Neuroinflammation is a hallmark of neurological disorders (such as stroke, traumatic brain injury, epilepsy, amyotrophic lateral sclerosis, Parkinson’s disease, and Alzheimer's disease), yet its immunological mechanisms are still not fully understood. The inflammatory response involves the activation of peripheral immune cells, monocytes/macrophages, neutrophils, lymphocytes, and CNS resident microglia. Activated immune cells produce cytokines and chemokines, which upon binding with their receptors trigger multiple inflammatory signaling pathways (notably TLR4/NF-κB and the NLRP3 inflammasome). Due to its complexity, intensity, and duration, neuroinflammation is often a double-edged sword. For example, the beneficial role of inflammation in removing cell debris and promoting tissue repair is well established; however, excessive and/or chronic inflammation is detrimental (promoting cell death, aggravating outcome, and impairing recovery). A better understanding of the molecular and cellular mechanisms which regulate the immune response (driving disease progression and severity) is needed in order to identify targets for the development of more effective treatments for patients with neurological disorders. Inflammation can be evaluated at multiple levels; these range from molecular, functional, and morphological changes in individual immune cells or specific organs to systemic changes. This collection includes but is not limited to the following innovative methodologies: (1) Analysis of gene expression signatures by single-cell RNA sequencing and nCounter system, (2) proteomic profiling by flow cytometry, (3) isolation of immune cells for in vitro and ex vivo analysis, (4) imaging with in vivo multiphoton microscopy and fluorescent in situ hybridization, and (5) multiplex immunoassays for biomarker screening.