eprintid: 224859
rev_number: 13
eprint_status: archive
userid: 11499
dir: disk0/00/22/48/59
datestamp: 2025-09-22 13:05:38
lastmod: 2025-09-22 13:05:38
status_changed: 2025-09-22 13:05:38
type: article
metadata_visibility: show
contact_email: matta.csaba@med.unideb.hu
creators_name: Botond, Gaál
creators_name: Roland, Takács
creators_name: Csaba, Matta
creators_name: Krisztián, Juhász
creators_name: Béla, Fülesdi
creators_name: Zoltán, Szekanecz
creators_name: Szilvia, Benkő
creators_name: László, Ducza
title: The Inflammasome-miR Axis in Alzheimer’s Disease and Chronic Pain: Molecular Mechanisms and Therapeutic Opportunities
ispublished: inpress
subjects: R850-854
full_text_status: public
keywords: Alzheimer’s disease;  Chronic pain , Neuroinflammation , Inflammasome , MicroRNA , Spinal cord , Glia
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-β (Aβ) 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.
date: 2025-06-25
date_type: published
publication: AGING AND DISEASE
id_number: doi:10.14336/AD.2025.0353
refereed: TRUE
issn: 21525250
official_url: http://doi.org/10.14336/AD.2025.0353
funders: Bolyai János Kutatási Ösztöndíj
fp7_project: no
fp7_type: info:eu-repo/semantics/article
citation:   Botond, Gaál and Roland, Takács and Csaba, Matta and Krisztián, Juhász and Béla, Fülesdi and Zoltán, Szekanecz and Szilvia, Benkő and László, Ducza  (2025) The Inflammasome-miR Axis in Alzheimer’s Disease and Chronic Pain: Molecular Mechanisms and Therapeutic Opportunities.  AGING AND DISEASE.   ISSN 21525250    (In Press)  
document_url: https://real.mtak.hu/224859/1/The%20Inflammasome-miR%20Axis%20in%20Alzheimer%26%23x02019%3Bs%20Disease%20and%20Chronic%20Pain_%20Molecular%20Mechanisms%20and%20Therapeutic%20Opportunities.pdf