Bcl-2 and Bax protein expression in Alzheimer’s disease
- Cite this article as:
- Tortosa, A., López, E. & Ferrer, I. Acta Neuropathol (1998) 95: 407. doi:10.1007/s004010050817
- 150 Downloads
β-Amyloid deposition and neurofibrillary degeneration are important pathological findings in the brains of patients with Alzheimer’s disease (AD). In the present study, we have examined Bcl-2 and Bax immunoreactivity in the hippocampus of AD cases, with special attention to the possible relationship between Bcl-2 and Bax immunoreactivity, and neurofibrillary degeneration and senile plaques. Different antibodies were used, including Bcl-2 (N-19), Bcl-2 (BioGenex), Bax (P-19) and Bax (N-20), and their specificity was tested on Western blots of brain homogenates. No differences between Bcl-2 and Bax immunoreactivity in tangle-bearing and non-tangle-bearing neurons were observed, thus suggesting that Bcl-2 and Bax do not participate in tangle formation. Overexpression of Bcl-2 protein in reactive glial cells surrounding senile plaques suggests that Bcl-2 may play a role in the survival of reactive glia. On the other hand, overexpression of Bax immunoreactivity in dystrophic neurites of senile plaques suggests that Bax is associated with neurite degeneration in senile plaques. Finally, Bax (P-19), but not Bax (N-20), immunoreactivity was localized in amyloid fibrils of senile plaques. Since Western blots to Bax (P-19) recognize multiple bands in addition to the expected band of about 21 kDa, it is suggested that Bax (P-19) immunoreactivity of amyloid fibrils is not specific.