Consistent with these observations, our data revealed that BDNF expression is downregulated in APP/PS1 Tg mice, and BDNF expression is markedly decreased in C57BL/6J mice injected with exogenous Aβ1−42 oligomers, which supports a critical roles of Aβ1−42 oligomers in suppressing the expression of BDNF during the course of AD development and progression. Here, APP is linked to Alzheimer disease.