Evidence that beta-amyloid protein in Alzheimer's disease is not derived by normal processing.
Science
; 248(4954): 492-5, 1990 Apr 27.
Article
en En
| MEDLINE
| ID: mdl-1691865
ABSTRACT
The beta-amyloid protein (beta/A4), derived from a larger amyloid precursor protein (APP), is the principal component of senile plaques in Alzheimer's disease. APP is an integral membrane glycoprotein and is secreted as a carboxyl-terminal truncated molecule. APP cleavage, which is a membrane-associated event, occurred at a site located within the beta/A4 region. This suggests that an intact amyloidogenic beta/A4 fragment is not generated during normal APP catabolism. Therefore, an early event in amyloid formation may involve altered APP processing that results in the release and subsequent deposition of intact beta/A4.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Precursores de Proteínas
/
Procesamiento Proteico-Postraduccional
/
Enfermedad de Alzheimer
/
Amiloide
Límite:
Aged
/
Animals
/
Humans
Idioma:
En
Revista:
Science
Año:
1990
Tipo del documento:
Article