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001-es BibID:	BIBFORM116002
035-os BibID:	(Scopus)85193370954 (WoS)001229829200018
Első szerző:	Ducza László (molekuláris biológus)
Cím:	The Neglected Sibling : NLRP2 Inflammasome in the Nervous System / László Ducza, Botond Gaál
Dátum:	2023
ISSN:	2152-5250
Megjegyzések:	While classical NOD-like receptor pyrin domain containing protein 1 (NLRP1) and NLRP3 inflammasomal proteins have been extensively investigated, the contribution of NLRP2 is still ill-defined in the nervous system. Given the putative significance of NLRP2 in orchestrating neuroinflammation, further inquiry is needed to gain a better understanding of its connectome, hence its specific targeting may hold a promising therapeutic implication. Therefore, bioinformatical approach for extracting information, specifically in the context of neuropathologies, is also undoubtedly preferred. To the best of our knowledge, there is no review study selectively targeting only NLRP2. Increasing, but still fragmentary evidence should encourage researchers to thoroughly investigate this inflammasome in various animal- and human models. Taken together, herein we aimed to review the current literature focusing on the role of NLRP2 inflammasome in the nervous system and more importantly, we provide an algorithm-based protein network of human NLRP2 for elucidating potentially valuable molecular partnerships that can be the beginning of a new discourse and future therapeutic considerations.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk inflammasome NLRP2 neurological disorders connectome
Megjelenés:	Aging and disease. - 15 : 5 (2023), p. 1-23. -
További szerzők:	Gaál Botond Ágoston (1982-) (anatómus, neurobiológus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM131018
035-os BibID:	(wos)001520635500001
Első szerző:	Gaál Botond Ágoston (anatómus, neurobiológus)
Cím:	The Inflammasome-miR Axis in Alzheimer's Disease and Chronic Pain : molecular Mechanisms and Therapeutic Opportunities / Gaál Botond, Takács Roland, Matta Csaba, Juhász Krisztián, Fülesdi Béla, Szekanecz Zoltán, Benkő Szilvia, Ducza László
Dátum:	2025
ISSN:	2152-5250
Megjegyzések:	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-? (A?) 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.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban folyóiratcikk Alzheimer's disease Chronic pain Neuroinflammation Inflammasome MicroRNA Spinal cord Glia
Megjelenés:	Aging and Disease. - [Epub ahead of print] (2025). -
További szerzők:	Takács Roland Ádám (1985-) (molekuláris biológus, biokémikus) Matta Csaba (1980-) (molekuláris biológus, genetikus, angol szakfordító) Juhász Krisztián Zoltán (1998-) (molekuláris biológus) Fülesdi Béla (1961-) (aneszteziológus) Szekanecz Zoltán (1964-) (reumatológus, belgyógyász, immunológus) Benkő Szilvia (1973-) (molekuláris biológus) Ducza László (1987-) (molekuláris biológus)
Pályázati támogatás:	FK-134304 OTKA EKÖP-24-4-II-DE-58 Egyéb EKÖP-24-3-I-DE-29 Egyéb K131844 OTKA BO/125/13 MTA K147109 OTKA
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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