Start Date
2018
Description
It is widely known that increased level of neuronal activity stimulates an inflammatory response in the brain and periphery tissue. A coordinated activity of the NVU cells such as microglia and astrocytes is necessary to regulate local inflammation in brain tissue. Recently, there is growing evidence that the NVU to be affected by the loss of Blood-brain barrier (BBB) integrity and permeability in neurodegenerative diseases (e.g. AD and ALS) as a result from the long-term effects of neuroinflammation1 . In other words, any signaling used to elicit NVC during inflammation must pass through the BBB. Also, current findings have shown that BBB disruption primarily occurs due to the disorganization of tight junction protein. Other findings have shown that certain cytokines (IL-1β and TNF-⍺) releases have a key role in inflammatory conditions2 . However, mechanisms by which inflammation affects BBB function and NVU together is not well understood. Hence, we further examine this mechanism in which systemic inflammation induces BBB disruption in vivo/in vitro by investigating possible markers, such as percent changes in cerebral blood volumes (% CBV), brain cytokine levels cytokines (IL-1β and TNF-⍺) and NVU cells (microglia and astrocytes).
Recommended Citation
Dho, Jinsung; Ha, Jiwon; Park, Hye Jin; and Suh, Minah, "Roles of Anti-Inflammatory Drugs and Systemic Inflammation in Neurovascular Coupling on rodent" (2018). Summer Research. 17.
https://digitalcommons.calvin.edu/summer_research/2018/Posters/17
Included in
Roles of Anti-Inflammatory Drugs and Systemic Inflammation in Neurovascular Coupling on rodent
It is widely known that increased level of neuronal activity stimulates an inflammatory response in the brain and periphery tissue. A coordinated activity of the NVU cells such as microglia and astrocytes is necessary to regulate local inflammation in brain tissue. Recently, there is growing evidence that the NVU to be affected by the loss of Blood-brain barrier (BBB) integrity and permeability in neurodegenerative diseases (e.g. AD and ALS) as a result from the long-term effects of neuroinflammation1 . In other words, any signaling used to elicit NVC during inflammation must pass through the BBB. Also, current findings have shown that BBB disruption primarily occurs due to the disorganization of tight junction protein. Other findings have shown that certain cytokines (IL-1β and TNF-⍺) releases have a key role in inflammatory conditions2 . However, mechanisms by which inflammation affects BBB function and NVU together is not well understood. Hence, we further examine this mechanism in which systemic inflammation induces BBB disruption in vivo/in vitro by investigating possible markers, such as percent changes in cerebral blood volumes (% CBV), brain cytokine levels cytokines (IL-1β and TNF-⍺) and NVU cells (microglia and astrocytes).