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10.1186/s13024-016-0088-1

http://scihub22266oqcxt.onion/10.1186/s13024-016-0088-1
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C4778358!4778358!26939933
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suck abstract from ncbi


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pmid26939933      Mol+Neurodegener 2016 ; 11 (ä): ä
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  • The NLRP3 and NLRP1 inflammasomes are activated in Alzheimer?s disease #MMPMID26939933
  • Saresella M; La Rosa F; Piancone F; Zoppis M; Marventano I; Calabrese E; Rainone V; Nemni R; Mancuso R; Clerici M
  • Mol Neurodegener 2016[]; 11 (ä): ä PMID26939933show ga
  • Background: Interleukin-1 beta (IL-1?) and its key regulator, the inflammasome, are suspected to play a role in the neuroinflammation observed in Alzheimer?s disease (AD); no conclusive data are nevertheless available in AD patients. Results: mRNA for inflammasome components (NLRP1, NLRP3, PYCARD, caspase 1, 5 and 8) and downstream effectors (IL-1?, IL-18) was up-regulated in severe and MILD AD. Monocytes co-expressing NLRP3 with caspase 1 or caspase 8 were significantly increased in severe AD alone, whereas those co-expressing NLRP1 and NLRP3 with PYCARD were augmented in both severe and MILD AD. Activation of the NLRP1 and NLRP3 inflammasomes in AD was confirmed by confocal microscopy proteins co-localization and by the significantly higher amounts of the pro-inflammatory cytokines IL-1? and IL-18 being produced by monocytes. In MCI, the expression of NLRP3, but not the one of PYCARD or caspase 1 was increased, indicating that functional inflammasomes are not assembled in these individuals: this was confirmed by lack of co-localization and of proinflammatory cytokines production. Conclusions: The activation of at least two different inflammasome complexes explains AD-associated neuroinflammation. Strategies targeting inflammasome activation could be useful in the therapy of AD.
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