Alzheimer's disease (AD) is a progressive and irreversible neurodegenerative 
disease, and corresponds to the most common cause of dementia worldwide. 
Although not fully understood, the pathophysiology of AD is largely represented 
by the neurotoxic events triggered by the beta-amyloid cascade and by 
cytoskeletal abnormalities subsequent to the hyperphosphorylation of 
microtubule-associated Tau protein in neurons. These processes lead respectively 
to the formation of neuritic plaques and neurofibrillary tangles, which are the 
pathological hallmarks of the disease. Clinical benefits of the available 
pharmacological treatment for AD with antidementia drugs (namely cholinesterase 
inhibitors and memantine) are unquestionable, although limited to a temporary, 
symptomatic support to cognitive and related functions. Over the past decade, 
substantial funding and research have been dedicated to the search and 
development of new pharmaceutical compounds with disease-modifying properties. 
The rationale of such approach is that by tackling key pathological processes in 
AD it may be possible to attenuate or even change its natural history. In the 
present review, we summarize the available evidence on the new therapeutic 
approaches that target amyloid and Tau pathology in AD, focusing on 
pharmaceutical compounds undergoing phase 2 and phase 3 randomized controlled 
trials.