Ihara Team

The present work is undertaken to enhance our understanding of the pathogenesis of Alzheimer�fs disease. Regarding anti-amyloid therapy, we seek to develop �g substrate-specific drug�h, in which cleavage of APP (?CTF) alone would be suppressed, whereas the cleavage of other substrates is not interfered with thus bringing few adverse effects. We also seek to clarify the role of A? oligomer by characterizing the new APP mutation found in Japan, which is ready to form A? oligomer but not fibrils. Finally, we test our hypothesis that unbalanced expression of tubulin and tau leads to tauopathy, and aim at exploring anti-tau therapeutics.