Neuroinflammation
Our understanding of the molecular pathogenesis of neuroinflammation is growing steadily. Progress in different areas of basic research, new animal models, and the generation of specific antibody markers to target essential proteins help find and improve the treatment of patients with neuroimmunological diseases.
Neuroinflammation broadly defines the collective reactive immune response in the brain and spinal cord in response to injury and disease. Inflammation in the central nervous system (CNS) is commonly associated with various degrees of tissue damage, such as loss of myelin and neurons.
The neuroinflammatory process is complex and involves the disruption of the blood-brain barrier (BBB), peripheral leukocyte infiltration, edema, and gliosis. The inflammatory response is characterized by a host of cellular and molecular aberrations within the brain.
Neuroinflammation arises within the CNS through phenotypic changes of different non-neuronal cell types in the brain, such as microglia, oligodendrocytes, and astrocytes, causing the release of various cytokines and chemokines, and finally, recruitment and infiltration of peripheral blood cells, mainly T-and B-cells, into the brain parenchyma.
Neuroinflammatory processes are the key causative factors behind brain and spinal cord injury. This is true not only for acute brain trauma and hypoxic-ischemic brain damage following a stroke but also for chronic infection and neurodegenerative diseases, such as Alzheimer's disease, amyotrophic lateral sclerosis (ALS), Lewy body dementia, and leukoencephalopathies like multiple sclerosis (MS). In addition, local peritumoral inflammation plays a role in the clinical progression and malignancy of glioblastomas, the most aggressive primary brain tumors.
Download the white paper where we discuss the role of microglia, oligodendrocytes, and astrocytes in the neuroinflammatory processes highlighting the relevant antibody markers with a particular focus on multiple sclerosis.
DOWNLOAD WHITE PAPER