Immunoreactivity for Bcl-2 protein within neurons in the Alzheimer's disease brain increases with disease severity.
Brain Res
; 697(1-2): 35-43, 1995 Oct 30.
Article
en En
| MEDLINE
| ID: mdl-8593592
ABSTRACT
Bcl-2 protein has been suggested to be one of the proteins preventing apoptosis in a variety of cell types. Recently, apoptosis has been suggested to have an important role in the pathogenesis of Alzheimer's disease (AD). We have utilized Bcl-2 immunohistochemical methods to examine Bcl-2 in the hippocampus and entorhinal cortex of AD patients ranging in clinical and neuropathological severity from mild to severe and compared these results to those obtained from age-matched controls. Immunoreactivity for Bcl-2 was predominantly found within neurons. Bcl-2 immunostaining within AD tissue was increased relative to controls in most neurons of the entorhinal cortex, subiculum, CA1, CA2, CA3, hilus and dentate gyrus. Relative Bcl-2 staining increased in parallel with increasing disease severity. However, neurons exhibiting immunoreactivity for markers of neurofibrillary tangle formation (AT8 and PHF-1) showed reduced Bcl-2 staining, suggesting that Bcl-2 may be down regulated in these degenerating neurons. Bcl-2 immunoreactivity within astrocytes and the vasculature was also increased in AD. These results suggest that Bcl-2 protein may have a role in compensation responses to AD pathology, perhaps affording to the remaining neurons a margin of protection from apoptosis.
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Bases de datos:
MEDLINE
Asunto principal:
Encéfalo
/
Proteínas Proto-Oncogénicas
/
Enfermedad de Alzheimer
/
Neuronas
Límite:
Aged
/
Aged80
/
Humans
Idioma:
En
Revista:
Brain Res
Año:
1995
Tipo del documento:
Article
País de afiliación:
Estados Unidos