P2‐077: HIPSC‐DERIVED CORTICAL NEURON HUMAN‐ON‐A‐CHIP SYSTEM TO STUDY Aβ‐ AND TAU‐INDUCED NEUROTOXICITIES IN ALZHEIMER'S DISEASE WITH AN IMPLICATION FOR DRUG DISCOVERY

tests (EPM, MWM), followed by sacrifice and estimation of amyloid beta, hyperphosphorylated tau, Bax and Bcl2. P 0.05 was considered significant. Results: In Neurobehavioral parameter, disease control group showed significant (p 0.05) increase in transfer latency as compared to sham. Metformin treatment significantly reduced the transfer latency as compared to disease control in both the behavioral tests. In disease control model, level of Ab(142) and hyperphosphorylated tau in brain was significantly higher as compared to sham.Treatment with metformin and memantine significantly reduced the Ab(1-42) and hyperphosphorylated tau level in brain as compared to the disease control group. Bax expression was higher and Bcl-2 expression was lower in disease control as compared to sham. Treatment with metformin decreased Bax expression and increased the Bcl-2 expression as compared to disease control. No significant effect on blood glucose level was observed post ICV injection of streptozotocin and even after the treatment with metformin. No significant difference was observed between the metformin and memantine groups. Conclusions: In Present study therapeutic metformin has shown favorable effect on memory and reduced the level of neurotoxic amyloid beta, hyperphosphorylated tau, apoptotic protein Bax and increased the anti-apoptotic Bcl-2 level in streptozotocin induced model of Alzheimer’s disease.