Alzheimer's disease(AD) is a primary neurodegenerative disorder mainly affecting aged people over 60 years old. It is characterized by extracellular senile plaques(SPs) and intracellular neurofibrillary tangles(NFTs)in patients' brains. The major component of SP is β-amyloid peptide(βA) with molecular weight of about 4 ku which is a neurotoxic derivative of β-amyloid precursor protein(APP) and can cause cell damage mainly through oxidative stress and being able to form calcium channels in lipid bilayers. The precursor, APP, whose function is not yet elucidated in detail but evidence exists that it may mediate cell adhesion, maintain synaptic plasticity and so on, can be processed in conventional secretary way by several putative secretases and alternatively in endosomal/lysosomal way. Longer βA is more predisposed to aggregate to form SP than its shorer counterpart, so some APP mutants may cause familial AD through producing more longer βAs or increasing the production of shorter ones. The changes of some factors which are important for the metabolism of APP, for example, mutations of presenilins, may also cause AD by increased generation of βA.