The method of in situ end-labeling of nuclear DNA fragmentation was used in the study of ten @entity1 (two biopsies, eight autopsies) with @entity13895 ( @entity3605 ). All the @entity1 had the typical morphological lesions including @entity528 , @entity7495 and @entity5219 . Four of them also showed @entity3669 ( @entity3669 ) deposits in the cerebral cortex, and two of them kuru-like plaques in the cerebellum. A few cells with DNA breaks were found in the two biopsy cases; one of them, suffering from a panencephalopathic form of the disease, showed positive nuclei not only in the cerebral cortex but also in the subcortical white matter. Variable numbers of positive nuclei were observed in the gray and white matter in the eight autopsy cases, in which, although the distribution of positive cells roughly correlated with the distribution of @entity528 , no clear relationship was found as regards the distribution and degree of cell labeling and the degree of @entity528 . Furthermore, large numbers of positive cells were concentrated in a particular area, whereas a few cells were seen in a neighboring equally affected area. Positive glial cells in the plexiform layer of the @entity1399 area of the hippocampus, and in the frontal white matter were frequently encountered. Staining of the cytoplasm in a minority of cells was interpreted as the result of nuclear DNA leakage. None of the stained cells had the typical morphology of apoptosis; most particularly, peripheral chromatin condensation and formation of apoptotic bodies were not seen in any case. @entity3669 deposits did not result in an increase of nuclear DNA breaks either within the area or in adjacent regions. Although positive cells were also observed in autopsy cases of controls which were processed in the same way, positive labeling as a whole was higher in @entity3605 than in age-matched controls. These results show that brain nuclear DNA is vulnerable in @entity3605 , and suggest that increased DNA vulnerability has a role in cell death and @entity528 . Since nuclear shrinkage and positive nuclear staining with the method of in situ end-labeling of nuclear DNA fragmentation are not exclusive to apoptosis, further information is needed to categorize cell death in @entity3605 as apoptosis. Necrosis or other forms of cell death, as well as increased DNA vulnerability to agonal changes of the individuals, and to postmortem delay in the fixation of the tissues, may account for additional positive staining in cases examined at autopsy.

Nuclear DNA fragmentation in XXXX : does a mere positive in situ nuclear end-labeling indicate apoptosis?

@entity1 :: ('9606', 'Species') :: ['patients'] @entity1399 :: ('759', 'Gene') :: ['CA1'] @entity5219 :: ('MESH:D005911', 'Disease') :: ['astrocytosis'] @entity3605 :: ('MESH:D007562', 'Disease') :: ['CJD'] @entity7495 :: ('MESH:D017825', 'Disease') :: ['spongiform change'] @entity13895 :: ('MESH:C565143', 'Disease') :: ['sporadic Creutzfeldt-Jakob disease'] @entity3669 :: ('5621', 'Gene') :: ['prion protein', 'PrP'] @entity528 :: ('MESH:D009410', 'Disease') :: ['neuron loss']
@entity3605 :: (MESH:D007562,Disease) :: ['Creutzfeldt-Jakob disease']
