Programmed cell death (apoptosis) in Alzheimer's disease and Creutzfeldt-Jakob disease.
The aim of our study was the estimation of the apoptosis process using in situ-end labelling of DNA breaks method on paraffin sections in 5 human cases of Alzheimer's disease (AD), 6 of Creutzfeldt-Jakob disease (CJD) and in 25 mice infected experimentally with the Fujisaki strain of CJD, killed sequentially at one-week intervals. The numbers of apoptotic cells in CJD-infected mice in the later stages of the disease and in terminally ill mice were progressively higher that at the early stage of the disease. Further, we found a correlation between the intensity of apoptosis and major lesions hallmark of disease--the intensity of spongiform changes in the cerebral cortex but not in the accumulation of PrP in CJD infected mice. The number of A beta-amyloid plaques in AD was not related to apoptotic index. Our study showed that apoptosis is a very important event in these neurodegenerative diseases and may become a basic mechanism in loss of neurons.
Jesionek-Kupnicka
D
D
Laboratory of Tumor Biology, School of Medicine, Lódź.
Buczyński
J
J
Kordek
R
R
Sobów
T
T
Kłoszewska
I
I
Papierz
W
W
Liberski
P P
PP
D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000032:analysis; D000818:Animals; D017209:Apoptosis; D001921:Brain / Q000473:pathology*; D001923:Brain Chemistry; D007562:Creutzfeldt-Jakob Syndrome / Q000378:metabolism / Q000473:pathology*; D053938:DNA Fragmentation; D006801:Humans; D020287:In Situ Nick-End Labeling; D051379:Mice; D009419:Nerve Tissue Proteins / Q000032:analysis; D018621:PrPC Proteins / Q000032:analysis
D016229:Amyloid beta-Peptides; D009419:Nerve Tissue Proteins; D018621:PrPC Proteins