Inflammatory responses to amyloidosis in a transgenic mouse model of Alzheimer's disease.

@article{Matsuoka2001InflammatoryRT,
  title={Inflammatory responses to amyloidosis in a transgenic mouse model of Alzheimer's disease.},
  author={Yasuji Matsuoka and M V Picciano and Brian Malester and John J Lafrancois and Cindy Zehr and J M Daeschner and John A. Olschowka and Maria Isabel Fonseca and M Kerry O'Banion and Andrea Joan Tenner and Cynthia A Lemere and Karen E Duff},
  journal={The American journal of pathology},
  year={2001},
  volume={158 4},
  pages={1345-54}
}
Mutations in the amyloid precursor protein (APP) and presenilin-1 and -2 genes (PS-1, -2) cause Alzheimer's disease (AD). Mice carrying both mutant genes (PS/APP) develop AD-like deposits composed of beta-amyloid (Abeta) at an early age. In this study, we have examined how Abeta deposition is associated with immune responses. Both fibrillar and nonfibrillar Abeta (diffuse) deposits were visible in the frontal cortex by 3 months, and the amyloid load increased dramatically with age. The number… CONTINUE READING