s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, synaptic dysfunction, and chronic neuroinflammation. Mounting evidence suggests that inflammasome activation plays a pivotal role in the onset and progression of AD by promoting neuronal damage, Tau pathology, and amyloid-{\ensuremath{\beta}} (A{\ensuremath{\beta}}) accumulation. Among the various inflammasome types expressed in the central nervous system (CNS), NLRP3 has received particular attention due to its strong association with both AD and pain-related neuroinflammation. Chronic pain, frequently observed in older adults and individuals with dementia, shares overlapping inflammatory mechanisms with AD, including glial activation and cytokine dysregulation. The inflammasome-microRNA (miR) axis has recently emerged as a key regulatory pathway modulating these neuroinflammatory responses. Specific inflammation-associated miRs, such as miR-22, miR-34a, miR-146a, miR-155, and miR-223, influence innate immune signaling and critically affect both neuronal homeostasis and pain sensitization. Emerging evidence also implicates dysfunction of the locus coeruleus-noradrenergic (LC-NE) system{--}an early target of AD pathology{--}in amplifying neuroinflammation and pain sensitivity, partly through interactions with dysregulated miRs. While previous studies have addressed the roles of inflamma-miRs in AD or chronic pain individually, this review uniquely examines their interconnected roles{--}highlighting how dysregulated miR expression and inflammasome activation may converge to drive persistent neuroinflammation across both conditions. By elucidating shared molecular pathways, we propose that targeting the inflammasome-miR axis may offer dual therapeutic potential: slowing AD progression while addressing pain-related neural dysfunction. As the prevalence of AD rises, such integrated insights are essential for the development of more precise, mechanism-based interventions.}
}