One of the most pressing issues in contemporary biomedical brain research is the search for ways to detect and prevent degenerative and neurodegenerative age-related changes at early stages of the process. At present, a significant body of information has been collected about the changes that occur in the aging neurons of the brain. However, for a comprehensive understanding of the mechanisms of this process, a detailed examination of changes in the neuronal microenvironment is necessary. One of the essential components of the neuronal microenvironment is astrocytes. Astrocytes provide metabolic support and protection for neuronal cells; neuron-astrocyte interactions underlie synaptic plasticity, and astrocytes regulate the processes of synapse formation, reorganization, and elimination (Verkhratsky and Nedergaard, 2014). When considering astrocytes, the morphology of these cells is particularly important. Astrocytes are characterized by multiple branching processes. Large, optically resolved processes create a framework, while small distal (beyond optical resolution) processes envelop synapses, forming astrocytic coverage and representing the main functional compartment of the astrocyte: their membranes are densely equipped with transporters that control ion homeostasis, remove glutamate from the synaptic cleft, and supply neuronal terminals with glutamine, ensuring synaptic transmission. The number of astrocytic branches and distal processes is not constant. The efficiency of astrocyte functioning as a component of the neuronal microenvironment directly depends on their morphology: a decrease in the number of large branches will be accompanied by a reduction in the area of the territorial domain under the control of the astrocyte, and a decrease in the number of small branches will result in a decrease in the quality of synaptic coverage. Our previously obtained results show that with age, there is atrophy of small astrocytic processes, leading to irreversible functional changes, ultimately altering the efficiency of neuronal and overall brain function (Popov et al., 2021). Is it possible to influence the process of healthy aging in order to slow it down, and what factors can affect it? Of particular interest are external factors such as diets, leading to changes in metabolism and various alterations in brain function. We have shown that in young animals, calorie restriction leads to the elongation of distal astrocytic processes, enhancing neurotransmitter uptake efficiency (Popov et al., 2020). Diets high in fat (HFD) have also yielded positive results in young animals: astrocyte expansion, improved neurotransmitter uptake, increased long-term potentiation, and enhanced exploratory behavior in mice (Popov et al., 2022). These results suggest that the age-related atrophy of astrocytes might be slowed down or temporarily halted through dietary adjustments. However, will these identified patterns hold true in the case of aging animals? And what is the mechanism behind the observed process? To fully explore this, it is necessary to examine several age groups subjected to different diets. We will use mice aged 9-12 and 20-24 months, corresponding to adult and aging states, as tested in our previous studies (Popov et al., 2021). Two diets previously tested in our work will be employed: Caloric restriction (CR) (Popov et al., 2020); High-fat diet (HFD) (Popov et al., 2023). We will investigate changes in astrocyte morphology, the number of their large and small distal processes, alterations in neurotransmitter uptake efficiency, and the formation of long-term potentiation. Detailed information on the protein-lipid composition of astrocyte cytoplasm (content, conformation, and functions), the energy state of mitochondria, and the efficiency of the electron transport chain will be obtained. In-vivo studies will measure calcium dynamics delivered to the brain stereotactically using genetically encoded sensors. Hippocampus-dependent behavioral tests will be conducted on freely moving animals for all age groups under the influence of the diets. In other words, a comprehensive range of studies from the molecular to the behavioral level will be carried out, leading to hypotheses about the mechanisms involved in this process. Deciphering these mechanisms will help identify therapeutic targets whose manipulation may contribute to compensatory restoration of morphological and functional characteristics of astrocytes that decline with aging, ultimately allowing for the slowing down or temporary halting of this process.