Academic literature on the topic 'Creatine, brain, mitochondria'
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Journal articles on the topic "Creatine, brain, mitochondria"
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O'Gorman, E., K. H. Fuchs, P. Tittmann, H. Gross, and T. Wallimann. "Crystalline mitochondrial inclusion bodies isolated from creatine depleted rat soleus muscle." Journal of Cell Science 110, no. 12 (June 15, 1997): 1403–11. http://dx.doi.org/10.1242/jcs.110.12.1403.
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Rats were fed a 2% guanidino propionic acid diet for up to 18 weeks to induce cellular creatine depletion by inhibition of creatine uptake by this creatine analogue. Ultrastructural analysis of creatine depleted tissues showed that mitochondrial intermembrane inclusion bodies appeared in all skeletal muscles analysed, after 11 weeks of feeding. Heart had relatively few even after 18 weeks of analogue feeding and none were evident in kidney, brain or liver. These structures were strongly immuno-positive for sarcomeric mitochondrial creatine kinase and upon removal from mitochondria, the inclusion bodies were shown to diffract to a resolution of 2.5 nm. Two-dimensional image analysis and three-dimensional reconstruction revealed arrays of creatine kinase octamers with additional components between the octameric structures. The same mitochondria had a 3-fold higher extractable specific creatine kinase activity than controls. Molecular mass gel filtration of inclusion body containing mitochondrial extracts from analogue fed rat solei revealed mitochondrial creatine kinase eluting as an aggregate of an apparent molecular mass > or = 2,000 kDa. Mitochondrial creatine kinase of control soleus mitochondrial extract eluted as an octamer, with a molecular mass of 340 kDa. Respiration measurements of control solei mitochondria displayed creatine mediated stimulation of oxidative phosphorylation that was absent in analogue-fed rat solei mitochondria. The latter also had 19% and 14% slower rates of state 4 and maximal state 3 respiration, respectively, than control mitochondria. These results indicate that mitochondrial creatine kinase co-crystallises with another component within the inter membrane space of select mitochondria in creatine depleted skeletal muscle, and is inactive in situ.
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Kottke, M., T. Wallimann, and D. Brdiczka. "Dual Electron Microscopic Localization of Mitochondrial Creatine Kinase in Brain Mitochondria." Biochemical Medicine and Metabolic Biology 51, no. 2 (April 1994): 105–17. http://dx.doi.org/10.1006/bmmb.1994.1015.
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Bojinca, Mihai, Violeta Claudia Bojinca, Andra Rodica Balanescu, and Serban Mihai Balanescu. "Macro Creatine Kinase (macro CK) in Clinical Practice." Revista de Chimie 69, no. 8 (September 15, 2018): 2107–9. http://dx.doi.org/10.37358/rc.18.8.6483.
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Creatine kinase (CK) is an important enzyme involved in energy metabolism. CK is found in the cytosol and mitochondria of various tissues, mainly those with increased energy necessities as skeletal muscle, cardiac muscle and brain, but also in visceral tissues. CK is a dimeric molecule composed of two identical or different subunits, type M - muscular and type B - brain. The combination of M and B subunits leads to formation of three isozymes: CK - MM found mainly in the skeletal muscle, CK - BB found mainly in the brain and CK - MB found mainly in the cardiac muscle, but also in small quantities in the skeletal muscle. The serum increase of different isozymes of CK is a consequence of cell disruption in various clinical situations like physical training, rhabdomyolysis, myositis, muscular dystrophy, myocardial infarction and others, CK being an important biomarker for this diseases. Macro CK is a complex of CK and immunoglobulin (macro CK type 1) or a polymer of mitochondrial CK (macro CK type 2) that induces false and persistent elevation of CK levels that could mislead the clinician. We present a review of the literature concerning the appearance and clinical significance of macro CK.
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Gonçalves, Cinara L., Gislaine T. Rezin, Gabriela K. Ferreira, Isabela C. Jeremias, Mariane R. Cardoso, Milena Carvalho-Silva, Alexandra I. Zugno, João Quevedo, and Emilio L. Streck. "Differential effects of escitalopram administration on metabolic parameters of cortical and subcortical brain regions of Wistar rats." Acta Neuropsychiatrica 24, no. 3 (June 2012): 147–54. http://dx.doi.org/10.1111/j.1601-5215.2011.00592.x.
