Neuroinflammation
Glial Cell Activation
Secretion of Proinflammatory Mediators Cytokine Secretion
BBB Breakdown and Peripheral Immune Cell Transmigration Neuroinflammation
Neuroinflammation, defined as an inflammatory reaction within nervous tissue, arises as a mechanism to protect the brain and spinal cord against potential harm from a variety of toxic stimuli including protein aggregates, neuronal injury, and infection. In recent years, research has shown that a sustained inflammatory response can contribute to the development and progression of many neurodegenerative diseases and neurological disorders. Bio-Techne offers an unparalleled selection of high-quality solutions for investigating all aspects of neuroinflammation.
Table of Contents
The Neuroinflammation Cycle ...... 3
Glial Cells in Neuroinflammation ...... 4-7
Detecting and Identifying Glial Cells ...... 4-5
Modulating Glial Cell Activation ...... 6-7
Cytokine Mediators of Neuroinflammation ...... 8-13
Detecting and Measuring Neuroinflammatory Factors...... 8-12
Investigate Inflammatory Signaling Pathways...... 13
Blood-Brain Barrier and Immune Cell Transmigration ...... 14-25
Detecting Components of the Blood-Brain Barrier ...... 14-17
Modulating Blood-Brain Barrier Transporter Functioning ...... 18
Evaluating Blood-Brain Barrier Dysfunction ...... 19
Detecting Peripheral Immune Cells ...... 20-24
Peripheral Immune Cell Markers ...... 20
Modulating Immune Cell Migration ...... 25
Spatially Map Neuroinflammatory Markers and Cell Types ...... 26-27 RNAscopeTM In Situ Hybridization Assays
2 Learn more | rndsystems.com/neuroinflammation The Neuroinflammation Cycle
Neuroinflammation is a complex response that involves activation of glial cells, secretion of inflammatory mediators, and production of reactive oxygen species (ROS) and nitric oxide (NO). It is a highly controlled process that tends to be quickly resolved. However, continued exposure to a harmful stimulus can lead to chronic neuroinflammation, which is characterized by the persistent activation of glial cells, sustained release of inflammatory mediators, breakdown of the blood-brain barrier (BBB), and increased migration of peripheral immune cells into the central nervous system (CNS). These events establish a feedback loop that perpetuates and prolongs neuroinflammation, leading to neurodegeneration.