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Our missions

We aim to protect the human dignity of aged people and their families by establishing presymptomatic diagnosis and preventive medicine against Alzheimer’s disease. We will also make the presenile Alzheimer’s disease preventable.

We will contribute to keeping the social security mechanisms sustainable. We will fight tax increases, which will be caused by the drastic aging of human populations in coming years.

1. Board Members and Wako Office

2. Our strategies

3. Next-generation mouse models of Alzheimer’s disease

4. List of some top scientists using our model mice

5. A cautionary note on Alzheimer immunotherapy

6. Market size of Alzheimer’s disease medications

7. To potential partners and collaborators:

8. 10 of the major publications since 2000

  1. Iwata, N., Tsubuki, S., Takaki, Y., Watanabe, K., Sekiguchi, M., Hosoki, E., Kawashima-Morishima, M., Lee, H.-.J., Hama, E., Sekine-Aizawa, Y., Saido, T.C. (2000). Identification of the major Aβ1-42-degrading catabolic pathway in brain parenchyma: Suppression leads to biochemical and pathological deposition. Nature Med., 6, 143-151.
  2. Iwata, N., Tsubuki, S., Takaki, Y., Shirotani, K., Lu, B., Gerard, N.P., Gerard, C., Hama, E., Lee, H.-J., Saido, T.C. (2001). Metabolic regulation of brain Aβ by neprilysin. Science, 292, 1550-1552.
  3. Saito, T., Takaki, Y., Iwata, N., Trojanowski, J., Saido T.C. (2003). Perspectives: Alzheimer’s disease, neuropeptides, neuropeptidase, and amyloid-β peptide metabolism. Science (SAGE-KE), http:// sageke.sciencemag.org/cgi/content/full/sageke; 2003/3/pe1. [2003(3) : PE1].
  4. Tsubuki, S., Takaki, Y., Saido, T.C. (2003). Dutch, Flemish, Italian, and Arctic mutations of APP and resistance of Aβ to physiologically relevant proteolytic degradation. Lancet, 361, 1957-1958.
  5. Iwata, N., Mizukami, H., Shirotani, K., Takaki, Y., Muramatsu, S., Gerard, N., Gerard, C., Ozawa, K., Saido, T.C. (2004). Presynaptic localization of neprilysin contributes to efficient clearance of amyloid β peptide in mouse brain. J. Neurosci., 24, 991-998.
  6. Saito, T., Iwata, N., Tsubuki, S., Takaki, Y., Takano, J., Huang, S.-H., Suemoto, T., Higuchi, M., Saido, T.C. (2005). Somatostatin regulates brain amyloid b peptide, Aβ42, through modulation of proteolytic degradation. Nature Med., 11, 434-439.
  7. Higuchi, M., Iwata, N., Matsuba, Y., Sato, K., Sasamoto, K., Saido T.C. (2005). 19F- and 1H-MRI detection of amyloid-β peptide in vivo. Nature Neurosci., 8, 527-533.
  8. Saito, T., Suemoto, T., Brouwers, N., Sleegers, K., Funamoto, S., Mihira, M., Matsuba, Y., Yamada, K., Nilsson, P., Takano, J., Nishimura, M., Iwata, N., Van Broeckhoven, C., Ihara, Y., Saido, T.C. (2011) Potent amyloidogenicity and pathogenicity of Aβ43. Nature Neurosci.,14, 1023-1032.
  9. Nilsson, P., Loganathan, K., Sekiguchi, M., Matsuba, Y., Hui, K., Tsubuki, S., Tanaka, M., Iwata, N., Saito, T., Saido, T.C. (2013) Aβ secretion and plaque formation depend on autophagy. Cell Reports, 5(19), 61-69, doi: 10.1016/j.celrep.2013.08.042.
  10. Saito, T., Matsuba, Y., Mihira, N., Takano, J., Nilsson, P., Itohara, S., Iwata, N., Saido, T.C. (2014) Single App knock-in mouse models of Alzheimer’s disease. Nat. Neurosci., 17, 661-663.