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Objective: Considering that mitochondria may be drug targets and some characteristics of drug–mitochondria interactions may still be misjudged because of the difficulty in foreseeing and understanding all possible implications of the complex pathophysiology of mitochondria, our study aimed to investigate the effect of escitalopram on the activity of enzymes of mitochondrial energy metabolism.Methods: Animals received daily administration of escitalopram dissolved in saline [10 mg/kg, intraperitoneal (IP)] at 1.0 ml/kg volume for 14 days. Control rats received an equivalent volume of saline, 1.0 ml/kg (IP), for the same treatment period. Twelve hours after last injection, rats were killed by decapitation and brain areas were rapidly isolated. The samples were homogenised and the activities of mitochondrial respiratory chain complexes, some enzymes of Krebs cycle (citrate synthase, malate dehydrogenase and succinate dehydrogenase) and creatine kinase were measured.Results: We verified that chronic administration of escitalopram decreased the activities of complexes I and II–III in cerebellum, hippocampus, striatum and posterior cortex whereas prefrontal cortex was not affected. Complex II activity was decreased only in striatum without affecting prefrontal cortex, hippocampus, cerebellum and posterior cortex. However, chronic administration of escitalopram did not affect complex IV and enzymes of Krebs cycle activities as well as creatine kinase.Conclusion: In this study we showed a decrease in the activities of complexes I and II–III in most of the brain structures analysed and complex II activity was decreased only in striatum. However, it remains to be determined if mitochondrial dysfunction is rather a causal or a consequential event of abnormal signalling.
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Kostadinova, Ivanka, Magdalena Kondeva-Burdina, Lyubomir Marinov, Lubomir L. Vezenkov, and Rumyana Simeonova. "Newly Synthesized Creatine Derivatives as Potential Neuroprotective and Antioxidant Agents on In Vitro Models of Parkinson’s Disease." Life 13, no. 1 (January 4, 2023): 139. http://dx.doi.org/10.3390/life13010139.
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Oxidative stress is one of the key factors responsible for many diseases–neurodegenerative (Parkinson and Alzheimer) diseases, diabetes, atherosclerosis, etc. Creatine, a natural amino acid derivative, is capable of exerting mild, direct antioxidant activity in cultured mammalian cells acutely injured with an array of different reactive oxygen species (ROS) generating compounds. The aim of the study was in vitro (on isolated rat brain sub-cellular fractions–synaptosomes, mitochondria and microsomes) evaluation of newly synthetized creatine derivatives for possible antioxidant and neuroprotective activity. The synaptosomes and mitochondria were obtained by multiple centrifugations with Percoll, while microsomes–only by multiple centrifugations. Varying models of oxidative stress were used to study the possible antioxidant and neuroprotective effects of the respective compounds: on synaptosomes–6-hydroxydopamine; on mitochondria–tert-butyl hydroperoxide; and on microsomes–iron/ascorbate (non-enzyme-induced lipid peroxidation). Administered alone, creatine derivatives and creatine (at concentration 38 µM) revealed neurotoxic and pro-oxidant effects on isolated rat brain subcellular fractions (synaptosomes, mitochondria and microsomes). In models of 6-hydroxydopamine (on synaptosomes), tert-butyl hydroperoxide (on mitochondria) and iron/ascorbate (on microsomes)-induced oxidative stress, the derivatives showed neuroprotective and antioxidant effects. These effects may be due to the preservation of the reduced glutathione level, ROS scavenging and membranes’ stabilizers against free radicals. Thus, they play a role in the antioxidative defense system and have a promising potential as therapeutic neuroprotective agents for the treatment of neurodegenerative disorders, connected with oxidative stress, such as Parkinson’s disease.
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Vyssokikh, Mikhail Y., Susanne Holtze, Olga A. Averina, Konstantin G. Lyamzaev, Alisa A. Panteleeva, Maria V. Marey, Roman A. Zinovkin, et al. "Mild depolarization of the inner mitochondrial membrane is a crucial component of an anti-aging program." Proceedings of the National Academy of Sciences 117, no. 12 (March 9, 2020): 6491–501. http://dx.doi.org/10.1073/pnas.1916414117.
