Alzheimer's disease, a complex and progressive neurological disorder, is the leading cause of late-life dementia. Pathologically, it is marked by the presence of amyloid plaques and neurofibrillary tangles in the brain. Over the past two decades, advancements in understanding the disease's pathogenesis have spurred research into new pharmacological treatments that target its underlying mechanisms. Currently available drugs, such as acetylcholinesterase inhibitors (rivastigmine, galantamine, donepezil) and the NMDA receptor antagonist memantine, primarily address symptoms and are effective only in the later stages of the disease. While these medications can slow disease progression and provide symptomatic relief, they do not offer a cure. Despite having a clear understanding of Alzheimer's neuropathology, the precise mechanisms driving the disease remain elusive. The lack of effective treatments that can stop the start and progression of the disease may be caused by our incomplete understanding of the pathogenic process. New therapeutic targets are now available due to the significant advancements made in pathophysiology over the past few years, which should allow for a direct attack on the underlying illness process. The various pathophysiological pathways that underlie Alzheimer's disease and how it is managed by conventional medication therapy, including current exploratory therapeutic options, are covered in this review article. Innovative, beneficial policies are essential to determine and progress therapeutic molecules to defend against AD.