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Nutrition and cerebral neurodegenerative diseases
Šálková, Michaela ; Vespalcová, Milena (referee) ; Vránová, Dana (advisor)
This bachelor‘s thesis is literary research and its topic is focused on the effect of nutrition on the development of neurodegenerative diseases. The thesis is divided into four parts. The first part deals with the structure and physiology of the human brain. In the second part are described all essential nutrients which the brain needs to maintain its functions. The third part focuses on neurodegenerative diseases and their epidemiology and pathophysiology. In this part are also examined nutrients which could be possibly useful in the prevention or which could be involved in the pathophysiology of the disease. Explored diseases include dementia, Alzheimer’s disease, Parkinson’s disease and unipolar depression.The aim of this thesis was to find accessible literature focused on this topic and make a discussion.
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Disorders of brain energy metabolism in Alzheimer's and Parkinson's disease
Řezáčová, Adéla ; Telenský, Petr (advisor) ; Kolář, David (referee)
Alzheimer's and Parkinson's diseases belong to group of neurodegenerative diseases that affect not only the patients, but also their surroundings. Patients of those diseases gradually lose their neurons. Both disorders are typical for pathophysiological accumulation of proteins which affect the functioning of neurons and astrocytes. These disorders are also characterised by mitochondrial senescence and its damages which itself manifest by dysfunction of various complexes. Furthermore, in both diseases, there can be found insulin resistance, which leads to an insufficient insulin signalization. Both diseases are also accompanied by impaired metabolisms of amino acids. With Alzheimer's disease, there is significantly lowered metabolism of glucose, whereas with Parkinson's disease, there is not enough stimulation for action potential to proceed in dopaminergic neurons in substantia nigra. These impairments in Alzheimer's disease cause cognitive dysfunction, while with Parkinson's disease, these defects predominantly lead to complications with motor function. By studying energetic changes in presented diseases could bring more effective treatment.
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Brain energy metabolism and its pathologies
Nová, Jana ; Telenský, Petr (advisor) ; Kolář, David (referee)
The brain belongs amongst metabolically most active organs and disturbances of brain energy metabolism are commonly cited as a critical factor predisposing to neurodegeneration. Brain metabolic substrates must be strictly regulated both spatially and temporarily to ensure the energy homeostasis of the brain. Research on energy metabolism of the brain identified several models revealing the interdependence of metabolic processes in the CNS. Powered by TCPDF (www.tcpdf.org)
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Mitochondrial dysfunction and neurodegenerative diseases
Novotná, Veronika ; Herink, Josef (advisor) ; Kovařík, Miroslav (referee)
Charles University in Prague Faculty of Pharmacy in Hradec Králové Department of Biological and Medical Sciences Author: Bc. Veronika Novotná Supervisor: doc. MUDr. Josef Herink, DrSc. Title of diploma thesis: Mitochondrial dysfunction and neurodegenerative diseases The diploma thesis deals with mitochondrial dysfunction and neurodegenerative diseases and it is divided into two main parts. The first part summarized the classification of neurodegenerative diseases and general charakteristic of mitochondria.Then a describe of the processes of oxidative stress, excitotoxicity, apoptosis and briefly decribe the nervous system. The second part deals with description of mitochondrial dysfunction in selected nerodegenerative diseases. The recent studies refer to connection between mitochondrial dysfunctions and formation of neurodegenerative diseases. Keywords: excitotoxicity, mitochondrial dysfunction, neurodegenerative disorders, neuronal cell death, oxidative damage
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The m6A pathway at the molecular level and its role in neurological diseases
Švendová, Aneta ; Černá, Barbora (advisor) ; Čočková, Zuzana (referee)
N6-methyladenosine is the most abundant modification in eukaryotic messenger RNA. This modification is reversible, thanks to a complex of methyltransferases and demethylases. The biological effects of m6 A are mediated through reader proteins. This complex mechanism of proteins contributes to many molecular processes such splicing, translation and transport. It also plays a role in many serious neurological diseases, such as Alzeheimer's disease, Parkinson's disease, major depressive disorder and attention deficit hyperactivity disorder. The purpose of this thesis is to describe the m6 A pathway, its regulation at the molecular level and to put it into context with neurological diseases of today. Key words: mRNA, mRNA metabolism, N6-methyladenosine, m6 A regulation, FTO, METTL, ALKBH5, neurodegenerative disorders, Alzheimer's disease, Parkinson's disease, major depressive disorder, ADHD
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The Generation of Transgenic Huntington's Disease Miniature Pig
Baxa, Monika
Huntingtons's disease (HD) is devastating neurodegenerative disorder manifesting by motor disturbances, cognitive decline and personal changes. The huge effort to find a cure for HD has brought several promising therapeutic treatments on the scene. Each of the prospective approaches needs to be investigated for safety, tolerability and efficacy. Mouse and rat models were a lot helpful in examination of pathological mechanisms of HD, but they are not sufficient for completion of pre-clinical testing. Therefore, we aimed to generate transgenic HD minipig to overcome the gap between rodents and humans. Minipig transgenic for the first 548 aminoacids of human mutant huntingtin gene (TgHD) under the control of human HD promotor was manipulated by lentiviral transduction of porcine one-cell stage embryos. Currently, six generations of minipigs expressing single copy of N-truncated human mutant huntingtin protein (mtHtt) with a repetition of 124 glutamines are at disposal. The more the model simulates the disease symptoms the better it is for translational research as the efficacy of the cure can be finer evaluated. Hence, the second aim was to demonstrate HD-like phenotype in our model. Testicular degeneration that preceded the clinical symptoms onset was observed as a consequence of expression of mtHtt....
