Neurofibrillary Tangles
Mostrando 1-12 de 117 artigos, teses e dissertações.
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1. Alzheimer's disease: is a vaccine possible?
The cause of Alzheimer's disease is still unknown, but the disease is distinctively characterized by the accumulation of β-amyloid plaques and neurofibrillary tangles in the brain. These features have become the primary focus of much of the research looking for new treatments for the disease, including immunotherapy and vaccines targeting β-amyloid in the
Braz J Med Biol Res. Publicado em: 2014-06
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2. Investigação do efeito neuroprotetor da atorvastatina em um modelo in vitro de toxicidade induzida pelo peptídeo ¿-amiloide
Alzheimer¿s disease is an age-related neurodegenerative disorder characterized by progressive memory loss, inability to perform the activities of daily living and personality changes. AD is characterized histopathologically by the presence of senile plaques, neurofibrillary tangles, synapse loss and neuronal death. Moreover, it is now recognized that neuroi
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 2012
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3. Estudos bioquímicos, funcionais e estruturais da septina humana SEPT2: fatores que determinam a formação de agregados / Functional and structural studies of human SEPT2: determinant factors triggering the sefl-assembly into amyloid fibrils
As septinas fazem parte de uma família de proteínas de ligação ao nucleotídeo guanina. As septinas têm mostrado ter um papel importante na citocinese e outros processos celulares, incluindo a determinação da polaridade celular e reorganização do citoesqueleto. Todos os membros da família de septinas são compostos por três domínios: um N-termina
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 26/10/2011
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4. Neuropsychological and neurobiological markers of the preclinical stage of Alzheimer's disease
Dementia, especially Alzheimer's disease, has a high prevalence in the elderly population. Therefore, identifying individuals who are at a high risk for early diagnosis is crucial to allow both pharmacological and behavioral therapeutic interventions, which in some cases can delay the progression of dementia. This paper describes neuropsychological and neuro
Psychology & Neuroscience. Publicado em: 2011
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5. Insights into Alzheimer disease pathogenesis from studies in transgenic animal models
Alzheimer disease is the most common cause of dementia among the elderly, accounting for ~60-70% of all cases of dementia. The neuropathological hallmarks of Alzheimer disease are senile plaques (mainly containing p-amyloid peptide derived from amyloid precursor protein) and neurofibrillary tangles (containing hyperphosphorylated Tau protein), along with neu
Clinics. Publicado em: 2011
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6. Glicogênio sintase quinase3B e proteína precursora do amilóide em plaquetas de indivíduos com comprometimento cognitivo leve e doença de Alzheimer / Glycogen synthase kinase 3B and amyloid precursor protein in adults platelets with cognitive impairment and Alzheimers disease
Alzheimers disease (AD) is a neurodegenerative disease characterized by progressive decline of memory and other cognitive functions, affecting mainly elderly. The abnormal metabolism of amyloid precursor protein (APP) and protein TAU hyperphosphorylation are cellular hallmarks of this disease. Glycogen synthase kinase 3B (GSK3B) is an enzyme highly expressed
Publicado em: 2010
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7. Alzheimer neurofibrillary tangles contain phosphorylated and hidden neurofilament epitopes.
Three monoclonal antibodies to neurofilaments (RT97, BF10 and 147), two of which also recognised neurofibrillary tangles (RT97 and BF10), have all been shown to be specific for phosphorylated epitopes. Treatment of histological sections with alkaline phosphatase prior to immunostaining resulted in reduction of axonal neurofilament staining with all three whi
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8. Neurofibrillary tangles of Alzheimer disease share antigenic determinants with the axonal microtubule-associated protein tau (tau)
The relationship of the neurofibrillary tangle, found in Alzheimer disease and aged brains, to normal or abnormal cytoskeletal proteins remains elusive. Although immunohistochemical studies have yielded disparate results, most antigenic determinants localized to neurofibrillary tangles are cytoskeletal constituents normally present in neuronal perikarya or d
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9. Diffuse neurofibrillary tangles with calcification: a new presenile dementia.
The term "diffuse neurofibrillary tangles with calcification" (DNTC) is proposed for a new form of presenile dementia. It is characterised by slowly progressive cortical dementia in the presenium, localised temporal or temporofrontal lobar atrophy, numerous neurofibrillary tangles widespread in the cerebral cortex, and pronounced calcareous deposits; 16 case
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10. Neurofibrillary tangles in dementia pugilistica are ubiquitinated.
Ubiquitin, a protein thought to be involved in the ATP-dependent non-lysosomal degradation of abnormal proteins, has already been identified as a component of neurofibrillary tangles in Alzheimer's disease. We have examined ubiquitin immunoreactivity in a unique collection of brains from 16 ex-boxers including 11 with dementia pugilistica. Neurofibrillary ta
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11. Recognition of Alzheimer paired helical filaments by monoclonal neurofilament antibodies is due to crossreaction with tau protein.
Neurofibrillary tangles and senile plaques are the principal pathological features of Alzheimer disease. Neurofibrillary tangles and the neurites of senile plaques contain paired helical filaments (PHF) that consist of two 10-nm filaments twisted into a double helix. The precursor proteins of PHF are not fully known. To identify these precursors, numerous im
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12. A quantitative study of the neurofibrillary tangles and the choline acetyltransferase activity in the cerebral cortex and the amygdala in Alzheimer's disease.
A quantitative study has been made of the number of neurofibrillary tangles and of the choline acetyltransferase activity in several sites in the cerebral hemispheres of eight patients who had had Alzheimer's disease. The neurofibrillary tangles were maximal in structures in the medial temporal lobe (uncus, amygdala, hippocampus and parahippocampal gyrus), s