ArticleJournal of neuroinflammation2026
IL-18 binding protein attenuates neuroinflammation and cognitive decline in Alzheimer's disease.
Article in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Neuroinflammation in Alzheimer’s disease (AD) extends beyond a secondary response to amyloid-β plaques and neurofibrillary tangles, representing a fundamental driver of disease pathogenesis. The NLRP3 inflammasome has emerged as a central mediator of neuroinflammation in AD, highlighting the importance of understanding its downstream effectors. Interleukin-18 (IL-18), a key proinflammatory cytokine activated by NLRP3 inflammasome, plays a crucial role in innate immunity and neuroinflammatory responses in neurodegenerative diseases and aging. However, its specific contribution to AD pathogenesis remains poorly understood. IL-18 binding protein (IL-18 BP), an endogenous inhibitor that suppresses IL-18-mediated inflammatory responses including IFNγ production, presents a potential therapeutic molecule, yet its regulatory role in AD has not been thoroughly investigated. This study aims to examine whether IL-18 and IL-18 BP are associated with neuroinflammation and neurodegeneration in AD progression and investigate the preventive effects of IL-18 BP in AD. Employing postmortem brain tissues of AD patients and AD mouse models, we confirmed that IL-18 and related proinflammatory signaling were activated in the absence of IL-18 BP in both AD patients and mice, including C/EBPβ transgenic mice, 3xTG (APP Swedish, MAPT P301L, PSEN1M146V), and 5xFAD (familial AD mutation) mice. Administration of IL-18 BP into the hippocampus alleviated inflammation and cognitive impairment during AD pathology progression in 3xTG mice compared to the vehicle administration group. These results suggest that IL-18 BP might be a new target for AD prevention by regulating IL-18-induced proinflammatory reactions and AD pathologies.
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