Alzheimer's sickness (AD) as of now introduces one of the greatest social insurance issues in the created nations. There is no viable treatment equipped for backing off illness movement. As of late the fundamental focal point of research on novel pharmacotherapies depended on the amyloid genic theory of AD, which sets that the beta-amyloid (Aβ) peptide is mainly in charge of subjective hindrance and neuronal demise. The objective of such medicines is (a) to lessen Aβ creation through the hindrance of β and γsecretase compounds and (b) to advance disintegration of existing cerebral Aβ plaques. Be that as it may, this approach has turned out to be just humbly viable. Late examinations propose an elective technique fixated on the hindrance of the downstream Aβ flagging, especially at the neural connection. Aβ oligomers may cause atypical N-methyl-D-aspartate receptor (NMDAR) enactment postsynaptically by framing edifices with the phone surface prion protein (PrPC). PrPC is enhanced at the neuronal postsynaptic thickness, where it communicates with Fyn tyrosine kinase.

• Aβ flagging
• N-methyl-D-aspartate receptor (NMDAR) enactment
• Inhibition of β and γsecretase chemicals
• Reduce Aβ generation