Neuronal apoptosis in XXXX .

@entity1 @entity32 @entity3605 @entity1579 @entity3669 @entity21 @entity528
@entity528 is a salient feature of @entity1579 ; however, its causes and mechanisms are unclear The possibility that it could occur through an apoptotic process has been postulated and is consistent with the lack of @entity32 in prion disorders as supported by experimental studies. In order to test this hypothesis in @entity1 , we examined samples of frontal and temporal cerebral cortex, striatum, thalamus, and cerebellum from 16 @entity1 who died from @entity3605 . They included 5 sporadic cases, 5 familial, 3 iatrogenic, and 3 cases with the new variant. These were compared with age and sex matched controls. Using in situ end labelling, we identified apoptotic neurons in all the cases of @entity3605 . A single labelled neuron was found in the eldest control. Apoptotic neurons were mostly found in damaged regions and their presence and abundance seemed to correlate closely with @entity528 . This supports the view that apoptosis of neurons is a feature of @entity1579 and may contribute to the @entity528 which is one of the main characteristics of these conditions. Neuronal apoptosis also correlated well with microglial activation, as demonstrated by the expression of major histocompatibility complex class II antigens, and @entity21 , as identified by beta-amyloid protein precursor immunostaining. In contrast, we found no obvious relationship between the topography and severity of neuronal apoptosis and the type, topography, and abundance of @entity3669 deposits as demonstrated by immunocytochemistry.
