Contribution of age on the inflammatory environment in the nigrostriatal pathway following traumatic brain injury

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Date

2015-05

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The Ohio State University

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Abstract

One of the leading risk factors for the development of a neurodegenerative disease is traumatic brain injury (TBI) through the secondary injury of prolonged inflammation. Aging populations have the most exaggerated immune responses following TBI that often result in hospitalization and/or death. While extensive research has investigated inflammatory mechanisms within the hippocampus that differ as animals age, little is known about the age-related changes in the ascending catecholaminergic systems of the brainstem. The current study investigated the effect of age on the expression of inflammatory proteins, motor learning deficits, and the integrity of the nigrostriatal pathway 28 days following traumatic brain injury. Age- and injury-related impairments in motor coordination and learning were observed 1 month after controlled cortical impact surgery. Interestingly, aged TBI-treated animals had increased tyrosine hydroxylase expression in the striatum and substantia nigra. Combined with low levels of pro- and anti-inflammatory cytokine expression observed across groups, this study points toward a novel compensatory mechanism following injury in the aged brain.

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Undergraduate Education Summer Research Fellowship
USG AEG

Keywords

nigrostriatal brain aging inflammation

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