Evaluation of the regeneration process of the sciatic nerve of a mouse animal model after application of freezing, crushing or electrocoagulation damage / Ocena procesu regeneracji nerwu kulszowego mysiego modelu zwierzecego po zastosowaniu uszkodzenia metoda mrozenia, zmiazdzenia i elektrokoagulacji.

The problem of regeneration of damaged peripheral nerves is an ongoing topic and has long been the subject of intensive research worldwide. This study examined the morphological and functional evaluation of the regeneration process within the damaged sciatic nerve, a mouse animal model. The effect of impaired expression of the TSC-1 gene on the process of nerve regeneration was evaluated, depending on the mode of damage. The research object consisted of 48, 2-month-old male TSC lines. The test group consisted of animals that underwent damage to the sciatic nerve by crushing, freezing and electrocoagulation, while the control group includes mice whose sciatic nerve was not damaged. Behavioral tests were conducted to evaluate the functional return of the limb, after 3,5,7 and 14 days. The first changes in the regeneration process of the damaged neurite are observed as early as day 3 after the injury, while on day 14 after the injury the functional return of the damaged limb was noted.

Neuroprotective effect of curcumin and its potential use in the treatment of neurodegenerative diseases / Neuroprotekcyjne dzialanie kurkuminy i jej potencjalne zastosowanie w leczeniu chorób neurodegeneracyjnych.

The development of methods used in molecular biology has allowed a milestone in medical and pharmaceutical sciences. Progress has also been made in the field of pharmacognosy, which places substances of natural origin contained in plant raw materials at the center of attention. The beneficial effects of some of them have been known for years, while scientific evidence of their health-promoting properties was lacking for a long time. This was also the case with curcumin and the long road from its isolation in pure form in 1842 to the knowledge of its chemical structure in 1910. Due to the chemical properties of the molecule, curcumin is attributed with many health-promoting properties. These affect many organ systems including the skin, visual pathway, respiratory system, circulatory system, digestive system and nervous system. One of the complications that follow nerve damage is the loss of locomotor function in the animal and the development of inflammation within it. Curcumin has anti-inflammatory properties. This is confirmed by its inhibition of nuclear factor κB, a mediator in inflammatory processes. In addition, a very important field associated with neuronal dysfunction is the aging process. This is caused, among other things, by the presence of reactive oxygen species. The neuroprotective effect of curcumin allows to reduce their concentration caused by the accumulation of mutations within the mitochondrial DNA. The beneficial effect on the nervous system is due to the penetration of curcumin across the blood-brain barrier. However, its poor solubility significantly limits the therapeutic properties resulting from curcumin supplementation. Methods are currently being developed to increase its bioavailability using nanoparticles.

Assessment of metabolomics in patients with multiple sclerosis as an indicator of disease development, including relapsing-remitting, primary progressive and secondary progressive stage / Ocena profilu metabolomicznego u pacjentów ze stwardnieniem rozsianym jako wskaznik rozwoju choroby z uwzglednieniem postaci rzutowo - remisyjnej, pierwotnie postepujacej i wtórnie postepujacej.

Metabolomics is a scientific field whose topics include qualitative and quantitative analysis of metabolites, defined as the total set of low-molecular-weight chemical compounds not exceeding 1500 Da. Along with genomics, transcriptomics, and proteomics, it is categorized as a field of science, currently using state-of-the-art diagnostic tools that, in the face of modern medicine, allow a holistic approach to the patient. The presence of metabolites in the analyzed biological material, in contrast to the information contained directly in the genetic material, reflects the current physiological state of the cell, and represents an integral relationship between genotype and phenotype, which can directly contribute in the future to the knowledge of the molecular basis in specific disease entities. An additional aspect that is in favor of metabolic analysis is their decidedly smaller number compared to at least genes, transcriptomes, and proteins. Despite the development of many "omics" technologies, there is a lack of integrative and linking studies to see the full picture of cellular pathways in the future. Such linkage would improve our insight into human pathologies, leading to a revolution in preclinical and clinical research in disease diagnosis, prognosis, drug response and drug development.

