In our experience, intracerebroventricular injection of STZ does induce tau phosphorylation at multiple sites. We inject STZ (150 μg/μl) to male Wistar rats at 3 months of age (BW: 350-450 g) to induce AD-like tau pathology. The STZ solution needs to be freshly prepared every time immediately before the injection by dissolved STZ (Sigma-Aldrich) in 100 mM of citrate buffer (pH 4.5). Injection 3 μl of such STZ solution to the cerebral ventricle does not cause death. Hyperphosphorylation of tau can be detected in the hippocampus two weeks after the STZ injection. Please also see http://www.ncbi.nlm.nih.gov/pubmed/16412093.

Let me give you some advices. Please, have a look below:

http://www.actaneurocomms.org/content/2/1/61

Chen Z., Zhong C. Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. Prog. Neurobiol. 2013. Vol. 108. P. 21-43. doi: 10.1016/j.pneurobio.2013.06.004.

Chen Y. et al. A non-transgenic mouse model (icv-STZ mouse) of Alzheimer's disease: similarities to and differences from the transgenic model (3xTg-AD mouse). Mol. Neurobiol. 201. Vo. 47, No 2. P.711-725. doi: 10.1007/s12035-012-8375-5.

Li Y., et al. GLP-1 receptor stimulation reduces amyloid-beta peptide accumulation and cytotoxicity in cellular and animal models of Alzheimer's disease. J. Alzheimers Dis. 2010. Vol. 19, No 4. P. 1205-1219. doi: 10.3233/JAD-2010-1314.

thank you sirs, i found the materials useful but the question now is what is the mechanism of action of icv-STZ in the brain to cause AD-like pathologies

If you can go through one of the earlier papers below;

Lannert H, Hoyer S (1998) Intracerebroventricular administration of streptozotocin

causes long-term diminutions in learning and memory abilities and in

cerebral energy metabolism in adult rats. Behav Neurosci 112: 1199–1208