| First Author | Harigaya Y | Year | 2006 |
| Journal | Neurosci Lett | Volume | 395 |
| Issue | 1 | Pages | 37-41 |
| PubMed ID | 16298484 | Mgi Jnum | J:107972 |
| Mgi Id | MGI:3622607 | Doi | 10.1016/j.neulet.2005.10.087 |
| Citation | Harigaya Y, et al. (2006) Type-specific evolution of amyloid plaque and angiopathy in APPsw mice. Neurosci Lett 395(1):37-41 |
| abstractText | To clarify how Abeta deposits start in the brain, we examined the early to late stages of senile plaques and amyloid angiopathy in APPsw mice. All types of human senile plaques were observed in the mouse brains. The premature forms of cored plaques appeared first in the cerebral cortex of mice at 7-8 months old. Then, amyloid angiopathy emerged, followed by diffuse plaques consisting of Abeta1-42. Modifications of the N-terminus of Abeta were late phase phenomena. The premature forms of cored plaques were composed of central Abeta1-40 amyloid cores, surrounding amorphous Abeta1-42 deposits, and accumulation of Abeta1-42 in some peripheral cells. These cells were incorporated in amyloid cores, and these plaques developed to large cored plaques composed of Abeta1-40 and Abeta1-42. The size and number of cored plaques were increased with age. These findings indicate different evolution paths for cored plaques and diffuse plaques, and suggest the presence of a pathway that initiates with the intracellular accumulation of Abeta1-42 and leads to the development of classic plaques in human brain tissues. |
