Amyloid beta-protein induces the cerebrovascular cellular pathology of Alzheimer's disease and related disorders
| Autor: | Susan M. Saporito-irwin, W E Van Nostrand, J Davis-Salinas |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Pathology
medicine.medical_specialty Cellular pathology Amyloid β Amyloid Peptide Disease Biology General Biochemistry Genetics and Molecular Biology Muscle Smooth Vascular Amyloid beta-Protein Precursor Meninges History and Philosophy of Science Smooth muscle Alzheimer Disease medicine Humans chemistry.chemical_classification Amyloid beta-Peptides General Neuroscience Models Cardiovascular Brain Cerebral Arteries medicine.disease Cerebral Veins Peptide Fragments Amino acid Cerebral Amyloid Angiopathy chemistry Solubility Nerve Degeneration Cerebral amyloid angiopathy |
| Zdroj: | Annals of the New York Academy of Sciences. 777 |
| ISSN: | 0077-8923 |
| Popis: | One of the hallmark pathologic characteristics of Alzheimer's disease (AD) and related disorders is deposition of the 39-42 amino acid amyloid beta-protein (A beta) in the walls of 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 implicated in the expression of the amyloid beta-protein precursor (A beta PP) and formation of A beta. We have established primary cultures of human cerebrovascular smooth muscle cells as a model for investigating the cellular pathologic processes involved in the cerebral amyloid angiopathy of AD and related disorders. Recently, we have shown that A beta 1-42, the predominant pathologic cerebrovascular form of A beta, causes extensive cellular degeneration that is accompanied by a striking increase in the levels of cellular A beta PP, potentially amyloidogenic carboxyl terminal A beta PP fragments, and soluble A beta peptide in the cultured human cerebrovascular smooth muscle cells. Together, these studies provide evidence that A beta contributes to the onset and progression of the cerebrovascular pathology associated with AD and related disorders and suggests the mechanism involves a molecular cascade with a novel product-precursor relationship that results in the adverse production and accumulation of A beta. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text