ADVANCES IN Tau PROTEIN INHIBITORS FOR ALZHEIMER'S DISEASE

A REVIEW

Abstract

Alzheimer's disease was originally defined as presenile dementia which has no an antecedent cause, for example alcohol, stroke on brain or a trauma on brain. It is neurodegenerative disease which is chronic in nature which starts slowly and as time passes get worsen. Neurofibrillary tangles composed primarily of tau proteins aggregates which are hyperphosphorylated forms of the microtubules associated protiens. The main reason of aggregation is an imbalance in phosphates and kinase activities leading to an abnormal phosphorylation of tau and its further aggregation. A wide range of therapeutic approaches for this specific tau kinase inhibition or to enhance the phosphate activity, which will indeed promote the stability of microtubule and thus will in turn reduce the aggregation of tau proteins and their clearance is also enhance its clearance by small molecule drugs or by means of immunotherapy. Most of the drugs which are promising in their activities are still in preclinical trails and some of them are: Crenezumab (a monoclonal antibody which is passive); ACI-24 & -35 (targets aβ and p-tau actively as an immunotherapy), Anti- tau antibody and Morphomer tau (compound which is small for the treatment). Thus this therapy improves current situation of patient and blocks tau protein aggregation leading cause of AD.