Presentation Title

Amyloid-Beta Exacerbates Deficits in Mice after Mild TBI

Student Presenter(s) and Advisor

Trevor BuhrFollow
Anne Houde, Lake Forest CollegeFollow

Location

Lilliard Science Center A 044

Abstract

Traumatic brain injury (TBI) is a leading cause of hospitalization and has been recently shown to cause long-term deficits in cognition and emotion.Links between TBI and Chronic Traumatic Encephalopathy, a neurodegenerative disease, have raised concern not only among healthcare practitioners, but also in the mainstream media, however the mechanisms behind such diseases remain elusive. Previous research on TBI brains has revealed the presence of specific proteins, such as amyloid-beta (Aβ), which are implicated in neurodegenerative diseases. My study investigates the role of Aβ after repeated TBI in mice bred to express the human precursor of Aβ.

Presentation Type

Individual Presentation

Start Date

4-10-2018 10:30 AM

End Date

4-10-2018 11:45 AM

Panel

Scientific Studies

Field of Study for Presentation

Biology, Neuroscience

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Apr 10th, 10:30 AM Apr 10th, 11:45 AM

Amyloid-Beta Exacerbates Deficits in Mice after Mild TBI

Lilliard Science Center A 044

Traumatic brain injury (TBI) is a leading cause of hospitalization and has been recently shown to cause long-term deficits in cognition and emotion.Links between TBI and Chronic Traumatic Encephalopathy, a neurodegenerative disease, have raised concern not only among healthcare practitioners, but also in the mainstream media, however the mechanisms behind such diseases remain elusive. Previous research on TBI brains has revealed the presence of specific proteins, such as amyloid-beta (Aβ), which are implicated in neurodegenerative diseases. My study investigates the role of Aβ after repeated TBI in mice bred to express the human precursor of Aβ.