ホーム > 認知症先進医療開発センター > English Pages > Department & Laboratories > Laboratory of Animal Models of Aging

Laboratory of Animal Models of Aging (Tsuda Lab)

Introduction

Alzheimer’s disease (AD) is a neuronal disorder with learning and memory defects as well as neuronal degenerations. Although many of approaches have been tried to identify the therapeutic drugs against this disease, there is currently no effective drug for the disorder. This therapeutic void reflects lack of ideal mouse model to evaluate the effect of the drugs in this field. To develop therapeutic drugs for AD, we tried to establish new AD models using Drosophila melanogaster (a fruitfly) and mouse. We have been searching for therapeutic drugs for AD by the combinatorial using of these AD models.

Research samples

Welcome to Tsuda lab home page!

Whats new?

  • Page updated.
  • Our laboratory started newly.
  • New resarch paper has been updated (See the publication).

Back to the top

Research

In Alzheimer’s disease, there are progressive neuronal dysfunctions and neurodegeneration in the brain. To tackle with Alzheimer’s disease (AD), we have been establishing animal models for AD using Drosophila melanogaster and mouse. In Drosophila model, we have established very synchronous system, which can observe the neuronal dysfunctions within a week. As a mouse model, we have established transgenic mouse, which can monitor the toxic effect of Amyloid-beta within 4 month after their birth. The combinatorial using of these animal models for AD, we have been seeking for therapeutic drugs for AD.

  1. Establishment of quantitative system for AD using Drosophila
  2. Analysis of Apoptotic inductions in AD
  3. Establishment of new mouse AD model.
  4. Drug screening using Drosophila and mouse AD models

Back to the top

People

Laboratory Head

Leo Tsuda, ph.D

Researcher

Young-Mi Lim, Ph.D

Yasutoyo Yamasaki, Ph.D

Research Assistant

Takami Azuma

Saori Ichihara

 

Back to the top

Publications 

Papers (within 5 yrs)

2016

・ Sofola-Adesakin, O., Khericha, M., Snoeren, I., Tsuda, L., Partridge, L. pGluAβ increases accumulation of Aβ in vivo and exacerbates its toxicity. Acta Neuropathologica Communications, 4(1): 109 (2016)

・ Omata, Y., Tharasegaran, S., Lim, YM., Yamasaki, Y., Ishigaki, Y., Tatsuno, T., Maruyama, M., and *Tsuda, L. Expression of amyloid-β in mouse cochlear hair cells caused early-onset auditory defect against high frequency sound stimulation. Aging, 8: 427-440 (2016) (Selected as Cover)

・ Lim, YM., *Tsuda, L. Ebi, a Drosophila homologue of TBL1, regulates the balance between cellular defense responses and neuronal survival. American Journal of Neurodegenerative Diseases, 5: 62-68 (2016)

2015

・ Seik Mohideen, S., Yamasaki, Y., Omata, Y., Tsuda, L., *Yoshiike, Y.  Nontoxic singlet oxygen generator as a therapeutic candidate for trating tauopathies. Scientific Reports, 5: 10821 (2015)

・ Lim, YM., Yagi, Y., *Tsuda, L. Cellular Defense and Sensory Cells Survival Require Distinct Functions of ebi in Drosophila. PLOS ONE, 10: e0141457 (2015)

2014

・ *Tsuda, L. and Lim, Y. The regulatory system for the G1-arrest during neuronal development in Drosophila. Dev Growth Diff, 56, 358-367 (2014)

・ Amcheslavsky A, Nie Y, Li Q, Tsuda L, Markstein M, and *Tony IP, Y. Gene expression profiling identifies the zinc-finger protein Charlatan as a regulator of intestinal stem cells in Drosophila. Development, 141, 2621-2632 (2014)

・ Omata, Y., Lim, YM., Akao, Y., and *Tsuda, L. Age-induced reduction of autophagy-related gene expression is associated with onset of Alzheimer’s disease. American Journal of Neurodegenerative Diseases, 3: 134-142 (2014)

2013

・ Lim, YM., Yamasaki, Y., and *Tsuda, L. Ebi alleviates excessive growth signaling through multiple epigenetic functions in Drosophila. Genes to Cells, 18, 909-920 (2013)

・ Yagi, Y., Lim, YM., Tsuda, L., and *Nishida, Y. fat facets induces polyubiquitination of Imd and inhibits the innate immune response in Drosophila. Genes to Cells, 18, 934-945 (2013).

2012

・ Lim, YM., Hayashi, S., and *Tsuda, L. Ebi/AP-1 suppresses pro-apoptotic gene expression and permits long-term survival of Drosophila sensory neurons. PLOS ONE, 7: e37028 (2012)

Pickup Papers

(1) *Tsuda, L., Kaido, M., Lim,Y.M., Kato, K., Aigaki, T., and *Hayashi, S. An NRSF/REST-like repressor under negative control of Su(H)/SMRTER/Ebi repressor complex regulates eye development in Drosophila. EMBO J, 25, 3191-3202 (2006)

(2) Tsuda, L., Nagaraj, R., *Zipursky, S.L., and *Banerjee, U. An EGFR/Ebi/Sno pathway promotes Delta expression by interacting Su(H)/SMRTER repression during inductive Notch signaling. Cell, 110, 625-637 (2002)

(3) Dong, X., Tsuda, L (Co-first author), Zavitz, KH., Lin, M., Li, S., Carthew, RW., and *Zipursky, SL. ebi regulates epidermal growth factor receptor signalig pathways in Drosophila. Genes Dev, 13, 954-964 (1999)

(4) Tsuda, L., Inoue, YH., Yoo, MA., Mizuno, M., Hata, M., Lim, YM., Adachi-Yamada, T., Ryo, H., Masamune, Y., *Nishida, Y. A protein kinase similar to MAP kinase activator acts downstream of the raf kinase in Drosophila. Cell, 72, 407-414 (1993)

 

Back to the top

Contact

7-430 Morioka, Obu , Aichi 474-8511, Japan

Email: ltsuda@ncgg.go.jp

Tel: +81-562-46-2311 (Ex.7523)

Back to the top

NCGG

  • National Center for Geriatrics and Gerontology
  • National Hospital for Geriatric Medicine, NCGG
  • Research Institute, NCGG
  • Center for Gerontology and Social Science

National Center for Geriatrics and Gerontology

7-430 Morioka-cho, Obu City, Aichi Prefecture, Japan