Implicative role of cytokines in neuroinflammation mediated AD and associated signaling pathways: Current progress in molecular signaling and therapeutics

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dc.contributor.authorKumari, Sneha
dc.contributor.authorDhapola, Rishika
dc.contributor.authorSharma, Prajjwal
dc.contributor.authorSingh, Sunil K.
dc.contributor.authorReddy, Dibbanti HariKrishna
dc.date.accessioned2024-01-21T10:44:51Z
dc.date.accessioned2024-08-13T13:21:52Z
dc.date.available2024-01-21T10:44:51Z
dc.date.available2024-08-13T13:21:52Z
dc.date.issued2023-10-30T00:00:00
dc.description.abstractAlzheimer's Disease (AD) is one of the most devastating age-related disorder causing significant social and economic burden worldwide. It affects the cognitive and social behavior of individuals and characterized by accumulation of A?, phosphorylated tau and cytokines formation. The synthesis and release of cytokines are regulated by specific groups of immune and non-immune cells in response to microglia or astrocyte activation through multiple pathways. Physiologically, microglia assert an anti-inflammatory, quiescent state with minimal cytokine expression and little phagocytic activity in motion to carry out their housekeeping role to eliminate pathogens, aggregated A? and tau protein. However, they develop a phagocytic nature and overexpress cytokine gene modules in response to certain stimuli in AD. Microglia and astrocytes upon chronic activation release an enormous amount of inflammatory cytokines due to interaction with formed A? and neurofibrillary tangle. Gut microbiota dysbiosis also stimulates the release of inflammatory cytokines contributing to AD pathogenesis. In addition, the dysregulation of few signaling pathways significantly influences the development of disease, and the pace of advancement also rises with age. This review sheds light on multiple pathways results into neuroinflammation triggered by activated cytokines worsening AD pathology and making it an appropriate target for AD treatment. This review also included drugs targeting different neuroinflammation pathways under clinical and preclinical studies that are found to be effective in attenuating the disease pathology. � 2023 Elsevier B.V.en_US
dc.identifier.doi10.1016/j.arr.2023.102098
dc.identifier.issn15681637
dc.identifier.urihttp://10.2.3.109/handle/32116/3879
dc.identifier.urlhttps://linkinghub.elsevier.com/retrieve/pii/S156816372300257X
dc.language.isoen_USen_US
dc.publisherElsevier Ireland Ltden_US
dc.subjectAstrocytesen_US
dc.subjectA?en_US
dc.subjectCytokinesen_US
dc.subjectDrugsen_US
dc.subjectGut microbiota�brain axisen_US
dc.subjectInterleukinen_US
dc.subjectMicrogliaen_US
dc.subjectNeuroinflammationen_US
dc.titleImplicative role of cytokines in neuroinflammation mediated AD and associated signaling pathways: Current progress in molecular signaling and therapeuticsen_US
dc.title.journalAgeing Research Reviewsen_US
dc.typeReviewen_US
dc.type.accesstypeClosed Accessen_US

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