Education

Biography

Dr. Masashi Asai is currently an Assistant Professor in the Department of Genome-based Drug Discovery, Graduate School of Biomedical Sciences, Nagasaki University. His Ph.D. thesis was approved by the Tokyo University of Science (Chiba, Japan) in 2006. He was an Assistant Professor at the Department of Pharmacology, Faculty of Medicine, Saitama Medical University, before joining Nagasaki University in 2012. He has been engaged in basic research and drug development for Alzheimer’s disease, and his current research projects focus on Alzheimer’s disease in people with Down syndrome.

Research Interest

• Alzheimer’s disease
• Down syndrome
• Amyloid-β peptide
• Amyloid precursor protein
• ADAM
• BACE
• Cathepsin
• Neprilysin
• DYRK1A
• RCAN1
• Protease inhibitors
• Kinase inhibitors
• NFAT
• Tau
• Calcineurin-NFAT signaling
• 21 chromosome

Scientific Activities

Awards

• The Encouragement Award for the best poster presentation in the 9th Conference on Proteases and Inhibitors in Patho-physiology and Therapeutics (2006)

Publications

1. Shirotani K*, Asai M, Iwata N. Paradigm shift from diagnosing patients based on common symptoms to categorizing patients into subtypes with different pathogenic mechanisms to guide treatment for Alzheimer’s disease. J Biochem. 2017;161(6):463-470.doi: 10.1093/jb/mvx015.
2. Kawakubo T, Mori R, Shirotani K, Iwata N*, Asai M*. Neprilysin is suppressed by dual-specificity tyrosine-phosphorylation regulated kinase 1A (DYRK1A) in Down-syndrome-derived fibroblasts. Biol Pharm Bull. 2017;40(3):327-333.doi: 10.1248/bpb.b16-00825.
3. Asai M*, Kinjo A, Kimura S, Mori R, Kawakubo T, Shirotani K, Yagishita S, Maruyama K, Iwata N*. Perturbed calcineurin-NFAT signaling is associated with the development of Alzheimer’s disease. Biol Pharm Bull. 2016;39(10):1646-1652.doi: 10.1248/bpb.b16-00350
4. Jiang H, Cheng XW*, Shi GP, Hu L, Inoue A, Yamamura Y, Wu H, Takeshita K, Li X, Huang Z, Song H, Asai M, Hao CN, Unno K, Koike T, Oshida Y, Okumura K, Murohara T, Kuzuya M. Cathepsin K-mediated Notch1 activation contributes to neovascularization in response to hypoxia. Nat Commun. 2014;5:3838.doi: 10.1038/ncomms4838.
5. Iwata N*, Sekiguchi M, Hattori Y, Takahashi A, Asai M, Ji B, Higuchi M, Staufenbiel M, Muramatsu S, Saido TC*. Global brain delivery of neprilysin gene by intravascular administration of AAV vector in mice. Sci Rep. 2013;3:1472.doi: 10.1038/srep01472.
6. Kondo T, Asai M, Tsukita K, Kutoku Y, Ohsawa Y, Sunada Y, Imamura K, Egawa N, Yahata N, Okita K, Takahashi K, Asaka I, Aoi T, Watanabe A, Watanabe K, Kadoya C, Nakano R, Watanabe D, Maruyama K, Hori O, Hibino S, Choshi T, Nakahata T, Hioki H, Kaneko T, Naitoh M, Yoshikawa K, Yamawaki S, Suzuki S, Hata R, Ueno S, Seki T, Kobayashi K, Toda T, Murakami K, Irie K, Klein WL, Mori H, Asada T, Takahashi R, Iwata N*, Yamanaka S, Inoue H*. Modeling Alzheimer’s disease with iPSCs reveals stress phenotypes associated with intracellular Aβ and differential drug responsiveness. Cell Stem Cell. 2013;12(4):487-496.doi: 10.1016/j.stem.2013.01.009.
