| Autor: |
Davis-Salinas J; Department of Microbiology and Molecular Genetics, University of California, Irvine 92717-4025, USA., Saporito-Irwin SM, Cotman CW, Van Nostrand WE |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of neurochemistry [J Neurochem] 1995 Aug; Vol. 65 (2), pp. 931-4. |
| DOI: |
10.1046/j.1471-4159.1995.65020931.x |
| Abstrakt: |
The progression of Alzheimer's disease and related disorders involves amyloid beta-protein (A beta) deposition and pathologic changes in the parenchyma as well as cerebral blood vessels. The cerebrovascular A beta deposits in these disorders are associated with degenerating smooth muscle cells in the vessel wall, which have been shown to express the A beta precursor (A beta PP) and A beta. Here, we show that A beta 1-42, an abundant cerebrovascular form of A beta, causes cellular degeneration in cultured human cerebrovascular smooth muscle cells. This stress response is accompanied by a striking increase in the levels of cellular A beta PP and soluble A beta peptide produced in these degenerating cells. These data provide the first experimental evidence that A beta can potentially contribute to the onset and progression of the cerebrovascular pathology. The present findings suggest that this mechanism may involve a molecular cascade with a novel product-precursor relationship that results in the adverse production and subsequent accumulation of A beta. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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