Alzheimer's disease (AD) is the most common cause of dementia among the elderly people. The prevailing hypothesis for the pathological progression of AD is the β-amyloid peptide (Aβ) cascade hypothesis: oligomeric forms of Aβ with cytotoxicity are the main cause of neuronal death in the brain of the AD patients. Thus, the inhibition of Aβ production and aggregation as well as improvement of its clearance appear to be the main strategy for drug development. However, the disturbing issue is that no significantly effective approach is available yet although a large number of compounds have been trialed on clinic. It questions the hypothesis that Aβ is the key pathologic factor leading to AD progression. The other possibility of failure is that loss of neural cells is so extensive that any treatment becomes not available when cognitive symptoms are apparent. New diagnostic ways may help to identify individuals before substantial neural damage has occurred. Treatments could then be attempted to stave off the onset of the disorders or the progression of the disease.