The cause and proximal consequences of Alzheimer's disease (AD), a progressive debilitating dementia remain largely unknown. Nonetheless an increasing number of genetic risk factors, including most recently bleomycin hydrolase, have been shown to be associated with the disease, offering the hope of revealing the mechanism of disease pathogenesis. Here we show that bleomycin hydrolase, known to be induced in an oxidative environment, is specifically increased in neurons marked for degeneration in AD. These findings support a key proximal role for bleomycin hydrolase, and oxidative stress in AD.