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The mitochondria of various tissues from mice, naked mole rats (NMRs), and bats possess two mechanistically similar systems to prevent the generation of mitochondrial reactive oxygen species (mROS): hexokinases I and II and creatine kinase bound to mitochondrial membranes. Both systems operate in a manner such that one of the kinase substrates (mitochondrial ATP) is electrophoretically transported by the ATP/ADP antiporter to the catalytic site of bound hexokinase or bound creatine kinase without ATP dilution in the cytosol. One of the kinase reaction products, ADP, is transported back to the mitochondrial matrix via the antiporter, again through an electrophoretic process without cytosol dilution. The system in question continuously supports H+-ATP synthase with ADP until glucose or creatine is available. Under these conditions, the membrane potential, ∆ψ, is maintained at a lower than maximal level (i.e., mild depolarization of mitochondria). This ∆ψ decrease is sufficient to completely inhibit mROS generation. In 2.5-y-old mice, mild depolarization disappears in the skeletal muscles, diaphragm, heart, spleen, and brain and partially in the lung and kidney. This age-dependent decrease in the levels of bound kinases is not observed in NMRs and bats for many years. As a result, ROS-mediated protein damage, which is substantial during the aging of short-lived mice, is stabilized at low levels during the aging of long-lived NMRs and bats. It is suggested that this mitochondrial mild depolarization is a crucial component of the mitochondrial anti-aging system.
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Kristian, Tibor, Arman J. Karimi, Adam Fearnow, Jaylyn Waddell, and Mary C. McKenna. "Perturbed Brain Glucose Metabolism Caused by Absent SIRT3 Activity." Cells 10, no. 9 (September 8, 2021): 2348. http://dx.doi.org/10.3390/cells10092348.
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Acetylation is a post-translational modification that regulates the activity of enzymes fundamentally involved in cellular and mitochondrial bioenergetic metabolism. NAD+ dependent deacetylase sirtuin 3 (SIRT3) is localized to mitochondria where it plays a key role in regulating acetylation of TCA cycle enzymes and the mitochondrial respiratory complexes. Although the SIRT3 target proteins in mitochondria have been identified, the effect of SIRT3 activity on mitochondrial glucose metabolism in the brain remains elusive. The impact of abolished SIRT3 activity on glucose metabolism was determined in SIRT3 knockout (KO) and wild type (WT) mice injected with [1,6-13C]glucose using ex vivo 13C-NMR spectroscopy. The 1H-NMR spectra and amino acid analysis showed no differences in the concentration of lactate, glutamate, alanine, succinate, or aspartate between SIRT3 KO and WT mice. However, glutamine, total creatine (Cr), and GABA were lower in SIRT3 KO brain. Incorporation of label from [1,6-13C]glucose metabolism into lactate or alanine was not affected in SIRT3 KO brain. However, the incorporation of the label into all isotopomers of glutamate, glutamine, GABA and aspartate was lower in SIRT3 KO brain, reflecting decreased activity of mitochondrial and TCA cycle metabolism in both neurons and astrocytes. This is most likely due to hyperacetylation of mitochondrial enzymes due to suppressed SIRT3 activity in the brain of SIRT3 KO mice. Thus, the absence of Sirt3 results in impaired mitochondrial oxidative energy metabolism and neurotransmitter synthesis in the brain. Since the SIRT3 activity is NAD+ dependent, these results might parallel changes in glucose metabolism under pathologic reduction in mitochondrial NAD+ pools.
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Kaldis, P., M. Stolz, M. Wyss, E. Zanolla, B. Rothen-Rutishauser, T. Vorherr, and T. Wallimann. "Identification of two distinctly localized mitochondrial creatine kinase isoenzymes in spermatozoa." Journal of Cell Science 109, no. 8 (August 1, 1996): 2079–88. http://dx.doi.org/10.1242/jcs.109.8.2079.
