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1/4. apoptosis in leukoaraiosis.

    We report a case of leukoaraiosis that was studied for apoptosis. In the neuropil, the number of cells that showed dna fragmentation was 2.5 times as great in the area of leukoaraiosis as in the adjacent white matter (P = .004) and 25 times as great as in the nearby cortex (P < .001). Our findings suggest that apoptosis, predominantly of oligodendrocytes, is involved in the pathogenesis of leukoaraiosis. Within the area of leukoaraiosis, we also found numerous small veins that were partially occluded by severe collagenous thickening of the vessel walls. This collagenosis may have contributed to or resulted from chronic ischemia in that area.
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keywords = apoptosis
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2/4. Cerebrovascular pathology in Alzheimer's disease and leukoaraiosis.

    A high percentage of patients with Alzheimer's disease (AD) show evidence of white matter degeneration known as leukoaraiosis (LA), which is due to chronic ischemia. We found that the periventricular veins tend to become occluded by multiple layers of collagen in the vessel walls in the elderly. This collagen deposition is particularly excessive in LA lesions. Therefore, it is present in the brains of many AD patients, along with other ischemia-causing cerebrovascular pathology. We found evidence that there is severe loss of oligodendrocytes in LA, due to extensive apoptosis. No evidence of inflammation was found in the LA lesions. In thick celloidin sections of AD brain, we have obtained detailed 3D views of small (early) deposits of amyloid (stained with beta-amyloid antibody) around capillaries (stained with collagen IV antibody).
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keywords = apoptosis
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3/4. Delayed diffuse neurodegeneration after cerebral concussion.

    A 27-month-old girl developed severe diffuse neurological disability that was progressive between 2 weeks and 2 years after a closed head injury. After stabilization of her disability for 1 year, mild improvement in neurological function began in the third year after the concussion. Multiple imaging studies of the neural axis remained normal during a 5-year period after the initial injury. Delayed and diffuse trauma-induced neuronal apoptosis is a pathogenic mechanism that could explain this unusual neurodegenerative syndrome.
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keywords = apoptosis
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4/4. cathepsin d deficiency is associated with a human neurodegenerative disorder.

    cathepsin d is a ubiquitously expressed lysosomal protease that is involved in proteolytic degradation, cell invasion, and apoptosis. In mice and sheep, cathepsin d deficiency is known to cause a fatal neurodegenerative disease. Here, we report a novel disorder in a child with early blindness and progressive psychomotor disability. Two missense mutations in the CTSD gene, F229I and W383C, were identified and were found to cause markedly reduced proteolytic activity and a diminished amount of cathepsin d in patient fibroblasts. Expression of cathepsin d mutants in cathepsin d(-/-) mouse fibroblasts revealed disturbed posttranslational processing and intracellular targeting for W383C and diminished maximal enzyme velocity for F229I. The structural effects of cathepsin d mutants were estimated by computer modeling, which suggested larger structural alterations for W383C than for F229I. Our studies broaden the group of human neurodegenerative disorders and add new insight into the cellular functions of human cathepsin d.
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keywords = apoptosis
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