Примеры использования Neurodegeneration на Английском языке и их переводы на Русский язык
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Neurodegeneration frequently results in dementia.
This impairment leads to neurodegeneration and FUS aggregate formation.
Its deregulation leads to a number of diseases,including cancer and neurodegeneration.
Key words:: neurodegeneration, piracetam, cerebral, verapamil, drosophila.
AD is currently conceptualized as a combined amyloidopathy and tau-related neurodegeneration.
Keywords: Alzheimer's disease; neurodegeneration; target-molecules; pharmacotherapy of Alzheimer's disease.
The next argument is that the majority of patients during the examination on a tomograph neurodegeneration is not detected.
And sectioning of the brain revealed neurodegeneration at a much higher rate than I would expect for her age.
P7C3 compounds have been shown in a number of publications to be beneficial in animal models for age-related neurodegeneration.
Special attention is given to the Meksidol effects in the treatment of neurodegeneration diseases, especially acute and chronic cerebral circulation disorders.
As far as AD neurodegeneration is concerned, there is a consensus suggesting that the inflammatory milieu associated with the neuro-inflammation inhibits the microglia phagocytosis 48.
Alzheimer's disease(AD) is a complex disease resulting in neurodegeneration and cognitive impairment.
Only in 5 cases we are dealing with real neurodegeneration, when dopamine-producing structures are being destroyed, and just in these cases L-dopa products should act.
However, implementation of novel technologies of regenerative medicine,including usage of induced pluripotent stem cells, in neurodegeneration needs essential evidence base.
There are a wide range of neurological disorders including neurodegeneration and brain injury, for which the ability to treat is limited by targeted delivery of therapeutic agents.
In September 2014, it was announced that Calico, in partnership with AbbVie, would be opening up an R&D facility focused on aging and age-related diseases,such as neurodegeneration and cancer.
Interestingly, the astrocytes expressing YKL-40 mark neuroinflammation or neurodegeneration zones in the mature brain[23, 24], thus confirming the role of astroglia in reparative angiogenesis regulation.
A bulk of evidence suggest that direct pathologic accumulation of A β oligomers in the nervous endings may lead to synaptic damage and, finally, to neurodegeneration in AD 21.
In AD, there is a characteristic pattern of tau-related,neurofibrillary neurodegeneration spreading from the medial temporal lobe to other multi-modal association areas and a corresponding pattern of memory loss spreading to other cognitive domains.
Improvement of physical activity in some patients immediately after RANC procedures,while others at a later date for continuing treatment is also inconsistent with neurodegeneration dofaminprodutsiruyuschih structures.
When neurodegeneration would not be patients who recover"that killed then killed" after the stroke, the death of brain areas is not accompanied by the restoration of the functions once they manage and dreams to the neighboring nerve centers take to the functions of the affected yet unfortunately, remain dreams.
This requires evidence of 1 amyloid deposition by autopsy, low cerebrospinal fluid(CSF) Aβ, orpositive amyloid positron emission tomography(PET) and 2 neurodegeneration by autopsy, high CSF ptau, and AD pattern of atrophy on structural imaging.
Symptoms of early infantile GM1(the most severe subtype, with onset shortly after birth) may include neurodegeneration, seizures, liver enlargement(hepatomegaly), spleen enlargement(splenomegaly), coarsening of facial features, skeletal irregularities, joint stiffness, distended abdomen, muscle weakness, exaggerated startle response to sound, and problems with gait.
Application of the models, utilizing direct cytotoxic effect of amyloid or chemical substances, impairing its metabolism(d-galactose, aluminium chloride),together with transgenic models allows identification of new target-molecules for pathogenetic therapy of Alzheimer's type neurodegeneration 54, 62, 72.
Applying for the treatment of Parkinson's disease RANC method in 90-95% of cases it is possible to achieve a significant improvement in the physical condition of the patient,because the true extent neurodegeneration reached"the point of no return", in my opinion, it is the only 5-10% of the total number affected so disease patients.
Without denying that neurodegeneration structures that produce dopamine and related disorders, there is, I still want to say that the same cases are very few and the total number of cases, these patients account for about 5-10 percent, and today's existing instrumental methods of diagnosis are quite capable of separating them from the bulk of who is a disease should be considered a significant functional disorder.
Amyloid toxicity is known[63] to be caused by impairment of neuron-astroglial metabolic coupling, inhibition of glycolysis and mitochondrial activity, glucose transport, and development of local insulin resistance, which alter cell functional activity and is the basis of cognitive dysfunction,progressing neurodegeneration, and neuroinflammation.
Endothelial dysfunction is one of important mechanisms of pathogenesis of brain development disturbances,its ischemic damage or neurodegeneration, which is related to disturbance of key metabolic and transportation processes, release of regulatory molecules, with disturbance of intercellular coupling, BBB structural and functional integrity and death of endothelial cells.
The developed transgenic models on animals demonstrated, that it is possible to reproduce some aspects of AD for a short period of time, with the clinical picture and neuropathologic changes appearing in 6-15 months,while expression of neurodegeneration markers displays region-specific character: various models of amyloid deposition may depend on the definite neuronal population, expressing a faulty gene, expression level, and topographic transgene distribution, as well as the levels of A β 1-40 and A β 1-42.
The authors have analyzed possible contribution mechanisms of these processes in endothelial dysfunction development as one of the pathogenetic components of neurodevelopmental disorders,ischemic brain injury, or neurodegeneration associated with alterations in key metabolic and transport processes, secretion of regulatory molecules, cell-to-cell communication in cerebral endothelial cells, as well as with endothelial cell death and the loss of structural and functional integrity of the blood-brain barrier.