Inflammasome adaptor ASC promotes sustained neuroinflammation and mild cognitive impairment in a closed-head injury model - PubMed
4 hours ago
- #cognitive impairment
- #neuroinflammation
- #closed-head injury
- Mild traumatic brain injury (mTBI) from closed-head injuries (CHI) can lead to neuropsychiatric disorders and increased risk for neurodegenerative diseases.
- Inflammasomes, particularly ASC (Apoptosis-associated Speck-like protein containing a Caspase recruitment domain), play a critical role in neuroinflammation post-CHI.
- Single-cell RNA sequencing showed ASC is predominantly expressed in microglial clusters after trauma.
- Sustained neuroinflammation, microglia activation, and astrocyte reactivity persisted up to 21 days post-mTBI, significantly reduced in Asc-/- mice.
- Mild cognitive impairment post-CHI was largely abrogated in Asc-/- mice, highlighting ASC's role in cognitive deficits.
- The study suggests ASC as a key inflammasome adaptor sustaining neuroinflammation and contributing to cognitive deficits after mild CHI.