Submission Date

7-19-2019

Document Type

Paper- Restricted to Campus Access

Department

Biology

Faculty Mentor

Jennifer King

Comments

Presented during the 21st Annual Summer Fellows Symposium, July 19, 2019 at Ursinus College.

Project Description

Neuroinflammation is a mechanism that occurs often in response to injury or infection. However when neuroinflammation is chronic, detrimental effects such as neurodegeneration can take place. The effects of neuroinflammation is implicated in neurodegenerative diseases such as Alzheimer's Disease (AD), Parkinson's Disease (PD), and multiple sclerosis (MS). A key component of neuroinflammation are microglia, a type of glial cell in the central nervous system (CNS) that plays a role in the immune function of the CNS. When activated, microglia phagocytose debris and release proinflammatory molecules like chemokines and cytokines. Prolonged activation, however, can weaken the blood brain barrier (BBB) and render it susceptible to inflammatory mediators. The goal of our study is to examine the effects of neuroinflammation on the phagocytic activity of BV2 cells, an immortalized microglial cell line. To accomplish this goal we will characterize our BV2 cells using immunofluorescence and use the HIV-TAT protein as our neuroinflammatory mediator.

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