Submission Date

7-23-2020

Document Type

Paper- Restricted to Campus Access

Department

Biology

Second Department

Neuroscience

Faculty Mentor

Jennifer King

Student Contributor

Trinady Banks

Second Student Contributor

Mekha Varghese

Comments

Presented during the 22nd Annual Summer Fellows Symposium, July 24, 2020 at Ursinus College.

A related presentation is available here.

Project Description

Neuroinflammation, the activation of the brain's innate immune system in response to inflammatory challenges, is characterized by a host of cellular and molecular changes within the central nervous system. During neuroinflammation, microglia provide trophic support and function as a defense mechanism by utilizing phagocytosis to eliminate harmful cellular debris and maintain homeostasis. In HIV associated neurocognitive disorders (HAND), microglia can be dysregulated, resulting in an increase in phagocytosis which can then be followed by neuronal cell death, or a decrease in phagocytosis, preventing the removal of harmful cellular debris. Previous studies have characterized the mechanisms that control phagocytic activity during an inflammatory state with variable findings. Additional investigation is necessary to uncover the specific role of microglial cytoskeletal proteins in neurodegenerative diseases, HIV associated neurocognitive diseases in particular. Our current study therefore further examines how cytoskeletal proteins modulate the activity of microglia phagocytic function in HIV-1 Tat induced neuroinflammation on BV-2 cells.

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