Cognitive Deficits after TBI are Exaggerated by Microglia-Associated Reactivity to Immune Challenge
Year: 2015
Type: article
Abstract: Inflammatory alterations in microglia biology occur with aging, traumatic CNS injury and neurodegenerative diseases.These changes represent a profile of microglia that are more reactive to secondary insults and exaggerated production of inflammatory cytokines by microglia.Furthermore, this coincides with the development of neuropsychological complications including cognitive decline and depression.In each of the models examined here, this prolonged neuroinflammation mediated by microglia is associated with cognitive and behavioral deficits and progressive pathologies.The causes of these impairments and what gives rise to a primed microglial population are not well understood.Head injury may provide the most direct evidence of a primed and pro-inflammatory profile that persist long after the injury.The studies from our lab (highlighted in chapter 1) have shown that that microglia and astrocytes play a dynamic role in sensing and interpreting signals from the peripheral immune system.As demonstrated in chapter 2, persistent glial inflammation or priming following TBI may adversely affect the ability of glia to appropriately respond to immune challenges, such as infection or illness, which occur regularly across the lifespan.Thus, impaired immunoregulation with aging, brain trauma, and neurodegenerative diseases precipitates a predisposition for cognitive and neurobehavioral deficits.This is particularly relevant because of an increased frequency of neuropsychiatric disorders and increased risk for the development of neurodegenerative disease after TBI.
Author: Megan M. Muccigrosso
Institution: The Ohio State University
Language: English
Subfield: Neurology
Field: Neuroscience
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W2621010284