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.