These data support the notion that selective autophagy can impact microglia activation by modulating IL-1beta and IL-18 production via NLRP3 degradation and thus present a mechanism how impaired autophagy could contribute to neuroinflammation in Alzheimer's disease.
Susceptibility disorders for AD, including obesity, type-2 diabetes, cardiovascular diseases and metabolic syndrome have been linked to increases in the proinflammatory cytokine, IL-18, which also regulates multiple AD related proteins.
Here, we demonstrate an increased expression of the inflammasome components NLRP3 and Caspase-1 and the products of inflammasome activation IL-1β and IL-18 along with GMF in the temporal cortex of AD brains.
The present study aims to analyze the levels of resistin, tumor necrosis factor alpha (TNF-<i>α</i>), interleukin (IL)-1<i>β</i>, IL-6, IL-18, and C-reactive protein (CRP) in patients with Alzheimer's disease (AD) and also investigate a potential relationship between resistin levels and TNF-<i>α</i>, IL-1<i>β</i>, IL-6, IL-18, and CRP levels in patients with AD.
The accumulation of proinflammatory cytokines, such as IL1B (interleukin 1 β) and IL18 (interleukin 18), as well as the dysfunctional autophagy pathway may damage hippocampal neuronal cells, thus leading to hippocampal-dependent impairment in learning and memory, which is associated with the pathogenesis of Alzheimer disease (AD).
Considering a single study may lack the power to provide reliable conclusion, we performed a meta-analysis to investigate the association between the IL-18-137 G/C and -607 C/A polymorphisms and AD susceptibility.
To clarify the role of IL-18 as a potential cause for AD susceptibility, we investigated the effect of two functional polymorphisms in IL-18 promoter: -607 C/A (rs1946518) and -137 G/C (rs187238) for the risk of sporadic late onset Alzheimer's disease (LOAD) in a Han Chinese population of 109 patients and 109 healthy controls matched for sex and age.
We previously demonstrated that the expression of the pro-inflammatory cytokine interleukin-18 (IL-18) colocalizes with plaques and hyperphoshorylated tau containing neurons in AD patients.
As IL-18 cytokine promoter gene polymorphisms have been previously described to have functional consequences on IL-18 expression, it is possible that individuals with a prevalent IL-18 gene variant have a dysregulated immune response, suggesting that IL-18 mediated immune mechanisms may play a crucial role in AD.
As IL-18 cytokine promoter gene polymorphisms have been previously described to have functional consequences on IL-18 expression, it is possible that individuals with a prevalent IL-18 gene variant have a dysregulated immune response, suggesting that IL-18 mediated immune mechanisms may play a crucial role in AD.