Transport of human beta-amyloid peptide through the rat blood-brain barrier after global cerebral ischemia.
In an attempt to produce an animal model of the Alzheimer's disease (AD), beta-amyloid-(1-42)-peptide (beta A1-42) was injected into the femoral vein in rats after single and repeated cardiac arrest (CA). After survival of 3.5 months, the brains immunoreactivity was evaluated using light microscopic immunocytochemistry of monoclonal beta-amyloid peptide (beta A) antibody 4G8 (mAb 4G8). Rats receiving beta A1-42 after CA demonstrated multifocal and widespread extravasation of beta A1-42 in extra- and intracellular space. The permeability to beta A1-42 was significantly higher in rats after repeated cerebral ischemia. As in AD, there were irregular diffuse amyloid plaque-like deposits and neuronal loss with reactive gliosis. Our data in ischemic rats with beta A1-42 represent a novel animal model of Alzheimer's pathology.
Pluta
R
R
Department of Neuropathology, Polish Academy of Sciences, Warsaw, Poland.
Misicka
A
A
Januszewski
S
S
Barcikowska
M
M
Lipkowski
A W
AW
D016229:Amyloid beta-Peptides / Q000493:pharmacokinetics*; D000818:Animals; D001812:Blood-Brain Barrier / Q000502:physiology*; D002545:Brain Ischemia / Q000378:metabolism*; D004195:Disease Models, Animal; D005119:Extravasation of Diagnostic and Therapeutic Materials; D006801:Humans; D010446:Peptide Fragments / Q000493:pharmacokinetics*; D051381:Rats; D017208:Rats, Wistar
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42)