bcl2, bax and nestin in the brains of patients with neurodegeneration and those of normal aging
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This study was conducted by employing specimens from the frontal cortices of Alzheimer, multiple-infarct dementia patients, and those of normal aging (age matched to patients). The objective was to evaluate and compare the bcl2, bax, and nestin patterns in these three groups. Using immunocytochemistry, it was observed that bcl2 and bax active sites were colocalized in 45% of cells in Alzheimer, 52% of cells in multiple infarct, and 30% of cells in normal aging. bcl2 and bax could also be separately located in cells of all three groups. bax cells were most prominent in number in Alzheimer patients and least prominent in normal aging. nestin was found in all three groups but was most prominent in the multiple-infarct patients. Both astrocytes and neurons demonstrated positive nestin sites. The difference in pattern between groups will lead to further understanding of cellular changes in neurodegenerative patients and those of normal aging.
Index EntriesAging Alzheimer multiple infarct bcl2 bax nestin frontal cortex
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- Carrio R., Lopez-Hoyos M., Jimeno J., Benedict M. A., Merino R., Benito A., Fernandez-Luna J. L., et al. (1996) A1 demonstrates restricted tissue distribution during embryonic development and functions to protect against cell death. Am. J. Pathol. 149, 2133–2142.Google Scholar
- D’Sa-Eipper C., Leonard J. R., Putcha G., Zheng T. S., Flavell R. A., Rakic P., et al. (2001) DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3. Development 28, 137–146.Google Scholar
- Liu D., Lu C., Wan R., Auyeung W. W., and Mattson M. P. (2002) Activation of mitochondrial ATP-dependent potassium channels protects neurons against ischemia-induced death by a mechanism involving suppression of Bax translocation and cytochrome c release. J. Cereb. Blood Flow Metab. 22, 431–443.PubMedCrossRefGoogle Scholar
- Tanaka T., Hanafusa N., Ingelfinger J. R., Ohse T., Fujita T., and Nangaku M. (2003) Hypoxia induces apoptosis in SV40-immortalized rat proximal tubular cells through the mitochondrial pathways, devoid of HIF1-mediated upregulation of Bax. Biochem. Biophys. Res. Commun. 309, 222–231.PubMedCrossRefGoogle Scholar