Aim: To assess the state of the oxidant-antioxidant system of the hippocampus and kidneys of rats with scopolamine-induced Alzheimer’s disease and with the administration of carbacetam, as a GABA receptor modulator, and to clarify the possible systemic oxidative process. Materials and Methods: The experiments were carried out on mature and old male rats. Alzheimer’s disease was simulated by scopolamine hydrochloride (Sigma, USA). It was introduced into the peritoneum in a dose of 1 mg/kg of the body weight once a day during 27 days. On the 28th day, carbacetam was administered in a dose of 5 mg/kg once a day during 14 days. Intensity of lipid peroxide oxidation (LPO) was evaluated by the content of products reacting with 2-thiobarbituric acid reactive substances (TBARS). The content of protein oxidation modification (POM), also known as protein oxidation, in homogenates was determined by the amount of their oxidative modification products with the help of spectrophotometric method. The state of antioxidant protection was assessed by catalase and SOD activity. Results: Simulated Alzheimer’s disease was found to cause affliction of the protein amino groups in the hippocampal neurons and endotheliocytes, and in the mesangial matrix of non-collapsed renal glomeruli of rats of different ages with more pronounced changes in brain cells. At the same time, there is a clear existing relationship between affliction of the nerve cells and kidneys, which makes a foundation for further study of pathogenic processes and interrelations in neurodegenerative processes. Conclusions: Thus, the group of rats of different ages with experimental Alzheimer’s disease presented increase of the lipid and protein peroxidation products with more pronounced lesion in the hippocampal cells than those of the kidneys. Moreover, decrease of the lipid and protein peroxidation products in the examined organs of rats with scopolamine-induced Alzheimer’s disease after administration of carbacetam indicates the involvement of the GABA-ergic system in the pathogenesis of damage to hippocampal neurons and kidney cells.