Poster (download) Mikhail Tyumentsev1, Natalia Muraleva2, Yulia Polienko3, Artyom Gorodetsky4, Elena Bagryanskaya51ICG SB RAS, landselur@bionet.nsc.ru2ICG SB RAS, Myraleva@bionet.nsc.ru3NIOCH SB RAS, polienko@nioch.nsc.ru4NIOCH SB RAS, gorodaa@nioch.nsc.ru5NIOCH SB RAS, egbagryanskaya@nioch.nsc.ru This study focuses on the relationship between mitochondrial dysfunction and redox-status in the context of the development of signs of Alzheimer’s disease (AD). Mitochondrial dysfunction is considered the missing link between brain aging and AD [1], the most common type of age-related dementia worldwide, but the exact causal relationship between mitochondrial dysfunction and the transition from healthy aging to AD remains to be fully understood. Oxidative stress is thought to play a significant role in this mitochondrial dysfunction, leading to cellular damage in redox imbalance. However, the extent of these processes and timing of their occurrence within the scope of AD remain hard to study, especially so in the early, pre-clinical stages of the disease. We explored the mechanisms underlying the disruption of mitochondrial function, their impact on the initiation and progression of pathological molecular cascades of AD, and assessed the changes in redox status as one of the main consequences of oxidative stress. This investigation was conducted using senescence-accelerated OXYS rats, which spontaneously develop all major signs of AD and largely reproduce the stages of the disease. We concluded that mitochondrial dysfunction appears to mediate or possibly even initiate AD-like pathology in OXYS rats. Importantly this takes place with no apparent connection to redox imbalance as on both transcriptional and biochemical levels OXYS rats display no significant changes in redox-status and ROS production as compared to controls.