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@ARTICLE{Li:285815,
      author       = {Li, Tao and Castro-Gomez, Mario Sergio and Botella Lucena,
                      Pablo and Vieira-Saecker, Ana and Schwartz, Stephanie and
                      Ding, Yingying and Deng, Yushuang and Gou, Maling and Stein,
                      Valentin and Golenbock, Douglas T and Latz, Eicke and
                      Heneka, Michael T},
      title        = {{I}nflammasome adaptor {ASC} promotes sustained
                      neuroinflammation and mild cognitive impairment in a
                      closed-head injury model.},
      journal      = {The journal of clinical investigation},
      volume       = {136},
      number       = {7},
      issn         = {0021-9738},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DZNE-2026-00351},
      pages        = {e199818},
      year         = {2026},
      abstract     = {Mild traumatic brain injury (mTBI) from a closed-head
                      injury (CHI) can lead to prevalent neuropsychiatric
                      disorders, including mood disorders and an increased risk
                      for neurodegenerative diseases and dementia. Inflammasomes
                      are molecular complexes crucial for neuroinflammation and
                      secondary damage after trauma, however their role in mild
                      CHI (mCHI) is poorly understood. In this study, we
                      investigate the cellular expression of inflammasome-related
                      genes and their functional significance in CHI models.
                      Single-cell RNA-seq analysis of cortical tissue after trauma
                      revealed selective expression of Asc (also known as Pycard),
                      which encodes the inflammasome adaptor apoptosis-associated
                      Speck-like protein containing a caspase recruitment domain
                      (ASC), predominantly in microglial clusters. Sustained
                      upregulation of inflammasome-related proteins, microglia
                      activation, and astrocyte reactivity persisted up to 21 days
                      in a model for mTBI, with significant reduction of this
                      pattern in Asc-/- mice. Importantly, mild cognitive
                      impairment induced after mCHI was largely abrogated in
                      Asc-/- mice. These findings suggest that ASC, as the primary
                      inflammasome adaptor, plays a critical role in sustaining
                      neuroinflammation and contributes to cognitive deficits
                      after mCHI. This study provides insights into the molecular
                      neuroinflammatory mechanisms underlying CHI, potentially
                      informing future therapeutic strategies.},
      keywords     = {Animals / CARD Signaling Adaptor Proteins: genetics / CARD
                      Signaling Adaptor Proteins: metabolism / Mice / Cognitive
                      Dysfunction: pathology / Cognitive Dysfunction: metabolism /
                      Cognitive Dysfunction: genetics / Cognitive Dysfunction:
                      etiology / Inflammasomes: genetics / Inflammasomes:
                      metabolism / Disease Models, Animal / Mice, Knockout /
                      Neuroinflammatory Diseases: pathology / Neuroinflammatory
                      Diseases: metabolism / Neuroinflammatory Diseases: genetics
                      / Neuroinflammatory Diseases: etiology / Male / Brain
                      Concussion: pathology / Brain Concussion: genetics / Brain
                      Concussion: metabolism / Microglia: pathology / Microglia:
                      metabolism / Mice, Inbred C57BL / Dementia (Other) /
                      Inflammation (Other) / Innate immunity (Other) /
                      Neuroscience (Other) / Transcriptomics (Other) / CARD
                      Signaling Adaptor Proteins (NLM Chemicals) / Inflammasomes
                      (NLM Chemicals) / Pycard protein, mouse (NLM Chemicals)},
      cin          = {AG Ehninger},
      ddc          = {610},
      cid          = {I:(DE-2719)1013005},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41734021},
      pmc          = {pmc:PMC13038205},
      doi          = {10.1172/JCI199818},
      url          = {https://pub.dzne.de/record/285815},
}