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000285815 1001_ $$aLi, Tao$$b0
000285815 245__ $$aInflammasome adaptor ASC promotes sustained neuroinflammation and mild cognitive impairment in a closed-head injury model.
000285815 260__ $$aAnn Arbor, Mich.$$bASCJ$$c2026
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000285815 520__ $$aMild traumatic brain injury (mTBI) from a closed-head injury (CHI) can lead to prevalent neuropsychiatric disorders, including mood disorders and an increased risk for neurodegenerative diseases and dementia. Inflammasomes are molecular complexes crucial for neuroinflammation and secondary damage after trauma, however their role in mild CHI (mCHI) is poorly understood. In this study, we investigate the cellular expression of inflammasome-related genes and their functional significance in CHI models. Single-cell RNA-seq analysis of cortical tissue after trauma revealed selective expression of Asc (also known as Pycard), which encodes the inflammasome adaptor apoptosis-associated Speck-like protein containing a caspase recruitment domain (ASC), predominantly in microglial clusters. Sustained upregulation of inflammasome-related proteins, microglia activation, and astrocyte reactivity persisted up to 21 days in a model for mTBI, with significant reduction of this pattern in Asc-/- mice. Importantly, mild cognitive impairment induced after mCHI was largely abrogated in Asc-/- mice. These findings suggest that ASC, as the primary inflammasome adaptor, plays a critical role in sustaining neuroinflammation and contributes to cognitive deficits after mCHI. This study provides insights into the molecular neuroinflammatory mechanisms underlying CHI, potentially informing future therapeutic strategies.
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000285815 650_7 $$2Other$$aDementia
000285815 650_7 $$2Other$$aInflammation
000285815 650_7 $$2Other$$aInnate immunity
000285815 650_7 $$2Other$$aNeuroscience
000285815 650_7 $$2Other$$aTranscriptomics
000285815 650_7 $$2NLM Chemicals$$aCARD Signaling Adaptor Proteins
000285815 650_7 $$2NLM Chemicals$$aInflammasomes
000285815 650_7 $$2NLM Chemicals$$aPycard protein, mouse
000285815 650_2 $$2MeSH$$aAnimals
000285815 650_2 $$2MeSH$$aCARD Signaling Adaptor Proteins: genetics
000285815 650_2 $$2MeSH$$aCARD Signaling Adaptor Proteins: metabolism
000285815 650_2 $$2MeSH$$aMice
000285815 650_2 $$2MeSH$$aCognitive Dysfunction: pathology
000285815 650_2 $$2MeSH$$aCognitive Dysfunction: metabolism
000285815 650_2 $$2MeSH$$aCognitive Dysfunction: genetics
000285815 650_2 $$2MeSH$$aCognitive Dysfunction: etiology
000285815 650_2 $$2MeSH$$aInflammasomes: genetics
000285815 650_2 $$2MeSH$$aInflammasomes: metabolism
000285815 650_2 $$2MeSH$$aDisease Models, Animal
000285815 650_2 $$2MeSH$$aMice, Knockout
000285815 650_2 $$2MeSH$$aNeuroinflammatory Diseases: pathology
000285815 650_2 $$2MeSH$$aNeuroinflammatory Diseases: metabolism
000285815 650_2 $$2MeSH$$aNeuroinflammatory Diseases: genetics
000285815 650_2 $$2MeSH$$aNeuroinflammatory Diseases: etiology
000285815 650_2 $$2MeSH$$aMale
000285815 650_2 $$2MeSH$$aBrain Concussion: pathology
000285815 650_2 $$2MeSH$$aBrain Concussion: genetics
000285815 650_2 $$2MeSH$$aBrain Concussion: metabolism
000285815 650_2 $$2MeSH$$aMicroglia: pathology
000285815 650_2 $$2MeSH$$aMicroglia: metabolism
000285815 650_2 $$2MeSH$$aMice, Inbred C57BL
000285815 7001_ $$0P:(DE-2719)9002230$$aCastro-Gomez, Mario Sergio$$b1$$udzne
000285815 7001_ $$aBotella Lucena, Pablo$$b2
000285815 7001_ $$0P:(DE-2719)9000382$$aVieira-Saecker, Ana$$b3
000285815 7001_ $$0P:(DE-2719)9000454$$aSchwartz, Stephanie$$b4
000285815 7001_ $$aDing, Yingying$$b5
000285815 7001_ $$0P:(DE-2719)9001013$$aDeng, Yushuang$$b6$$udzne
000285815 7001_ $$aGou, Maling$$b7
000285815 7001_ $$aStein, Valentin$$b8
000285815 7001_ $$0P:(DE-2719)9001335$$aGolenbock, Douglas T$$b9
000285815 7001_ $$0P:(DE-2719)2000062$$aLatz, Eicke$$b10$$udzne
000285815 7001_ $$0P:(DE-2719)2000008$$aHeneka, Michael T$$b11
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