BCL-2 AND BAX PROTEIN EXPRESSION IN ALZHEIMERS-DISEASE

Citation
A. Tortosa et al., BCL-2 AND BAX PROTEIN EXPRESSION IN ALZHEIMERS-DISEASE, Acta Neuropathologica, 95(4), 1998, pp. 407-412
Citations number
32
Categorie Soggetti
Neurosciences,"Clinical Neurology",Pathology
Journal title
ISSN journal
00016322
Volume
95
Issue
4
Year of publication
1998
Pages
407 - 412
Database
ISI
SICI code
0001-6322(1998)95:4<407:BABPEI>2.0.ZU;2-Q
Abstract
beta-Amyloid deposition and neurofibrillary degeneration are important pathological findings in the brains of patients with Alzheimer's dise ase (AD). In the present study, we have examined Bcl-2 and Bax immunor eactivity in the hippocampus of AD cases, with special attention to th e possible relationship between Bcl-2 and Bax immunoreactivity, and ne urofibrillary degeneration and senile plaques. Different antibodies we re 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 hom ogenates. No differences between Bcl-2 and Bax immunoreactivity in tan gle-bearing and non-tangle-bearing neurons were observed, thus suggest ing that Bcl-2 and Bax do not participate in tangle formation. Overexp ression of Bcl-2 protein in reactive glial cells surrounding senile pl aques suggests that Bcl-2 may play a role in the survival of reactive glia. On the other hand, overexpression of Bax immunoreactivity in dys trophic neurites of senile plaques suggests that Bax is associated wit h neurite degeneration in senile plaques. Finally, Bax (P-19), but not Bax (N-20), immunoreactivity was localized in amyloid fibrils of seni le plaques. Since Western blots to Bax (P-19) recognize multiple bands in addition to the expected band of about 21 kDa, it is suggested tha t Bax (P-19) immunoreactivity of amyloid fibrils is not specific.