Currently available drugs against Alzheimer's disease (AD) target cholinergic 
and glutamatergic neurotransmissions without affecting the underlying disease 
process. Putative disease-modifying drugs are in development and target 
β-amyloid (Aβ) peptide and tau protein, the principal neurophatological 
hallmarks of the disease. Areas covered: Phase III clinical studies of emerging 
anti-Aβ drugs for the treatment of AD were searched in US and EU clinical trial 
registries and in the medical literature until May 2016. Expert opinion: Drugs 
in Phase III clinical development for AD include one inhibitor of the 
β-secretase cleaving enzyme (BACE) (verubecestat), three anti-Aβ monoclonal 
antibodies (solanezumab, gantenerumab, and aducanumab), an inhibitor of receptor 
for advanced glycation end products (RAGE) (azeliragon) and the combination of 
cromolyn sodium and ibuprofen (ALZT-OP1). These drugs are mainly being tested in 
subjects during early phases of AD or in subjects at preclinical stage of 
familial AD or even in asymptomatic subjects at high risk of developing AD. The 
hope is to intervene in the disease process when it is not too late. However, 
previous clinical failures with anti-Aβ drugs and the lack of fully 
understanding of the pathophysiological role of Aβ in the development of AD, put 
the new drugs at substantial risk of failure.