| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Outline of Final Research Achievements |
Inflammasomes can be activated not only by extracorporeal pathogens like virus and bacterium, but also by the internal factors including intracellular matrix to induce inflammation during neurodegeneration. ASC (apoptosis-associated speck-like protein containing a CARD) is a key component to activate inflammasomes. We investigated the effects of knock out of ASC on the severity of ischemic brain damage and traumatic brain injury. Compared to wild type, targeted disruption of ASC significantly suppressed increases in TNFα and IL-1β within the ischemic brain, and showed a tendency of less infarct volume after ischemia. Furthermore, this disruption significantly precluded increases in TNFα and IL-1β within the brain subjected to mild traumatic injury and attenuated space-navigation disability after mild traumatic brain injury (MTBI). These findings suggest that the inhibition of inflammasomes’ activation can ameliorate the secondary neurodegeneration after brain ischemia or MTBI.
|