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The creatine kinase (CK) isoenzyme system is essential for motility in rooster and sea urchin sperm. In the present study, biochemical characterization as well as immunofluorescence and confocal laser microscopy with highly specific antibodies against various chicken CK isoenzymes revealed that cytosolic brain-type CK isoenzyme (B-CK) is the only CK isoenzyme in rooster seminal plasma, while three isoenzymes, cytosolic B-CK, sarcomeric mitochondrial CK (Mib-CK), and a variant of ubiquitous Mi-CK (‘Mia-CK variant’), are found in rooster spermatozoa. These three isoenzymes are localized in different regions of the sperm cell. B-CK and Mib-CK were localized along the entire sperm tail and in the mitochondria-rich midpiece, respectively. The ‘Mia-CK variant’, on the other hand, was found predominantly at the head-midpiece boundary, in a non-uniform manner in the midpiece itself and, surprisingly, at the distal end of the sperm tail as well as at the acrosome. Several lines of evidence show that the ‘Mia-CK variant’ shares some characteristics with purified Mia-CK from chicken brain, but also displays distinctive features. This is the first evidence for two different Mi-CK isoenzymes occurring in one cell and, additionally, for the co-expression of Mib-CK and cytosolic brain-type B-CK in the same cell. The relevance of these findings for sperm physiology and energetics is discussed.
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Hemmer, W., I. Riesinger, T. Wallimann, H. M. Eppenberger, and A. F. Quest. "Brain-type creatine kinase in photoreceptor cell outer segments: role of a phosphocreatine circuit in outer segment energy metabolism and phototransduction." Journal of Cell Science 106, no. 2 (October 1, 1993): 671–83. http://dx.doi.org/10.1242/jcs.106.2.671.
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Different isoforms of creatine kinase, an important enzyme of vertebrate energy metabolism, were localized in bovine photoreceptor cells, with particular emphasis on the identification and quantification of the brain-type isoform within the outer segment compartment. Using immunofluorescence and immunoelectron microscopy, brain-type creatine kinase was shown to be present in bovine photoreceptor cell outer and inner segments. The presence of this isoenzyme in rod outer segments was additionally confirmed by immunoblotting and immunolabeling of isolated rod outer segments. The content of creatine kinase in rod outer segments was quantified by measuring creatine kinase activity after membrane disruption with detergent. The ATP regeneration potential provided by the creatine kinase in isolated, washed bovine rod outer segments was 1.2 +/- (0.4) i.u. mg-1 rhodopsin. This value was calculated to be at least an order of magnitude larger than that necessary to replenish the energy required for cGMP resynthesis in rod outer segments, and high enough to regenerate the entire ATP pool of rod outer segments within the time span of a photic cycle. A mitochondrial creatine kinase isoenzyme was located within the ellipsoid portions of bovine rod and cone inner segments by immunofluorescence microscopy and, using immunogold staining, was specifically localized in the mitochondria clustered within bovine rod and cone inner segments. These results suggest that vertebrate photoreceptor cells contain a functional phosphocreatine circuit. Outer segment creatine kinase may play an important role in phototransduction by providing energy for the visual cycle, maintaining high local ATP/ADP ratios and consuming protons produced by enzymes located in the outer segment.
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Walzel, Bernd, Oliver Speer, Ernie Boehm, Søren Kristiansen, Sharon Chan, Kierian Clarke, Joseph P. Magyar, Erik A. Richter, and Theo Wallimann. "New creatine transporter assay and identification of distinct creatine transporter isoforms in muscle." American Journal of Physiology-Endocrinology and Metabolism 283, no. 2 (August 1, 2002): E390—E401. http://dx.doi.org/10.1152/ajpendo.00428.2001.
