Alzheimer's disease (AD) is a neurodegenerative disorder that impairs mainly the 
memory and cognitive function in elderly. Extracellular beta amyloid deposition 
and intracellular tau hyperphosphorylation are the two pathological events that 
are thought to cause neuronal dysfunction in AD. Since the detailed mechanisms 
that underlie the pathogenesis of AD are still not clear, the current treatments 
are those drugs that can alleviate the symptoms of AD patients. Recent studies 
have indicated that these symptom-reliving drugs also have the ability of 
regulating amyloid precursor protein processing and tau phosphorylation. Thus 
the pharmacological mechanism of these drugs may be too simply-evaluated. This 
review summarizes the current status of AD therapy and some potential 
preclinical considerations that target beta amyloid and tau protein are also 
discussed.