The Mitochondrial Membrane Potential as a Screening Tool for Immunostimulation
The rise of neuroinflammatory disorders highlights the importance of early detection and intervention for more effective treatment options. Neuroinflammation is associated with the pathogenesis of many neurological disorders, including Major Depressive Disorder, Alzheimer's disease, and Multiple Sclerosis. There has been a focus on neurons to advance our understanding of the underlying mechanisms of neuroinflammation and its role in neurodegeneration. However, recent studies have highlighted the pivotal role of glial cells, particularly microglia, in neuroinflammation due to their active participation in the immune response. This study investigates glial-specific indicators of morphology, metabolic changes, and drug efficacy in neuroinflammatory conditions. By analyzing the glial-specific activity of microglia at various levels, we uncover distinct patterns that correlate with disease progression. These findings offer insights into the early stages of neurological diseases and provide potential biomarkers for early detection. Moreover, this study explores the modulation of microglial metabolic activity as a screen for therapeutic approaches. We examine the impact of pharmacological interventions on glial cells and their subsequent effects on disease outcomes. In summary, this dissertation expands the current understanding of the dynamic interplay between glial cells, neuroinflammation, and disease progression, ultimately contributing to the development of a novel drug screening tool. Identifying glial-specific metabolic indicators and evaluating drug efficacy offer promising avenues for early detection and targeted therapeutic interventions in neurological diseases.
Publication Details
- Journal
- Digital Scholarship - UNLV (University of Nevada Reno)
- Published
- 2024-10-02
- DOI
- https://doi.org/10.34917/37650861
- Primary Topic
- Neuroinflammation and Neurodegeneration Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00