Alzheimer’s Disease (AD) is the highly prevalent type of dementia, according to medical literature. The condition, which gets worse over time and eventually results in death, has no known total cure. Alois Alzheimer, a German psychiatric and neuropathologist, first described it in 1906, and he is the inspiration for its name. There are a number of theories as to what causes this condition, one of the oldest of which is the cholinergic hypothesis,1 according to which the development of AD is sped up by a deficiency in cholinergic signalling. The isoprenoid hypothesis demonstrated isoprenoid changes in AD,2 which are distinct from the symptoms seen in normal ageing, which is why it is referred to as premature ageing. The amyloid hypothesis3,4 describes the formation of aggregated amyloid fibrils, which are one of the toxic forms of protein. The tau hypothesis is one of the most recent hypotheses in which amyloid plaques are formed that have no relation to neuron loss,5 and tau is the main causative factor of this hypothesis. The loss of microtubule-stabilizing tau protein, which leads to cytoskeleton degradation, has been proposed as a mechanism for neurotoxicity. Current treatments only address the disease’s symptoms. There are no treatments available that can stop or reverse the progression of the disease. The number of people who will have the condition by 2050 will be astonishing-100 million. As of 2022, more than 1,000 clinical studies testing various drugs for Alzheimer’s disease have been completed or are ongoing. In both mild and moderate Alzheimer’s disease, acetyl cholinesterase inhibitors like donepezil, rivastigmine, and galantamine offer momentary relief, while memantine, a low-affinity N-methyl D-aspartate receptor antagonist, is permitted for use in moderate-to-severe Alzheimer’s disease.6 Huperzine A has also attracted the attention of US medical researchers. It can also be used to treat diseases characterised by neurodegeneration. As a result, Huperzine A has been discovered to be an inhibitor of the enzyme acetylcholinesterase.7 Though some of them are currently undergoing clinical trials for Alzheimer’s disease, one strategy has been used to develop vaccination therapies, and the field of Alzheimer’s research has recently been shaken by three phase failures. Phase 3 clinical trials for vaccine development and grounds for their rejection included: a) Semagecestat (LY450139), a gamma secretase inhibitor that prevents the generation of the A Beta peptide, failed to meet its key end goals in 2011. Bapineuzumab (Pfizer/ Janssen Alzheimer Immunotherapy) and solanezumab, two anti-Abeta monoclonal antibodies that were being investigated in phase 3 studies, failed to achieve their key end goals, which were an improvement in cognition and daily living activities. c) The failures of Tarenflurbil Phase 3 in 2008 and Tramiprosate Phase 3 in 2007.8 The development of above amyloidcentric vaccines based on the amyloid cascade hypothesis failed in phase three trials. This failure of vaccination therapy suggests that we might be able to treat Alzheimer’s disease by activating PP2A. (Protein Phosphatase 2A enzyme). Because a very low level of this enzyme was sufficient to cause Alzheimer’s disease, researchers focused on activating this enzyme or inhibiting the generation of PP2A inhibitors by new chemical entities, which became the new trends in Alzheimer’s drug discovery.