Author Type

Undergraduate Student

Date of Award

Spring 4-29-2025

Document Type

Thesis

Publication Status

Version of Record

Submission Date

July 2026

College Granting Degree

Harriet L. Wilkes Honors College

Thesis/Dissertation Advisor [Chair]

Claudia Rodrigues

Thesis/Dissertation Co-Chair

Chitra Chandrasekhar

Abstract

This paper aims to summarize the key differences in neuroinflammation across various contexts beyond neurodegenerative diseases, specifically senescence, diet, infection, cancer treatments, and psychostimulant usage. While each of these conditions presents unique inflammatory characteristics, they share core mechanistic themes, particularly the disruption of the blood-brain barrier (BBB). BBB dysfunction serves as a crucial regulatory point, influenced by endothelial cells (ECs) within the neurovascular unit (NVU). ECs play an essential role in neuroinflammation through pathways involving tight junction (TJ) proteins and matrix metalloproteinases (MMPs), which mediate BBB integrity and permeability. Additionally, ECs interact with various cellular components and signaling pathways, further shaping inflammatory responses. By examining the distinct features and shared mechanisms of neuroinflammation in different contexts, this paper highlights the complexity of BBB regulation and the varied cellular interactions that contribute to neuroinflammatory progression.

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