The Fundamental Role of Neuroinflammation at the Beginning and Progression of Alzheimer’s Disease

Abstract

The majority of astrocytes are responsible for the expression and release of S100B, a 21-kDa calcium-binding protein of the EFhand type (helix E-loop-helix F). It is mostly present in the neurological system and, depending on concentration, has different (beneficial, detrimental) effects on neurons, astrocytes, and microglia. an effect on the survival and development of both glia and neuronal cells. Patients with Down Syndrome and Alzheimer's Disease (AD) have brains that are overexpressed with the S100 protein Down Syndrome (DS). Increased S100B concentrations are linked to brain trauma and ischemia, most likely due to astrocyte destruction. As S100B appears to influence multiple neuropathological mechanisms in (AD) , a pivotal role for S100B as a significant contributor to (AD) pathology has emerged. Studies of S100B overexpression, S100B localization, multiple relationships between S100B and increase amyloid precursor protein, the interaction between S100B and dystrophic neuritis plaques, and change in a neurofibrillary tangle in Alzheimer's disease focus on providing evidence for the involvement of S100B in Alzheimer's disease pathology and neuronal loss. The significance of S100B in head trauma and degenerative brain disease is the central subject of this review. Overexpressing s100B, which also causes more astrogliosis and microgliosis, speeds up the pathogenesis of Alzheimer's disease. Numerous clinical problems have been associated with an increase in S100B, a neurotropic signaling protein.