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Role of post-translational modifications, O-GlcNAcylation and Phosphorylation, in neurodegenerative disorders and brain hypometabolism
Špundová, Tereza ; Růžička, Jiří (advisor) ; Čočková, Zuzana (referee)
Post-translational modifications are major mechanisms that highly increase the variability in protein function. O-GlcNAcylation and phosphorylation are among the most extensively studied post-translational modifications in research to date. In physiological conditions, O- GlcNAcylation acts as a metabolic sensor that links glucose metabolism to normal neuronal functioning. Reversible phosphorylation is one of the mechanisms that can downregulate metabolism by regulating the rates of flux through metabolic pathways. The impairments in the regulation of these modifications are linked to with neurodegenerative disorders and hypometabolism. This thesis focuses on the crosstalk and correlation between these two modifications, their reciprocal relationship and their mutual impact on their regulations in models of neurodegenerative diseases and disease non-related models. Keywords: hypometabolism, O-GlcNAcylation, phosphorylation, post- translational modifications, neurodegenerative disorders, hibernation, caloric restriction, memory, learning
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The Generation of Transgenic Huntington's Disease Miniature Pig
Baxa, Monika
Huntingtons's disease (HD) is devastating neurodegenerative disorder manifesting by motor disturbances, cognitive decline and personal changes. The huge effort to find a cure for HD has brought several promising therapeutic treatments on the scene. Each of the prospective approaches needs to be investigated for safety, tolerability and efficacy. Mouse and rat models were a lot helpful in examination of pathological mechanisms of HD, but they are not sufficient for completion of pre-clinical testing. Therefore, we aimed to generate transgenic HD minipig to overcome the gap between rodents and humans. Minipig transgenic for the first 548 aminoacids of human mutant huntingtin gene (TgHD) under the control of human HD promotor was manipulated by lentiviral transduction of porcine one-cell stage embryos. Currently, six generations of minipigs expressing single copy of N-truncated human mutant huntingtin protein (mtHtt) with a repetition of 124 glutamines are at disposal. The more the model simulates the disease symptoms the better it is for translational research as the efficacy of the cure can be finer evaluated. Hence, the second aim was to demonstrate HD-like phenotype in our model. Testicular degeneration that preceded the clinical symptoms onset was observed as a consequence of expression of mtHtt....
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The Generation of Transgenic Huntington's Disease Miniature Pig
Baxa, Monika ; Motlík, Jan (advisor) ; Procházka, Jan (referee) ; Petr, Jaroslav (referee)
Huntingtons's disease (HD) is devastating neurodegenerative disorder manifesting by motor disturbances, cognitive decline and personal changes. The huge effort to find a cure for HD has brought several promising therapeutic treatments on the scene. Each of the prospective approaches needs to be investigated for safety, tolerability and efficacy. Mouse and rat models were a lot helpful in examination of pathological mechanisms of HD, but they are not sufficient for completion of pre-clinical testing. Therefore, we aimed to generate transgenic HD minipig to overcome the gap between rodents and humans. Minipig transgenic for the first 548 aminoacids of human mutant huntingtin gene (TgHD) under the control of human HD promotor was manipulated by lentiviral transduction of porcine one-cell stage embryos. Currently, six generations of minipigs expressing single copy of N-truncated human mutant huntingtin protein (mtHtt) with a repetition of 124 glutamines are at disposal. The more the model simulates the disease symptoms the better it is for translational research as the efficacy of the cure can be finer evaluated. Hence, the second aim was to demonstrate HD-like phenotype in our model. Testicular degeneration that preceded the clinical symptoms onset was observed as a consequence of expression of mtHtt....
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Mitochondrial dysfunction and neurodegenerative diseases
Novotná, Veronika ; Herink, Josef (advisor) ; Kovařík, Miroslav (referee)
Charles University in Prague Faculty of Pharmacy in Hradec Králové Department of Biological and Medical Sciences Author: Bc. Veronika Novotná Supervisor: doc. MUDr. Josef Herink, DrSc. Title of diploma thesis: Mitochondrial dysfunction and neurodegenerative diseases The diploma thesis deals with mitochondrial dysfunction and neurodegenerative diseases and it is divided into two main parts. The first part summarized the classification of neurodegenerative diseases and general charakteristic of mitochondria.Then a describe of the processes of oxidative stress, excitotoxicity, apoptosis and briefly decribe the nervous system. The second part deals with description of mitochondrial dysfunction in selected nerodegenerative diseases. The recent studies refer to connection between mitochondrial dysfunctions and formation of neurodegenerative diseases. Keywords: excitotoxicity, mitochondrial dysfunction, neurodegenerative disorders, neuronal cell death, oxidative damage
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