Brain plasticity is at the basis of many cognitive functions, including learning and memory. It includes several mechanisms of synaptic and extrasynaptic changes, neurogenesis, and the formation and elimination of synapses. The plasticity of synaptic transmission involves the expression of immediate early genes (IEGs) that regulate neuronal activity, thereby supporting learning and memory. In addition, IEGs are involved in the regulation of brain cells’ metabolism, proliferation, and survival, in the establishment of multicellular ensembles, and, presumably, in cell competition in the tissue. In this review, we analyze the current understanding of the role of IEGs (c-Fos, c-Myc, Arg3.1/Arc) in controlling brain plasticity in physiological and pathological conditions, including brain aging and neurodegeneration. This work might inspire new gene therapy strategies targeting IEGs to regulate synaptic plasticity, and potentially prevent or mitigate neurodegenerative diseases.

There is growing evidence that the remodeling of cerebral microvessels plays an important role in plastic changes in the brain associated with development, experience, learning, and memory consolidation. At the same time, abnormal neoangiogenesis, and deregulated regulation of microvascular regression, or pruning, could contribute to the pathogenesis of neurodevelopmental diseases, stroke, and neurodegeneration. Aberrant remodeling of microvesselsis associated with blood–brain barrier breakdown, development of neuroinflammation, inadequate microcirculation in active brain regions, and leads to the dysfunction of the neurovascular unit and progressive neurological deficits. In this review, we summarize current data on the mechanisms of blood vessel regression and pruning in brain plasticity and in Alzheimer’s-type neurodegeneration. We discuss some novel approaches to modulating cerebral remodeling and preventing degeneration-coupled aberrant microvascular activity in chronic neurodegeneration.

In recent times, there has been a significant increase in researchers’ interest in the functions of microRNAs and the role of these molecules in the pathogenesis of many multifactorial diseases. This is related to the diagnostic and prognostic potential of microRNA expression levels as well as the prospects of using it in personalized targeted therapy. This review of the literature analyzes existing scientific data on the involvement of microRNAs in the molecular and cellular mechanisms underlying the development of pathologies such as Alzheimer’s disease, cerebral ischemia and reperfusion injury, and dysfunction of the blood–brain barrier.

Background: Microvessels in tumor tissue play a crucial role in meeting the metabolic needs of transformed cells, controlling the entry of xenobiotics into tumor tissue, and regulating local inflammation that promotes metastasis. Methylene blue has photosensitizing properties and can also affect dysfunctional mitochondria. Methods: The study was performed on the primary culture of CECs. The cells underwent photodynamic treatment through 660 nm laser irradiation at a power density of 300 mW/cm². The MTT, TMRE, and TUNEL assays were used to assess the survival, redox metabolism, mitochondrial activity, and apoptosis of CECs. Additionally, the metabolic activity of cells was evaluated using FLIM by measuring the fluorescence lifetime of NADH and FAD. Results: When CECs were incubated with MB, there was an increase in mitochondrial activity that was dependent on the concentration of MB. Additionally, mitochondrial activity increased when the CECs were exposed to 660 nm laser irradiation at an energy dose of up to 5 J/cm². Following PDT, a slight shift towards oxidative phosphorylation was observed. Conclusions: In vitro application of MB accumulation or laser irradiation causes a shift in the redox status of CECs towards increased reducing activity, without causing any cell damage. However, the combined action of PS and laser radiation has the opposite effect on the redox status of cells, resulting in an increase in the oxidized form of FAD.