In DN-DISC1 mice, a mouse model for major mental illnesses, the model that expresses 
pathological phenotypes relevant to 
schizophrenia, 
mood disorders, and 
addiction simultaneously, the inventors of the present invention found pronounced levels of 
oxidative stress in the 
prefrontal cortex, but not in the 
striatum. These mice also displayed greater amounts of GAPDH-Siah1 binding, a 
protein-
protein interaction that is activated under 
exposure to 
oxidative stress. The present inventors investigated the role of 
oxidative stress in other organ systems. As detailed herein, the inventors found that GAPDH-Siah1 binding was increased in mouse models of cardiac failure. It was also found, that certain novel analogs of deprenyl, significantly inhibited GAPDH-Siah1 binding in cardiac tissue. Thus, with experimental data provided herein, it is clear that this GAPDH-Siah1 binding 
cascade is a crucial mechanism involved in major 
mental illness, such as 
schizophrenia, 
mood disorders, and 
addiction, as well as in stress-associated diseases involving other organs where GAPDH is expressed.The present invention provides compounds and composition comprising analogs of deprenyl and their use in the inhibition of nuclear GAPDH-Siah1 binding and the activation of p300 and MEF2. Also provided herein are methods of prevention and treatment of 
stress induced disorders of the body, including, for example, major 
mental illness, such as 
schizophrenia, 
mood disorders, and 
addiction, as well as in stress-associated diseases involving other organs, such as 
cardiac hypertrophy, 
in vivo, comprising administering to a 
mammal a therapeutically effective amount of analogs of deprenyl.