Glial expression of the beta-amyloid peptide in cardiac arrest.
We have investigated in the rat, immunocytochemically, the expression of beta-amyloid peptide in glial cells following ischemia-reperfusion brain injury. The postischemic brain injuries were studied at survival times from 2 days to 12 months. The reactive astrocytes with indirect staining for beta-amyloid peptide were observed in brain till 7 days postischemia. beta-Amyloid positive astrocytes disappeared transiently on the 14 days and then reappeared in the 6 months and again disappeared at 9 months after brain injury. Transient ischemia temporarily induced beta-amyloid peptide expression in reactive astrocytes, but this expression peaked at 7 days and 6 months. A glial appearance of beta-amyloid peptide direct staining occurred at a time when extensive neuronal loss was evident.
Pluta
Ryszard
R
Department of Neuropathology, Medical Research Centre, Polish Academy of Sciences, Pawińskiego 5 Str., 02-106 Warsaw, Poland. pluta@medres.cmdik.pan.pl
D016229:Amyloid beta-Peptides / Q000096:biosynthesis*; D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D048429:Cell Size; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006323:Heart Arrest / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D009457:Neuroglia / Q000378:metabolism* / Q000473:pathology; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D009836:Oligodendroglia / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology; D013534:Survival
D016229:Amyloid beta-Peptides; D005904:Glial Fibrillary Acidic Protein