Japanese (日本語)

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.

Email: saidotc@wb4.so-net.ne.jp

The following are our major strategies. I believe a numbers of companies will save and make billions of dollars by working with us.
 

1. Licensing the next-generation mouse models of AD.
2. Clinical application of gene therapy to prevention of Alzheimer’s disease.
3. Medications for prevention of Alzheimer’s disease.
4. Plasma-based presymptomatic diagnosis of Alzheimer’s disease.
5. Consultation on Alzheimer’s disease research and development (with emphasis on the new mouse models).
6. Generation of non-human primate models of Alzheimer’s disease.

10 of the major publications since 2000

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.

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.

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].

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.

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.

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.

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.

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.

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.

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.