Previous studies have reported that non-human primates and rodents exposed to lead during brain development may become dependent on the deposition of pre-determined β-amyloid protein (Aβ), and exhibit upregulation of β-site amyloid precursor protein expression in old age. However, further evidence is required to elucidate the precise relationship and molecular mechanisms underlying the effects of early lead exposure on excessive Aβ production in adult mammals. The present study investigated the effects of lead exposure on expression of β-amyloid precursor protein cleavage enzyme-1 (BACE-1) in the rat retina and the production of Aβ in early development, using the retina as a window for studying Alzheimers disease. Adult rats were intraocularly injected with different doses of lead acetate (10 μmol/L, 100 μmol/L, 1 mmol/L, 10 mmol/L and 100 mmol/L). The results revealed that retinal lead concentration, BACE-1 and its cleavage products β-C-terminal fragment and retina Aβ1-40 were all significantly increased in almost all of the lead exposure groups 48 hours later in a dose-dependent manner. The only exception was the 10 μmol/L group. The distribution of BACE-1 in the retina did not exhibit obvious changes, and no distinctive increase in the activation of retinal microglia was apparent. Similarly, retinal synaptophysin expression did not exhibit any clear changes. These data suggest that lead exposure can result in the upregulation of retinal neuron BACE-1 expression in the early period of development and further increase the overproduction of Aβ1-40 in the retina. Our results provided novel insight into the molecular mechanisms underlying environmentally-induced Alzheimers disease.