APP and Alzheimer disease: We have shown that AD-related cellular stressors—such as the presence of reactive oxygen species (ROS) and amyloid-beta (Aβ)—increase PM20D1 expression, that PM20D1 expression is upregulated in symptomatic APP/PS1 AD mice and human AD samples, and that genetic manipulation of PM20D1 levels can modify the progression of the disease in APP/PS1 mice: When PM20D1 was overexpressed, disease progression was delayed; when PM20D1 was decreased, disease progression was accelerated.