Alzheimer's disease is a multifactorial neurodegenerative disorder which causes 60-80% of all dementia. Main characteristic is progressive cognitive decline caused by accumulation of β-amyloid plaques and neurofibrillary tangles in cerebral cortex. There are 2 types of Alzheimer's disease, familial and sporadic with differences in cause and age of onset. Due to disease complexity, Molecular pathogenesis of Alzheimer's Disease is desribed by several hypothesis, with main ones being: β-amyloid hypothesis, Tau hypothesis, cholinergic hypothesis, hypothesis of oxidative stress, inflammation hypothesis and metal dishomeostasis hypothesis. One of these hypothesis, cholinergic hypothesis has set the base for drugs that work as cholinesterase inhibitors. There are currently 3 approved cholinesterase inhibitors used in treatment of Alzheimer's disease: Donepezil, Galantamine and Rivastigmine. Those medications together with NMDA receptor agonist Memantine are classified as drugs that treat symptoms of Alzheimer's disease. Other type of treatment used are drugs that delay clinical decline, with currently only immunotherapeutic Aducanumab being approved for use. Sucess of this drug that binds and removes Aβ plaques encouraged scientist to study other hypothesis and use their findings as a targets in future therapies. New research, therefore use not only β-amyloid as their main target but also tau protein, inflammation and oxidative stress. This thesis gives detailed description of the connection between hypothesis and pathofiziology of AD and presents existing therapeutic options with purpose of better understanding their mechanism of action, all in order to set the foundation on which future research will be based.