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Despite the pivotal role of creatine (Cr) and phosphocreatine (PCr) in muscle metabolism, relatively little is known about sarcolemmal creatine transport, creatine transporter (CRT) isoforms, and subcellular localization of the CRT proteins. To be able to quantify creatine transport across the sarcolemma, we have developed a new in vitro assay using rat sarcolemmal giant vesicles. The rat giant sarcolemmal vesicle assay reveals the presence of a specific high-affinity and saturable transport system for Cr in the sarcolemma (Michaelis-Menten constant 52.4 ± 9.4 μM and maximal velocity value 17.3 ± 3.1 pmol · min−1 · mg vesicle protein−1), which cotransports Cr into skeletal muscle together with Na+ and Cl− ions. The regulation of Cr transport in giant vesicles by substrates, analogs, and inhibitors, as well as by phorbol 12-myristate 13-acetate and insulin, was studied. Two antibodies raised against COOH- and NH2-terminal synthetic peptides of CRT sequences both recognize two major polypeptides on Western blots with apparent molecular masses of 70 and 55 kDa, respectively. The highest CRT expression occurs in heart, brain, and kidney, and although creatine kinase is absent in liver cells, CRT is also found in this tissue. Surprisingly, immunofluorescence staining of cultured adult rat heart cardiomyocytes with specific anti-CRT antibodies, as well as cell fractionation and cell surface biotinylation studies, revealed that only a minor CRT species with an intermediate molecular mass of ∼58 kDa is present in the sarcolemma, whereas the previously identified major CRT-related protein species of 70 and 55 kDa are specifically located in mitochondria. Our studies indicate that mitochondria may represent a major compartment of CRT localization, thus providing a new aspect to the current debate about the existence and whereabouts of intracellular Cr and PCr compartments that have been inferred from [14C]PCr/Cr measurements in vivo as well as from recent in vivo NMR studies.
Dissertations / Theses on the topic "Creatine, brain, mitochondria"
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Shao, Changxing. "OXIDATIVE STRESS AND MITOCHONDRIAL DYSFUNCTION IN TRAUMATIC BRAIN INJURY IN AGING." UKnowledge, 2007. http://uknowledge.uky.edu/gradschool_diss/533.
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Traumatic brain injury (TBI) is a prominent disease in developed countries, and age is an important factor in functional outcome. Although aged patients typically show diminished recovery compared to young patients, and have higher mortality and morbidity following TBI, the mechanism is not well understood. To date, there is no effective therapeutic for TBI. Previous studies indicate a secondary injury in TBI begins immediately after impact, and is likely the major contribution to delayed neuron dysfunction and loss. Studies also suggest mitochondrial dysfunction and increased free radical species (ROS) production following TBI may play a key role in the process. To evaluate oxidative damage following TBI, especially in aging, young (3 months), middle aged (12 months) and aged (22 months) Fisher-344 rats were subjected to a unilateral controlled cortical impact (CCI) injury, and tissue sparing, 4-hydroxynonenal (HNE) and acrolein levels, and antioxidant enzyme activities, and DNA oxidative damage were measured. In order to evaluate changes in mitochondria following TBI, mitochondrial protein levels were investigated using young adult animals. To evaluate a potential therapeutic for TBI, the effect of creatine on oxidative damage was evaluated. These studies show an age dependent increase of oxidative damage following TBI, demonstrated by increased levels of 4-HNE, acrolein and 8-hydroxyguanine. Middle aged and aged animals showed increased tissue loss compared to young animals 7 days post injury. Mitochondrial proteins involved in the respiratory chain, carrier proteins and channel proteins were significantly decreased 24 h post injury in ipsilateral cortex, but increased in both ipsilateral and contralateral hippocampus. To study potentially protective compounds in TBI, animals were fed with creatine two weeks before TBI and showed less oxidative damage and increased antioxidant capacity, which suggests creatine may be a potential drug for clinical treatment of TBI. The work described in this dissertation is the first to show increased oxidative damage and diminished antioxidant capacity in TBI in aging. The study of mitochondriafollowing TBI using quantitative proteomics is also the first time to show multiple mitochondrial proteins change following TBI. These data are also the first to show creatine can increase antioxidant defenses. These studies contribute to our understanding the mechanisms of secondary injury in TBI in aging.
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Molinaro, Angelo. "New insights into creatine transporter deficiency: identification of neuropathological and metabolic targets for treatment." Doctoral thesis, 2019. http://hdl.handle.net/2158/1154767.
Full textBook chapters on the topic "Creatine, brain, mitochondria"
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Zhang, Yuhua, Melvin G. McInnis, and Sebastian Zöllner. "Genetic techniques and applications to bipolar disorder." In The Bipolar Brain, 192–99. Oxford University Press, 2022. http://dx.doi.org/10.1093/med/9780197574522.003.0010.
