The term neuronutrition has been proposed as part of nutritional neuroscience, studying the effects of various dietary components on behavior and cognition. Other researchers underline that neuronutrition includes the use of various nutrients and diets to prevent and treat neurological disorders. The aim of this narrative review was to explore the current understanding of the term neuronutrition as the key concept for brain health, its potential molecular targets, and perspectives of its nutritional approach to the prevention and treatment of Alzheimer’s and Parkinson’s diseases, multiple sclerosis, anxiety, depressive disorders, migraine, and chronic pain. Neuronutrition can be defined as a part of neuroscience that studies the influence of various aspects of nutrition (nutrients, diet, eating behavior, food environment, etc.) on the development of nervous disorders and includes nutrition, clinical dietetics, and neurology. There is evidence that the neuronutritional approach can influence neuroepigenetic modifications, immunological regulation, metabolic control, and behavioral patterns. The main molecular targets in neuronutrition include neuroinflammation, oxidative/nitrosative stress and mitochondrial dysfunction, gut–brain axis disturbance, and neurotransmitter imbalance. To effectively apply neuronutrition for maintaining brain health, a personalized approach is needed, which includes the adaptation of the scientific findings to the genetic, biochemical, psycho-physiological, and environmental features of each individual.

Lymphangiogenesis plays an important role in development of renal parenchyma inflammation during kidney injury. Vascular endothelial growth factor type C (VEGF-C), cytokine that regulates lymphangiogenesis, is a potential early biomarker for acute kidney injury. Aim. To study the concentration of VEGF-C in renal homogenate and blood serum of newborn rats with experimental intraabdominal hypertension (IAH) of varying severity and duration, to establish a relationship with morphological changes in the renal tissue. Materials and methods. The experiment was conducted on 50 newborn Wistar rats. Rats were divided into 5 groups of 10 rats each: groups 1 and 2 with mild IAH lasting 5 and 10 days, respectively, and groups 3 and 4 with severe IAH lasting 5 and 10 days, respectively, and the control group. IAH was modelled by injecting sterile vaseline into the abdominal cavity to a predetermined level of IAH under the control of intra-vesical manometry. VEGF-C content was measured by ELISA. Morphological examination of the biopsy material and its photography were carried out using a Leica DM2000 microscope. The Mann—Whitney, Kruskal—Wallis, Wilcoxon tests, as well as one-way ANOVA, were used for statistical analysis. Results. The level of VEGF-C in the renal homogenate was increased in all groups (pc < 0.001); the degree of VEGF-C increase depended on the severity of IAH (p < 0.05) but not on the duration of IAH exposure. The VEGF-C blood serum level was increased only in group 3 (pc = 0.011). Morphological analysis showed hydropic dystrophy: changes in the height of the tubular epithelium, an increase in interstitial edema, expansion of the urinary spaces of glomeruli. The degree of morphological changes depended on the severity and duration of IAH. Conclusion. Changes in VEGF-C level assessed in the renal homogenate correlated with morphological changes in renal tissue of rats with different severity and duration of IAH.