—As the population ages, age-related cognitive impairments are becoming an increasingly pressing problem. Currently, the role of polyamines (putrescine, spermidine, and spermine) in the pathogenesis of cognitive impairments of various origin is actively discussed. It was shown that the content of polyamines in the brain tissue decreases with age. Exogenous administration of polyamines makes it possible to avoid cognitive impairment and/or influence the pathogenetic processes associated with disease progression. There are 3 known ways that polyamines can enter the human body: food, synthesis by intestinal bacteria, and biosynthesis in the body. Currently, one of the most promising approaches to the prevention of cognitive impairment is the use of foods with a high content of polyamines, as well as the use of various probiotics that affect intestinal bacteria that synthesize polyamines. Since 2018, in a number of European countries projects have been launched aimed at evaluation of the impact of a diet high in polyamines on cognitive processes. The review, based on analysis of modern scientific literature and the authors' own data, presents material on the effect of polyamines on cognitive processes and the role of polyamines in the regulation of neurotransmitter processes, and discusses the role of polyamines in cognitive disorders in mental and neurological diseases.

The fungal glycoprotein l-lysine α-oxidase (LO) catalyzes the oxidative deamination of l-lysine (l-lys). LO may be internalized in the intestine and shows antitumor, antibacterial, and antiviral effects in vivo. The main mechanisms of its effects have been shown to be depletion of the essential amino acid l-lys and action of reactive oxidative species produced by the reaction. Here, we report that LO penetrates into the brain and is retained there for up to 48 h after intravenous injection, which might be explained by specific pharmacokinetics. LO actively intervenes in amino acid metabolism in the brain. The most significant impact of LO was towards amino acids, which are directly exposed to its action (l-lys, l-orn, l-arg). In addition, the enzyme significantly affected the redistribution of amino acids directly associated with the tricarboxylic acid (TCA) cycle (l-asp and l-glu). We discovered that the depletion of l-orn, the precursor of polyamines (PA), led to a significant and long-term decrease in the concentration of polyamines, which are responsible for regulation of many processes including cell proliferation. Thus, LO may be used to reduce levels of l-lys and PA in the brain.

Using electron paramagnetic resonance, the dose-dependence effect of dopamine on methemoglobin formation in erythrocytes of patients with Parkinson’s disease under the activation of oxidative stress induced by acrolein and the possibilities for the correction of this pathological process using carnosine in vitro experiments have been examined. It was shown that incubation of erythrocytes with 1.5 mM dopamine did not change the methemoglobin content, while incubation with 15 mM dopamine caused a two fold increase in the methemoglobin content compared to its initial level; 10 μM acrolein increased methemoglobin formation threefold. Administration of 15 mM dopamine and, after 1 h, 10 μM acrolein to the incubation system increased methemoglobin formation tenfold compared to its initial level. Preincubation of erythrocytes with 5 mM carnosine followed by acrolein addition prevented the increase in the methemoglobin content, while carnosine had no effect on methemoglobin formation induced by dopamine.

The contents of polyamines in the brains of SAMP1/SAMR1 mice (senescence accelerated mice prone/resistance) of two different age groups (10-day-old and 8-month-old) were investigated. The SAMP1 mice line is a unique model object with a genetically determined mechanism of aging, which is related to a deficiency of the antioxidant body status. We found that the contents of the studied polyamines (spermine, spermidine, and putrescine) in the brains of adult mice of both strains are much lower than in the brains of 10-day animals, although rapidly aging SAMP1 mice had a significantly higher putrescine and significantly lower spermidine level in comparison with SAMR1 mice. The level of spermine in 10-day-old SAMP1 brains was lower by 57% than in the brains of SAMR1 mice (“control”). Our results confirm that polyamine exchange in the brains of rapidly aging mice is already disturbed at early ontogenesis stages (10 days of life) and it can negatively affect the development of animals.

—A brief review of the authors’ work on the use of low-temperature EPR spectroscopy in blood tests of patients with Parkinson’s disease and tissues of rat organs taken in experiments that simulate the early stages of parkinsonism is presented. An analysis of the obtained and published data suggests that the process of hemoglobin degradation can be included in the list of fundamental characteristics of the pathogenesis of Parkinson’s disease.