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The methods and technologies behind the analyses of genetic data and information have advanced considerably since the identification and expansion of DNA sequence-based markers, genotypes, that map the human genome. The capacity for generating large numbers of genotypes have provided a base for developing innovative methods of analysis. The approach has shifted from family-based linkage analyses to population-based association analyses and emerging results have opened new directions for inquiry. In disorders with non-Mendelian inheritance, tens to hundreds of susceptibility loci have been identified, and methods adapted to assess a polygenic risk score are being tested. Methods for estimating epigenetic influences on gene expression are actively being developed and tested. The mitochondria are an exciting frontier in the search for causality. As current methods and technologies are considered, there is momentum and innovation driving the process. Emerging data and results demand new approaches, which create new data and results.
Conference papers on the topic "Creatine, brain, mitochondria"
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Rezende, Maria Clara Lopes, Maria Luiza Franco de Oliveira, Júlia Campos Fabri, Maria Júlia Filgueiras Granato, Mariana Vanon Moreira, and Leandro Vespoli Campos. "Neuroprotective Effects of Creatine Supplementation in Neurodegenerative Diseases." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.234.
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Introduction: Creatine is important in providing energy for the resynthesis of adenosine triphosphate (ATP) and in the deposition of intracellular energy, being present mainly in muscle fibers and in the brain. Supplementation with exogenous creatine can be used in neurodegenerative disorders that are related to bioenergetic deficits in the etiology and progression of the disease. Objective: Highlight the neuroprotective mechanisms of creatine supplementation in neurodegenerative diseases. Methods: In April 2021, a search was carried out on MEDLINE, with the descriptors: “Creatine” and “Neuroprotection”; and its variations, obtained in MeSH. Studies published in the last five years were included. Results: Of the 122 articles found, four were used in this work. They concluded that creatine supplementation contributes to brain bioenergetics by increasing phosphocreatine deposits, restoring mitochondrial functions and decreasing susceptibility to apoptosis. In addition, creatine intake shortly after the diagnosis of Huntington’s and Parkinson’s Diseases can be used as a complementary therapy, because improve performance in tasks of memory and intelligence. Finally, it buffers cellular concentrations of ATP, being a possible therapeutic strategy to delay or stop neurodegeneration diseases. Conclusion: Creatine promote important neuroprotective effect, but further studies on the subject are needed.
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Киреева, Виктория, Viktoriya Kireeva, Ю. Усольцев, Yu Usolcev, Ж. Капустенская, Zh Kapustenskaya, Е. Кожевникова, et al. "Intermediate results 2016 of a search study of translational diagnostic methods Mitochondrial dysfunction in patients with chronic myocardial ischemia and/or head Brain." In Topical issues of translational medicine: a collection of articles dedicated to the 5th anniversary of the day The creation of a department for biomedical research and technology of the Irkutsk Scientific Center Siberian Branch of RAS. Москва: INFRA-M Academic Publishing LLC., 2017. http://dx.doi.org/10.12737/conferencearticle_58be81ec94893.
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Purpose of the study. To rate prognostic properties of changes in mitochondrial DNA concentration in the blood plasma of patients with chronic cerebral ischemia and ischemic heart disease in relation to the disease and the effectiveness of the therapy. Materials and methods. The study involved patients suffering from coronary heart disease (CHD) and chronic cerebral ischemia (CCI) with stable and unstable atherosclerotic plaques, who have signed informed consent to the data processing within the framework of scientific research. The patients were admitted to the hospital for examination and treatment of CHD and CCI in Cardiology and Neurology Unit of the Hospital of ISC SB RAS. The subjects underwent laboratory and instrumental examination and analysis of the level of free circulating serum mitochondrial DNA by real-time PCR (copies/ml). The examination results considered as satisfactory were compared with the mtDNA levels before and after the treatment. Results. The average value of the mtDNA levels before and after the treatment in patients of neurological and cardiological profile were significantly different: 1 093 686 copies/ml vs 418 046 copies/ml, respectively (p = 0.02). Unlike women, men mtDNA levels statistically significantly (p = 0.03) decreased after the treatment. We revealed statistically significant differences in mtDNA level indicators before and after the treatment, depending on the definition of the series (p = 0.0010) for rank test Kruskal – Wallis test. The results of the proposed research will help to identify prognostic factors of destabilization of cell damage and plaques in endothelial dysfunction, atherosclerosis and its complications, to conduct clinical test of the method for predicting and diagnostics of cellular damage in chronic ischemia on a background of atherosclerosis.