Alzheimer's disease (AD)is a neurodegenerative disorder characterized by memoryimpairment, cognitive decline and neuronal loss. Its pathogenesis involves a variety offactors, among which amyloid-β (Aβ) is critical in neurons and the body. Aβ is thedecomposition product of human amyloid precursor protein(APP) through various amyloidprocessing routes and non-amyloid processing routes, and is cleared through various wayssuch as cerebrospinal fuid and inter-tissue fluid lymphatic drainage, cell clearance, bloodand brain barrier transport and enzymatic hydrolysis. The generation and clearance of Aβ is a dyamic and balanced process, and the imbalance of its balance will accumulate Aβ in the brain, leading to neuronal cell death, impaired synaptic function and neuronalnetwork changes, inducing and exacerbate AD symptoms. This review expounded themechanisms of Aβ generation, clearance and metabolism in AD, summarized theinteraction mechanisms of Aβ with neurons, astrocytes, urea cycle, etc, and provided newideas for further discovery of new therapeutic and diagnostic targets for AD.