Neurological disorders (ND) are the central nervous system (CNS) related complications
originated by enhanced oxidative stress, mitochondrial failure and overexpression of proteins
like S100B. S100B is a helix-loop-helix protein with the calcium-binding domain associated with
various neurological disorders through activation of the MAPK pathway, increased NF-kB expression
resulting in cell survival, proliferation and gene up-regulation. S100B protein plays a crucial
role in Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, Schizophrenia and epilepsy because
the high expression of this protein directly targets astrocytes and promotes neuroinflammation.
Under stressful conditions, S100B produces toxic effects mediated through receptor for advanced
glycation end products (AGE) binding. S100B also mediates neuroprotection, minimizes
microgliosis and reduces the expression of tumor necrosis factor (TNF-alpha) but that are concentration-
dependent mechanisms. Increased level of S100B is useful for assessing the release of inflammatory
markers, nitric oxide and excitotoxicity dependent neuronal loss. The present review
summarizes the role of S100B in various neurological disorders and potential therapeutic measures
to reduce the prevalence of neurological disorders.