BMP4 overexpression induces the upregulation of APP/Tau and memory deficits in Alzheimer’s disease

Abstract Alzheimer’s disease (AD) is a chronic progressive degenerative of the nervous system. Its pathogenesis complex and related to abnormal expression amyloid β (Aβ), APP, Tau proteins. Evidence has demonstrated that bone morphogenetic protein 4 (BMP4) highly expressed in transgenic mouse models AD endogenous levels BMP4 mainly affect hippocampal function. To determine whether participates development, mice were constructed overexpress under control neuron-specific enolase (NSE) promoter. We also performed MTT, FACS, transfection, TUNEL, Western blotting assays define role cells. found middle-aged exhibited impaired memory via Morris water maze experiment. Moreover, their tissues high AD-related proteins, including Aβ, PSEN-1, Tau, P-Tau (Thr181), (Thr231). Furthermore, multiple cell lines, overexpression increased whereas downregulation opposing effects. Consistent with these results, modulation affected apoptosis regulation BAX Bcl-2 Our findings indicate might be potential factor induce AD.