Poster Title

Neuronal Degeneration and Short-term Memory Impairment after TBI

Grade Level at Time of Presentation

Senior

Institution

University of Louisville

KY House District #

48

KY Senate District #

26

Department

Department of Physiology

Abstract

Traumatic brain injury (TBI) was associated with impaired short-term memory with causes of vehicle accidents and falls. Protein plaques containing fibrinogen (Fg), are associated with memory loss. After TBI, Fg in blood was higher than normal (>~2 mg/ml), which resulted in increased Fg in extravascular space. Therefore, Fg bonded to its endothelial receptor intercellular adhesion molecule-1 (ICAM-1). Fg then interacted with cellular prion protein (PrPC), which had a strong effect on the loss of memory and cognition. Mechanisms of Fg and PrPC complex formation and its functional implication are not known. This present study tested the level of Fg-PrPC complex formation, neuronal degeneration and the short-term memory after mild TBI and severe TBI. We hypothesized that after a mild to moderate injury, there was an enhanced deposition of Fg & Fg-PrPC complex formation that leaded to reduction in short-term memory, while severe trauma caused exacerbation of these effects and greater neuronal degeneration. We used C57BL/6J wild type (WT) mice models. TBI was made by using a TBI 0310 (Precision Systems and Instrumentation device with a 2mm diameter flat tip). Impactor settings were 3.5 m/sec velocity, 500msec stimulation duration with 0.5mm depth for mild-to-moderate TBI and 2mm depth severe TBI. Expressions of Fg, ICAM-1, PrPc and neuronal degeneration were seen using immunohistochemistry and confocal microscopy. Observed effects of Short-term memory post TBI were tested by Novel Object Recognition Test Two Trial Recognition Test & Spontaneous Alternation Test. Results showed with TBI-induced inflammation and Fg to endothelial ICAM-1 interaction, deposition of Fg in extravascular space increased; resulting in enhanced Fg-PrPC complex formation. There also was an increase in neuronal degeneration & reduction in short-term memory, involved with the upregulation of TrkB. To conclude, it might not be unexpected that these effects were exacerbated after a severe brain injury.

This document is currently not available here.

Share

COinS
 

Neuronal Degeneration and Short-term Memory Impairment after TBI

Traumatic brain injury (TBI) was associated with impaired short-term memory with causes of vehicle accidents and falls. Protein plaques containing fibrinogen (Fg), are associated with memory loss. After TBI, Fg in blood was higher than normal (>~2 mg/ml), which resulted in increased Fg in extravascular space. Therefore, Fg bonded to its endothelial receptor intercellular adhesion molecule-1 (ICAM-1). Fg then interacted with cellular prion protein (PrPC), which had a strong effect on the loss of memory and cognition. Mechanisms of Fg and PrPC complex formation and its functional implication are not known. This present study tested the level of Fg-PrPC complex formation, neuronal degeneration and the short-term memory after mild TBI and severe TBI. We hypothesized that after a mild to moderate injury, there was an enhanced deposition of Fg & Fg-PrPC complex formation that leaded to reduction in short-term memory, while severe trauma caused exacerbation of these effects and greater neuronal degeneration. We used C57BL/6J wild type (WT) mice models. TBI was made by using a TBI 0310 (Precision Systems and Instrumentation device with a 2mm diameter flat tip). Impactor settings were 3.5 m/sec velocity, 500msec stimulation duration with 0.5mm depth for mild-to-moderate TBI and 2mm depth severe TBI. Expressions of Fg, ICAM-1, PrPc and neuronal degeneration were seen using immunohistochemistry and confocal microscopy. Observed effects of Short-term memory post TBI were tested by Novel Object Recognition Test Two Trial Recognition Test & Spontaneous Alternation Test. Results showed with TBI-induced inflammation and Fg to endothelial ICAM-1 interaction, deposition of Fg in extravascular space increased; resulting in enhanced Fg-PrPC complex formation. There also was an increase in neuronal degeneration & reduction in short-term memory, involved with the upregulation of TrkB. To conclude, it might not be unexpected that these effects were exacerbated after a severe brain injury.