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EN
Objective: The aim of the work is to compare the results of research on the oral language of people with neurodegenerative diseases. On the basis of literature, research results and available information, research methodologies in the subject and test results are presented. Speech variables that have been considered in the studies were presented, including linguistic, phonetic and phonological features, prosodic, acoustic, lexical, semantic, syntactic and morpho-syntactic features. Material and methods: A comprehensive review and analysis of literature, articles in peer-reviewed journals, in the field of language disorders resulting from brain damage resulting from neurodegenerative diseases. Conclusions: Studies show that the speech analysis is a crucial diagnosis tool, which can be used for early neurodegenerative changes recognition. No such studies have been carried out in the Polish language so far.
PL
Starzenie się organizmu jest procesem złożonym prowadzącym do zwiększonego ryzyka głównie takich chorób, jak choroby sercowo-naczyniowe i neurodegeneracyjne, ale również do cukrzycy. Związek z chorobami sercowo-naczyniowymi i naczyń mózgowych zależy nie tytko od czynników występujących u osób w wieku podeszłym, ale również od samego postępu procesu starzenia się. Podczas procesu starzenia zachodzą zmiany strukturalne, fizjologiczne i funkcjonalne w sercu i naczyniach tętniczych i żylnych. Kliniczne konsekwencje tych zmian to zawał serca, udar mózgu, nadciśnienie, niewydolność serca. Narastanie występowania cukrzycy jest szczególnie alarmujące z tego względu, iż choroba ta zwiększa ryzyko wielu chorób związanych z wiekiem, w tym chorób sercowo-naczyniowych. Patogeneza cukrzycy w wieku podeszłym charakteryzuje się dwiema cechami: wzrostem insulinooporności i upośledzeniem sekrecji insuliny. W pracy przedstawiono mechanizmy prowadzące do rozwoju chorób sercowo-naczyniowych i cukrzycy u osób w wieku podeszłym.
EN
Aging is a complex process that is linked to an increased risk of major diseases such as cardiovascular and neurodegenerative disease, but also diabetes mellitus. The influence of aging on cardiovascular and cerebrovascular diseases is due not only to increase in risk factors in the elderly but also to independent and inevitable effect of aging itself. During aging are observed structural, and physiological and functional changes in the heart and vasculars. Clinical consequences of these changes is myocardial infarction, stroke, hypertension, heart failure. The higher incidence of diabetes is especially alarming considering that diabetes in itself increases the risk for multiple other age-related diseases such as cardiovascular disease. The pathogenesis of diabetes in aging is characterized by two major features: peripheral insulin resistance and impaired insulin secretion. This paper reviews the mechanisms that lead to cardiovascular diseases and diabetes in the elderly.
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EN
Because of its special function in the body, diseases of the central nervous system can be very dramatic, especially if they affect the centres controlling the most vital functions of the body. They can develop as primary diseases or as secondary diseases, i.e. complications of another disease, the focus of which is located outside the nervous system. Diseases of the nervous system may affect its peripheral part (inflammation of nerves, polyneuropathies, radicular syndrome) or its central part (neuroinfections, developmental anomalies, dementia, trauma, tumors, epilepsy, stroke). There are also neurological diseases causing simultaneous changes to the peripheral and central parts. They are demyelination diseases, such as multiple sclerosis and transverse myelitis. There are also diseases affecting the spinal cord selectively. Muscle diseases such as myasthenia and muscular dystrophy, in which disorders of neuromuscular transmission are observed, may also be considered as neurological diseases. There is also a group of neurological diseases in which mental disorders can occur. Such diseases include, most importantly, dementia (Alzheimer’s disease, dementia with Levy bodies, fronto-temporal dementia) and encephalopathies (metabolic, traumatic, ischemic). During later stages of a neurological disease, mental symptoms resulting directly from numerous injuries to the central nervous system may occur. Neurodegenerative diseases in domestic animals are quite rare. However, they represent a very important and very large group of diseases. Many of these degenerations are similar to diseases occurring in humans, which makes it possible to understand them better by carrying out research on animals. Unfortunately, in many cases all we know about these diseases are their clinical symptoms, pathological changes that occur in their course and conclusions drawn from genealogical examinations. The introduction of more recent examination methods and new instruments makes it possible to obtain increasingly detailed knowledge of these diseases on the molecular level and, above all, a better understanding of their causes. Neurodegenerative disorders are among the most life-altering diseases and are therefore very costly to society.
