Alzheimer’s disease (AD) is one of the most common forms of dementia and has been a
global concern for several years. Due to the multi-factorial nature of the disease, AD has become irreversible,
fatal and imposes a tremendous socio-economic burden. Even though experimental medicines
suggested moderate benefits, AD still lacks an effective treatment strategy for the management
of symptoms or cure. Among the various hypotheses that describe development and progression of
AD, the amyloid hypothesis has been a long-term adherent to the AD due to the involvement of various
forms of Amyloid beta (Aβ) peptides in the impairment of neuronal and cognitive functions.
Hence, majority of the drug discovery approaches in the past have focused on the prevention of the
accumulation of Aβ peptides. Currently, there are several agents in the phase III clinical trials that target
Aβ or the various macromolecules triggering Aβ deposition. In this review, we present the state of
the art knowledge on the functional aspects of the key players involved in the amyloid hypothesis.
Furthermore, we also discuss anti-amyloid agents present in the Phase III clinical trials.