In the DN-DISC1 mouse, a mouse model for major psychosis that expresses a pathological phenotype associated with schizophrenia, mood disorders, and addiction (耽溺), the inventors of the present invention simultaneously We found significant levels of oxidative stress in the prefrontal cortex, but not in the striatum. These mice also showed a greater amount of GAPDH-Siah1 binding, a protein-protein interaction that was activated under exposure to oxidative stress. We studied the role of oxidative stress in other organ systems. As detailed herein, the inventors have found that GAPDH-Siah1 binding is increased in a mouse model of heart failure. In addition, certain novel analogs of deprenyl were found to significantly suppress GAPDH-Siah1 binding in heart tissue. Thus, with the experimental data provided here, this GAPDH-Siah1 binding cascade is implicated in major psychosis such as schizophrenia, mood disorders, and addiction, and in other organs where GAPDH is expressed Clearly, it is an important mechanism involved in stress-related diseases. The present invention provides compounds and compositions that include analogs of deprenyl, as well as their use in inhibiting nuclear GAPDH-Siah1 binding and activation of p300 and MEF2. Also here, for example, in major psychoses, such as schizophrenia, mood disorders, and addictions, as well as in stress-related diseases involving other organs, such as cardiac hypertrophy Methods for preventing and treating bodily stress-induced disorders, including those in vivo, include administering to mammals a therapeutically effective amount of an analog of deprenyl.DN-DISC1マウス、主要な精神病のためのマウスモデルで、統合失調症、気分障害、嗜癖（耽溺）に関連する病理学的表現型を発現するモデルにおいては、本発明の発明者らは、同時に、前頭前野において酸化ストレスの顕著なレベルを見出したが、線条体では異なっていた。これらのマウスはまた、GAPDH-Siah1結合、酸化ストレスへの曝露下で活性化されるタンパク質-タンパク質相互作用のより多くの量を示した。本発明者らは、他の器官系における酸化ストレスの役割を研究した。ここで詳述するように、本発明者らは、GAPDH-Siah1結合が心不全のマウスモデルで増加することを見出した。さらに、デプレニルのある種の新規な類似体が、心臓組織においてGAPDH-Siah1結合を著しく抑制することを見出した。このように、ここで提供される実験データにより、このGAPDH-Siah1結
