Vitamin E but not 17β-estradiol protects against vascular toxicity induced by β-amyloid wild type and the dutch amyloid variant
Author
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Muñoz, Francisco J.
Author
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Opazo, Carlos
Author
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Gil-Gómez, Gabriel
Author
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Tapia, Gladys
Author
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Fernández, Virginia
Author
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Valverde, Miguel A.
Author
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Inestrosa, Nibaldo C.
Admission date
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2019-01-29T17:51:53Z
Available date
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2019-01-29T17:51:53Z
Publication date
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2002
Cita de ítem
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Journal of Neuroscience, Volumen 22, Issue 8, 2018, Pages 3081-3089
Identifier
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02706474
Identifier
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https://repositorio.uchile.cl/handle/2250/163599
Abstract
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Amyloid β-peptide (Aβ) fibril deposition on cerebral vessels produces cerebral amyloid angiopathy that appears in the majority of Alzheimer's disease patients. An early onset of a cerebral amyloid angiopathy variant called hereditary cerebral hemorrhage with amyloidosis of the Dutch type is caused by a point mutation in Aβ yielding AβGlu22→Gln. The present study addresses the effect of amyloid fibrils from both wild-type and mutated Aβ on vascular cells, as well as the putative protective role of antioxidants on amyloid angiopathy. For this purpose, we studied the cytotoxicity induced by Aβ1-40 Glu22→Gln and Aβ1-40 wild-type fibrils on human venule endothelial cells and rat aorta smooth muscle cells. We observed that AβGlu22→Gln fibrils are more toxic for vascular cells than the wild-type fibrils. We also evaluated the cytotoxicity of Aβ fibrils bound with acetyl-cholinesterase (AChE), a common component of amyloid deposits. Aβ1-40 wild-type-AChE fibrillar complexes, similar to neurona