Accepted_test

Age is the main risk factor for Alzheimer's disease (AD) and age-related macular degeneration (AMD). There are no effective ways to prevent and treat these neurodegenerative diseases. Risk factors and mechanisms of the pathogenesis of AD and AMD are intersecting. Among them, oxidative stress, mitochondrial dysfunctions and impaired maintenance of proteostasis with the accumulation of extracellular deposits - senile plaques in the brain of AD patients, and in the drusen of AMD patients. These abnormalities may be associated with alteration of MAPK signaling pathways (sp) regulation with age. The aim of study was compare changes in the activity of ERK1/2, p38MAPK and JNK in brain and retina with age and during the development of AD and AMD. We used OXYS rats as the models of accelerated aging, one of the manifestations of which is the simultaneous development of signs of AD and AMD. Our results showed that during physiological aging of Wistar rats and during accelerated aging of OXYS rats in the retina and brain structures, the direction of changes in the activity of MAPK sp both at the level of gene expression and at the protein level is the same. It was found that the manifestation and progression of signs of AD and AMD pathology in OXYS rats occur against the background of enhanced phosphorylation of p38MAPK, ERK1/2 and JNK which makes it possible to consider an increase in the activity of MAPK sp as a common mechanism for the development of AD and AMD.