Alzheimer disease （AD） is characterized by clinical progressive decline in cognitive function and behavioral abnormalities， and eventually dementia. Its neuropathological features include tau protein neurofibrillary tangles， senile plaques formed by the accumulation of β-amyloid （Aβ）. Other changes include reactive microglia proliferation and widespread loss of neurons， white matter， and synapses. Since amyloid pathology may precede tau protein pathology and the appearance of AD brain atrophy and clinical symptoms， the correlation between Aβ metabolic abnormalities and AD is elaborated in this paper.