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@ARTICLE{Braatz:257344,
      author       = {Braatz, Charlotte and Komes, Max and Ravichandran, Kishore
                      and Garcia de Fragas, Matheus and Griep, Angelika and
                      Schwartz, Stephanie and McManus, Roisin and Heneka, Michael
                      T},
      title        = {{NLRP}3-directed antisense oligonucleotides reduce
                      microglial immunoactivities in vitro.},
      journal      = {Journal of neurochemistry},
      volume       = {168},
      number       = {10},
      issn         = {0022-3042},
      address      = {Oxford},
      publisher    = {Wiley-Blackwell},
      reportid     = {DZNE-2023-00413},
      pages        = {3467 - 3481},
      year         = {2024},
      abstract     = {Alzheimer's disease (AD) is associated with the cerebral
                      deposition of Amyloid-β (Aβ) peptide, which leads to NLRP3
                      inflammasome activation and subsequent release of
                      interleukin-1β (IL-1β) and interleukin-18 (IL-18). NLRP3
                      reduction has been found to increase microglial clearance,
                      protect from synapse loss, and suppress both the changes to
                      synaptic plasticity and spatial memory dysfunction observed
                      in murine AD models. Here, we test whether NLRP3-directed
                      antisense oligonucleotides (ASOs) can be harnessed as immune
                      modulators in primary murine microglia and human THP-1
                      cells. NLRP3 mRNA degradation was achieved at 72 h of ASO
                      treatment in primary murine microglia. Consequently,
                      NLRP3-directed ASOs significantly reduced the levels of
                      cleaved caspase-1 and mature IL-1β when microglia were
                      either activated by LPS and nigericin or LPS and Aβ. In
                      human THP-1 cells NLRP3-targeted ASOs also significantly
                      reduced the LPS plus nigericin- or LPS plus Aβ-induced
                      release of mature IL-1β. Together, NLRP3-directed ASOs can
                      suppress NLRP3 inflammasome activity and subsequent release
                      of IL-1β in primary murine microglia and THP-1 cells. ASOs
                      may represent a new and alternative approach to modulate
                      NLRP3 inflammasome activation in neurodegenerative diseases,
                      in addition to attempts to inhibit the complex
                      pharmacologically.},
      keywords     = {Microglia: metabolism / Microglia: drug effects / Animals /
                      NLR Family, Pyrin Domain-Containing 3 Protein: metabolism /
                      Humans / Mice / Oligonucleotides, Antisense: pharmacology /
                      Mice, Inbred C57BL / Amyloid beta-Peptides: metabolism /
                      Interleukin-1beta: metabolism / Inflammasomes: metabolism /
                      THP-1 Cells / Cells, Cultured / Alzheimer's disease (Other)
                      / Aβ (Other) / NLRP3 inflammasome (Other) / antisense
                      oligonucleotides (Other) / innate immunity (Other) /
                      microglia (Other) / neuroinflammation (Other)},
      cin          = {Biomarker / AG Heneka},
      ddc          = {610},
      cid          = {I:(DE-2719)1011301 / I:(DE-2719)1011303},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36799439},
      doi          = {10.1111/jnc.15778},
      url          = {https://pub.dzne.de/record/257344},
}