Role of protein’s and future treatment options for Alzheimer’s Disease

Abstract

Alzheimer‘s disease is a progressive brain disorder that slowly destroys the memorizing skill, decline in cognitive function and thinking ability which is one of the main causes of dementia. The exact cause of AD is still unknown but several studies suggest that extracellular accumulation of amyloid-beta oligomers and intracellular hyperphosphorylated tau peptides mainly responsible for this disease. Amyloid beta is 40-42 amino acid long polypeptide chain that is produced amyloid precursor protein through β-secretase and ɣ secretase enzymatic cleavage. Impaired amyloid accumulation causes synaptic dysfunction, mitochondrial dysfunction that cause neurodegeneration. Tau is intrinsically disordered protein which is required for stabilizing microtubules but hyperphosphorylation of tau protein cause them to dissociate from microtubules causes axonal loss. Acetylcholine esterase inhibitor and NMDA receptors antagonist are currently available drugs for AD that reduce AD symptoms. Currently scientists are working several AD drugs targeting the pathological hall marks of AD (Aβ and tau).