7. Yahata N, Asai M, Kitaoka S, Takahashi K, Asaka I, Hioki H, Kaneko T, Maruyama K, Saido TC, Nakahata T, Asada T, Yamanaka S, Iwata N*, Inoue H*. Anti-Aβ drug screening platform using human iPS cell-derived neurons for the treatment of Alzheimer’s disease. PLoS One. 2011;6(9):e25788.doi: 10.1371/journal.pone.0025788.
8. Asai M*, Yagishita S, Iwata N, Saido TC, Ishiura S, Maruyama K. An alternative metabolic pathway of amyloid precursor protein C-terminal fragments viacathepsin B in a human neuroglioma model. FASEB J. 2011;25(10):3720-3730.doi: 10.1096/fj.11-182154.
9. Asai M*, Iwata N, Tomita T, Iwatsubo T, Ishiura S, Saido TC, Maruyama K. Efficient four-drug cocktail therapy targeting amyloid-β peptide for Alzheimer’s disease. J Neurosci Res. 2010;88(16):3588-3597.doi: 10.1002/jnr.22503.
10. Tanabe C, Ebina M, Asai M, Futai E, Sasagawa N, Katano K, Fukami H, Ishiura S*. 1,3-Capryloyl-2-arachidonoyl glycerol activates alpha-secretase activity and suppresses Abeta40 secretion in A172 cells. Neurosci Lett. 2009;450(3):324-326.doi: 10.1016/j.neulet.2008.
11. Asai M*, Iwata N, Yoshikawa A, Aizaki Y, Ishiura S, Saido TC, Maruyama K*. Berberine alters the processing of Alzheimer’s amyloid precursor protein to decrease Aβ secretion. BiochemBiophys Res Commun. 2007;352(2):498-502.doi: 10.1016/j.bbrc.2006.11.043.
12. Hattori C, Asai M, Onishi H, Sasagawa N, Hashimoto Y, Saido TC, Maruyama K, Mizutani S, Ishiura S*. BACE1 interacts with lipid raft proteins. J Neurosci Res. 2006;84(4):912-927.doi: 10.1002/jnr.20981.
13. Asai M, Hattori C, Iwata N, Saido TC, Sasagawa N, Szabó B, Hashimoto Y, Maruyama K, Tanuma S, Kiso Y, Ishiura S*. The novel β-secretase inhibitor KMI-429 reduces amyloid β peptide production in amyloid precursor protein transgenic and wild-type mice. J Neurochem. 2006;96(2):533-540. doi: 10.1111/j.1471-4159.2005.03576.x.
14. Kimura T, Shuto D, Kasai S, Liu P, Hidaka K, Hamada T, Hayashi Y, Hattori C, Asai M, Kitazume S, Saido TC, Ishiura S, Kiso Y*. KMI-358 and KMI-370, highly potent and small-sized BACE1 inhibitors containing phenylnorstatine. Bioorg Med Chem Lett. 2004;14(6):1527-1531.doi: 10.1016/j.bmcl.2003.12.088.
15. Asai M, Hattori C, Szabó B, Sasagawa N, Maruyama K, Tanuma S, Ishiura S*. Putative function of ADAM9, ADAM10, and ADAM17 as APP α-secretase. BiochemBiophys Res Commun. 2003;301(1):231-235.doi: 10.1016/S0006-291X(02)02999-6.
16. Hattori C, Asai M, Oma Y, Kino Y, Sasagawa N, Saido TC, Maruyama K, Ishiura S*. BACE1 interacts with nicastrin. BiochemBiophys Res Commun. 2002;293(4):1228-1232.doi: 10.1016/S0006-291X(02)00351-0.
17. Ishiura S*,Hotoda N, Szabó B, Asai M, Hattori C, Tanaka E, Koike H, Sasagawa N.Alzheimer amyloid α-secretase: aspecial target for drug development. Psychogeriatrics,2001;1(4):273-276.doi: 10.1111/j.1479-8301.2001.tb00016.x.