Alzheimer‟s disease (AD) is a debilitating neurodegenerative disorder associated with impaired cortical as well as cognitive functions.One of the causes of AD is the accumulation of beta-amyloid (A) plaques outside and surrounding the nerve cell. The accumulation of A peptides inside the neurons involves in cognitive impairment, synaptic dysfunction and constitution of amyloid plaques. Aβ aggregation is believed to play a critical role in the pathogenesis of AD. As a result, therapeutics aimed at disrupting or reversing Aβ aggregation have garnered significant attention in recent years.Still no effective treatment has been made which can slow down the progression of these A plaques. Based on various researches, different anti-A drugs have been made to decrease the production of A plaques by inhibiting the  and -secretase enzymes and also to stimulate the breakdown of preexisting A plaques in the brain. Globally, many drug companies have performed clinical trials on AD patients, based upon amyloid hypothesis, to synthesize anti-amyloid drugs. Many researchers have dismissed the A hypothesis of AD due to the failure of several amyloid-targeted therapies in various clinical trials performed on AD patients, as discussed in this article. Researchers are still developing and testing various therapies for an ideal drug of AD, in ongoing clinical trials. In this article, such anti-amyloid drugs are discussed which can prevent the formation of A oligomer and suppress their toxicity.