MITOGEN ACTIVATED PROTEIN KINASE AT THE CROSSROADS OF ALZHEIMER’S DISEASES

Abstract

Alzheimer’s disease (AD) is associated with various neurodegenerative alterations and inflammation thought to play a major role in its pathogenesis. The Mammalian stress activated protein kinase (SAPK), p38 mitogen-activated protein kinases (MAPKs), a family of serine/threonine protein kinases, activated in response to wide range of cellular stresses as well as in response to inflammatory mediators. A large body of evidences indicates that p38MAPK activity is critical for normal immune and inflammatory response. Moreover, the p38 MAPK pathway is considered to be a key regulator of various inflammatory pathways which are activated during normal aging and AD therapy. The p38MAPK pathway which is a key regulator of pro-inflammatory cytokines biosynthesis at the transcriptional and translational levels, which makes different components of this pathway, a potential targets for the treatment of autoimmune and inflammatory diseases. Furthermore, p38 MAPK is over expressed in AD and have been linked to Aβ deposition and Tau tangle formation. Favourable modulator of p38 MAPK found to beneficial in a variety of experimental models of AD, further implicating p38 MAPK in AD pathogenesis. In this review, we provide an overview on p38 MAPK and its implication in the pathogenesis of Alzheimer’s diseases.