Interactions of laminin with the amyloid beta peptide. Implications for Alzheimer's disease.
Braz J Med Biol Res
; 34(5): 597-601, 2001 May.
Article
em En
| MEDLINE
| ID: mdl-11323745
Extensive neuronal cell loss is observed in Alzheimer's disease. Laminin immunoreactivity colocalizes with senile plaques, the characteristic extracellular histopathological lesions of Alzheimer brain, which consist of the amyloid beta (A(beta)) peptide polymerized into amyloid fibrils. These lesions have neurotoxic effects and have been proposed to be a main cause of neurodegeneration. In order to understand the pathological significance of the interaction between laminin and amyloid, we investigated the effect of laminin on amyloid structure and toxicity. We found that laminin interacts with the A(beta)1-40 peptide, blocking fibril formation and even inducing depolymerization of preformed fibrils. Protofilaments known to be intermediate species of A(beta) fibril formation were also detected as intermediate species of laminin-induced A(beta) fibril depolymerization. Moreover, laminin-amyloid interactions inhibited the toxic effects on rat primary hippocampal neurons. As a whole, our results indicate a putative anti-amyloidogenic role of laminin which may be of biological and therapeutic interest for controlling amyloidosis, such as those observed in cerebral angiopathy and Alzheimer's disease.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Laminina
/
Precursor de Proteína beta-Amiloide
/
Matriz Extracelular
/
Doença de Alzheimer
Limite:
Animals
/
Humans
Idioma:
En
Revista:
Braz J Med Biol Res
Ano de publicação:
2001
Tipo de documento:
Article
País de afiliação:
Chile
País de publicação:
Brasil