Tumor necrosis factor (TNF) is one of the most extensively studied cytokine with about 19 distinct superfamily members and many more to be found. Prominent among these members is tumor necrosis factor alpha (TNF-α) that is known to be a potent promoter of inflammation, as well as many normal physiological functions in homeostasis and health and antimicrobial immunity. Nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) is one of the most important transcription factors that activate transcription of many proinflammatory genes, and the unraveling of TNF-α induced NFκB activation forms the foundation of TNF-α as major cytokine of neuroinflammation. This review discusses summary of literature on unique role of TNF-α in neuroinflammation and various agents that mediate neuroinflammation via TNF-α modulation.
Part of the book: Cytokines
Stroke remains global health care problem that constitutes world’s second-leading perpetrator of mortality and third most pronounced cause of all disabilities. The hallmark of cerebral stroke is the persistent loss of cerebral function consequence of abnormality of the blood supply. The ultimate goal of stroke care is to recover and maximize the cerebral functions lost due to the cerebral damage. Therefore, understanding the mechanism of cerebral damage after stroke is fundamental to comprehension of mechanisms of recovery following stroke, as well as key towards eliminating devastating human disability as a result of stroke. Therapeutic strategies aim to harness and enhance neuroplasticity offers reasonable level of hope towards maximizing recovery from post stroke impairments. This paper therefore, highlighted the mechanism of cerebral damage after stroke as well as elucidates the concept of neuroplasticity as key for recovery following stroke.
Part of the book: Cerebral and Cerebellar Cortex