Pro-apoptotic protein Bax and anti-apoptotic protein Bcl-2 expression in streptozotocin model of Alzheimer's disease

It was demonstrated that neuronal insulin receptor is dysfunctional in Alzheimer's disease. Experimental intracerebroventricular (ICV) administration of streptozotocin (STZ) causes insulin receptor signaling perturbation within the brain. This condition has been designated as cerebral diabetes and has been regarded as probable model of Alzheimer's disease (AD). As it is stil unclear whether apoptotis is present in AD or not and whether the expression of pro-apoptotic and anti-apoptotic markers is changed in AD, we used STZ model of AD to ass the relationship between pro-apoptotic and anti-apoptotic proteins in AD. The objective of this study was to determine if ICV administration of STZ might induce apoptotic cascade activation. Methods: Animals were divided into 2 groups (five per group) and treated ICV either by STZ (1 mg/kg) or vehicle (control). Immunohistochemistry was performed 3 months after the treatment. Temporal gyrus tissue samples were used. Anti-Bax polyclonal aantibody (Santa Cruz) and anti-Bcl-2 polyclonal aantibody (DAKO) were used. Staining was measured semiquantitatively as the percentage of immunopositive cells and intensity of staining. Results: In temporal gyrus of STZ-treated rats percentage of Bax-positive neurons as well as the intensity of its staining were significantly increased in comparison to the control. There was no difference in Bcl-2 expression between the two groups of animals. Conclusion: Results of this study indicate that, in STZ model of AD, ICV administration of STZ might induce activation of apoptotic cascade through over-expression of pro-apoptotic factor Bax.