EN
A fat-rich and low-carbohydrate ketogenic diet has been successfully used in epilepsy treatment in children and adults for many years. Lately, advances have been made in the use of ketogenics as therapy for other disorders such the tuberous sclerosis complex, brain tumors and neurodegenerative diseases: Alzheimer’s disease and Parkinson’s disease. Many studies have also shown its neuroprotective abilities. This neuroprotection is connected with the molecular mechanisms of a ketogenic diet and ketone metabolism. This review shows how a ketogenic diet induces ketosis, how it works and how the molecular mechanisms of a ketogenic diet may be used in the therapy of central nervous system disorders.
PL
Wysokotłuszczowa, niskowęglowodanowa dieta ketogenna jest terapią, która od wielu lat z sukcesem jest stosowana u dzieci i dorosłych w leczeniu epilepsji. Późniejsze badania pozwoliły na rozszerzenie poszukiwań jej terapeutycznego zastosowania o stwardnienie guzowate, guzy mózgu i schorzenia neurodegeneracyjne, jak choroba Alzheimera i choroba Parkinsona. Wiele badań wykazało również neuroprotekcyjne właściwości tej terapii. Indukowanie neuroprotekcji jest związane z molekularnymi mechanizmami działania diety ketogennej i metabolizmem ciał ketonowych. Niniejsza praca opisuje działanie diety ketogennej oraz jej mechanizmy molekularne, które mogą być wykorzystywane w terapii chorób centralnego układu nerwowego.
EN
Glutathione S-transferase pi (GST pi) inactivates a large variety of toxic, electrophilic compounds. The substrates of GST pi include environmental toxins and intracellular reactive oxygen species, factors significant in the pathogenesis of neurodegenerative diseases. The aim of the present study was to investigate the expression of glutathione S-transferase pi in transgenic mouse models of neurodegeneration on both the mRNA and protein levels. Experiments were conducted on the frontal cortex of transgenic B6-C3H hybrids SOD1, Cra1 and SOD1/Cra1, aged 70 and 140 days. The SOD1 mice express a human SOD1ᴳ⁹³ᴬ mutation, the Cra1 strain carries mutation in the cytoplasmic dynein heavy chain 1 (Dnchc1), and the double heterozygote SOD1/Cra1 mice show a delayed disease progression as well as an increased lifespan compared with the SOD1 strain. A wild strain of mice were used as a control. The expression of GST pi mRNA in younger mice (age 70 days) was found to be similar in all studied groups of animals. In older (aged 140 days) controls and Cra1 mice the GST pi expression was at a similar level and it did not significantly differ from younger animals. In SOD1 and SOD1/Cra1 strains, the mRNA-GST pi expression was lower when compared to 140-day-old controls and the Cra1 strain. Moreover, it was significantly lower than in corresponding 70-day-old animals. A decrease in the GST pi expression on the mRNA level was accompanied by a decrease in the protein level. High and unchanged GST pi expression in the frontal cortex of Cra1 mice indicates that the antioxidant-detoxification system plays an important role in protection against neurodegeneration. A significant decrease of GST pi expression in the frontal cortex of SOD1 and SOD1/Cra1 mice at the symptomatic stage of the disease suggests that the expression of this enzyme is related more to the G93A mutation in the SOD1 gene than to the efficient axonal transport.
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tom 50
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nr 3
198-208
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