The mTOR pathway and transgenic animals with deletion of the TSC gene in the regeneration of the nervous system and selected models of sciatic nerve damage / Szlak mTOR i zwierzeta transgeniczne z delecja genu TSC w procesie regeneracji ukladu nerwowego i wybranych modelach uszkodzen nerwu kulszowego.

Traumatic damage to the nervous system has been a common occurrence for years, reducing patients' quality of life. The mammalian target of rapamycin (mTOR) pathway plays a key role in nervous system physiology, including by controlling nerve cell survival and differentiation. Excessive activation of the mTOR pathway leads to an increase in cell cycle protein activity and apoptosis of nerve cells. Moreover, current findings suggest the involvement of the mTOR pathway in neuroplasticity. The use of transgenic animals with deletion of the TSC gene as well as various models of sciatic nerve damage, allows activation of the mTOR pathway. Currently, the results confirm that inactivation of point mutations in TSC-1 or TSC-2 genes, activates the canonical signaling pathway of the mTORC-1 complex, in turn, reactivation of the mTORC-1 pathway through the absence of the TSC-1 gene in mature neurons induces axonal regeneration. Dysfunction of the mTORC-1 pathway in Schwann cells (SC) inhibits myelination of nerve fibers. The aim of the present study is to understand the physiology and role of the mTOR pathway as well as to demonstrate the impact of TSC gene deletion in the regeneration of the nervous system. Current research on the activity of the mTOR pathway may provide new strategies to intensify peripheral nerve regeneration.

Bcl-2-proteins and neurotrophins as important factors for the survival of peripheral neurons in transgenic animals / Bialka z rodziny Bcl-2 oraz neurotrofiny jako istotny czynnik decydujacy o przezywalnosci neuronów obwodowych u zwierzat transgenicznych.

Apoptosis is an orderly, active process with the activation of certain genes that allows the cell to follow the path of programmed death. During embryogenesis, programmed cell death templates are essential for the proper formation of organs and the functioning of the nervous system in the regression of primary or abnormal structures. Increased cell mortality in the mature nervous system can lead to various neurodegenerative diseases. For these reasons, the Bcl-2 protein family is being studied intensively in connection with the function of the nervous system. Programmed cell death (PCD) makes it possible to eliminate superfluous cells and thus contribute to the maintenance of homeostasis in the body. Malregulation of apoptosis is characteristic of tumour processes, degenerative changes and autoimmune diseases. Research into gene expression of pro- and anti-apoptotic proteins using knock-out technology is currently raising great hopes for the treatment of patients affected by neurodegenerative changes.

Cerebral metabolism of glucose and selected glucose transporters in neurodegenerative diseases / Mózgowy metabolizm glukozy i wybranych jej transporterów w chorobach neurodegeneracyjnych.

Cerebral glucose metabolism is an issue of researchers' interest for a long time. Disturbed transport and metabolism of glucose in the brain lead to development of numerous neurological pathologies. Recently, a significant correlation between perturbed cerebral glucose metabolism and development of neurodegenerative diseases has been shown. Glucose, a monosaccharide, is the main source of energy for brain cells. Brain is the organ which is the most sensitive to changes in blood glucose level. Perturbed glucose transport leads to disorders of the central glucose metabolism. Neurodegenerative diseases are defined in the literature as progressive and irreversible degeneration of nerve tissue, causing cell death as a result of degenerative processes. The aim of this article is to discuss the physiology and the role of selected glucose transporters in the development of neurodegenerative diseases: expression of selected GLUT1 and GLUT3 transporters in Alzheimer's and Huntington's diseases. Understanding of the cerebral glucose metabolism may be a crucial factor in fight with central nervous system diseases.