Angiogenesis has been suggested as a direct contributor to Alzheimer's disease (AD) pathology. The major pathological hallmarks of AD are the presence of neurofibrillary tangles and, β-amyloid plaques associated with activated microglia, astrocytes, degenerating neurons and vascular toxicity. In this study, Aβ1-40 and Aβ1-42 peptides, both components of the senile plaques in AD, were used to study their angiogenic activity in vitro, by using normal human cerebral endothelial cells (HCECs), and in vivo, by using the chick embryo chorioallantoic membrane (CAM) assay. Results showed that both peptides stimulate in vitro endothelial cell proliferation, chemotaxis and morphogenesis in Matrigel. Moreover, by using the aorta ring assay, both peptides stimulated the formation of capillary-like structures. An angiogenic response was induced in the CAM assay, similar to that induced by fibroblast growth factor-2 (FGF-2), a well-known angiogenic cytokine. Overall, these data support the hypothesis that Aβ peptides may contribute to angiogenesis occurring in AD and suggest that limiting the pro-angiogenic activity of Aβ peptides may therefore provide a useful target to control angiogenesis associated to AD and therefore limit the disease progression.
|Number of pages||7|
|Journal||International Journal of Molecular Medicine|
|Publication status||Published - Apr 2007|
- Alzheimer's disease
- Beta amyloid
ASJC Scopus subject areas