FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2129470375> ?p ?o ?g. }

• W2129470375 endingPage "6549" @default.
• W2129470375 startingPage "6539" @default.
• W2129470375 abstract "Inflammation is a key pathological hallmark of Alzheimer's disease (AD), although its impact on disease progression and neurodegeneration remains an area of active investigation. Among numerous inflammatory cytokines associated with AD, IL-1β in particular has been implicated in playing a pathogenic role. In this study, we sought to investigate whether inhibition of IL-1β signaling provides disease-modifying benefits in an AD mouse model and, if so, by what molecular mechanisms. We report that chronic dosing of 3xTg-AD mice with an IL-1R blocking Ab significantly alters brain inflammatory responses, alleviates cognitive deficits, markedly attenuates tau pathology, and partly reduces certain fibrillar and oligomeric forms of amyloid-β. Alterations in inflammatory responses correspond to reduced NF-κB activity. Furthermore, inhibition of IL-1 signaling reduces the activity of several tau kinases in the brain, including cdk5/p25, GSK-3β, and p38-MAPK, and also reduces phosphorylated tau levels. We also detected a reduction in the astrocyte-derived cytokine, S100B, and in the extent of neuronal Wnt/β-catenin signaling in 3xTg-AD brains, and provided in vitro evidence that these changes may, in part, provide a mechanistic link between IL-1 signaling and GSK-3β activation. Taken together, our results suggest that the IL-1 signaling cascade may be involved in one of the key disease mechanisms for AD." @default.
• W2129470375 created "2016-06-24" @default.
• W2129470375 creator A5008959840 @default.
• W2129470375 creator A5009317100 @default.
• W2129470375 creator A5024086237 @default.
• W2129470375 creator A5026487650 @default.
• W2129470375 creator A5030274546 @default.
• W2129470375 creator A5054340538 @default.
• W2129470375 creator A5066782263 @default.
• W2129470375 creator A5087603338 @default.
• W2129470375 date "2011-12-15" @default.
• W2129470375 modified "2023-10-10" @default.
• W2129470375 title "Blocking IL-1 Signaling Rescues Cognition, Attenuates Tau Pathology, and Restores Neuronal β-Catenin Pathway Function in an Alzheimer’s Disease Model" @default.
• W2129470375 cites W1563440444 @default.
• W2129470375 cites W1705725530 @default.
• W2129470375 cites W1784761870 @default.
• W2129470375 cites W1965214584 @default.
• W2129470375 cites W1965942744 @default.
• W2129470375 cites W1966831629 @default.
• W2129470375 cites W1972637602 @default.
• W2129470375 cites W1973216353 @default.
• W2129470375 cites W1974194572 @default.
• W2129470375 cites W1976445933 @default.
• W2129470375 cites W1976829076 @default.
• W2129470375 cites W1977896329 @default.
• W2129470375 cites W1979150324 @default.
• W2129470375 cites W1981962503 @default.
• W2129470375 cites W1984307826 @default.
• W2129470375 cites W1986830236 @default.
• W2129470375 cites W1991377288 @default.
• W2129470375 cites W1994394172 @default.
• W2129470375 cites W1994953714 @default.
• W2129470375 cites W1998981667 @default.
• W2129470375 cites W2001334299 @default.
• W2129470375 cites W2005470401 @default.
• W2129470375 cites W2009174342 @default.
• W2129470375 cites W2009390338 @default.
• W2129470375 cites W2013274571 @default.
• W2129470375 cites W2016575029 @default.
• W2129470375 cites W2017079501 @default.
• W2129470375 cites W2018447297 @default.
• W2129470375 cites W2018708829 @default.
• W2129470375 cites W2020194826 @default.
• W2129470375 cites W2031864556 @default.
• W2129470375 cites W2032365749 @default.
• W2129470375 cites W2033773472 @default.
• W2129470375 cites W2035887863 @default.
• W2129470375 cites W2036094153 @default.
• W2129470375 cites W2037366132 @default.
• W2129470375 cites W2038733641 @default.
• W2129470375 cites W2041425500 @default.
• W2129470375 cites W2049733399 @default.
• W2129470375 cites W2050685224 @default.
• W2129470375 cites W2052092557 @default.
• W2129470375 cites W2054159913 @default.
• W2129470375 cites W2055002633 @default.
• W2129470375 cites W2055316677 @default.
• W2129470375 cites W2057249855 @default.
• W2129470375 cites W2060096067 @default.
• W2129470375 cites W2061576298 @default.
• W2129470375 cites W2062772621 @default.
• W2129470375 cites W2065419688 @default.
• W2129470375 cites W2065656296 @default.
• W2129470375 cites W2068477037 @default.
• W2129470375 cites W2071695496 @default.
• W2129470375 cites W2075725519 @default.
• W2129470375 cites W2076334107 @default.
• W2129470375 cites W2079158266 @default.
• W2129470375 cites W2079381217 @default.
• W2129470375 cites W2083556882 @default.
• W2129470375 cites W2084043574 @default.
• W2129470375 cites W2094958540 @default.
• W2129470375 cites W2096158347 @default.
• W2129470375 cites W2102842633 @default.
• W2129470375 cites W2103428562 @default.
• W2129470375 cites W2105385589 @default.
• W2129470375 cites W2108233365 @default.
• W2129470375 cites W2114358785 @default.
• W2129470375 cites W2120537929 @default.
• W2129470375 cites W2121820194 @default.
• W2129470375 cites W2133595485 @default.
• W2129470375 cites W2136936410 @default.
• W2129470375 cites W2145210308 @default.
• W2129470375 cites W2145283772 @default.
• W2129470375 cites W2147654688 @default.
• W2129470375 cites W2152119060 @default.
• W2129470375 cites W2152728580 @default.
• W2129470375 cites W2153206087 @default.
• W2129470375 cites W2154758696 @default.
• W2129470375 cites W2157079522 @default.
• W2129470375 cites W2164535032 @default.
• W2129470375 cites W2164627569 @default.
• W2129470375 cites W32083764 @default.
• W2129470375 cites W3214092816 @default.
• W2129470375 cites W8494518 @default.
• W2129470375 doi "https://doi.org/10.4049/jimmunol.1100620" @default.
• W2129470375 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4072218" @default.
• W2129470375 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22095718" @default.

• next