It is printed in the A4 size.To the laboratory site

 - Nursing Science - Community Health and Community Health Nursing
Home Healthcare Nursing
As the population ages, the need to fully understand the pathogenesis of dementia and to develop its effective method for care is vital to our nation. Therefore, the mission of our section is to help the person with the disease, and caregivers, family members to empower the abilities that remain. Within this mission, one objective is to foster new lines by bringing together basic and clinical science with an emphasis on Alzheimer’s disease and related disorders. We welcome the young scientists who have interests in dementia research.

  Ayae Kinoshita, MD, PhD
Professor
Research and Education
1)Pathogenesis of Alzheimer’s disease
The exact nature of neuronal dysfunction in Alzheimer’s disease remains largely unknown. For the last 10 years, we have focused on the protein Presenilin 1 (PS1), a causative protein for familial Alzheimer’s disease in order to reveal its pathogenesis. We are now currently pursuing the mechanisms which influence the PS1 localization and functions. We identified several factors to regulate PS1 function and are now currently analyzing them in vitro and in vivo.
2)Development of internet-based telenursing
In order to support the homecare for the dementia patients, there is a need for the bi-directional, communicative and economical approach between the patients and the medical staff. We develop and provide a new strategy to help the dementia patients and caregivers by internet-based webcamera.


Home Healthcare Nursing
Professor Ayae Kinoshita
Assistant
 Professor


Masakazu Kubota
List for Tel,
Fax & E-Mail
here
URL http://kinoshita-lab.hs.med.kyoto-u.ac.jp/
The research of the N-cadherin cleavage by Presenilin 1. The PS1-mediated N-cadherin cleavage releases its cytoplasmic domain from the membrane and transactivate beta-catenin. PS1 is considered to have an important effect on regulating signal transduction.
Our hypothesis of Alzheimer’s disease pathogenesis. PS1 dysfunction may
be causally linked to synaptic failures and other neuronal damages. We consider PS1
as a molecular switch to regulate various signaling cascades by cleaving membranous
proteins.
An example of a new IT-based support system for the dementia patients and caregivers.
Recent Publications
1. 木下彩栄 老年性認知症「ガイドライン 外来診療2009」日経メディカル p395-402
2. Uemura K, Lill CM, Banks M, Asada M, Aoyagi N, Ando K, Kubota M, Kihara T, Nishimoto T, Sugimoto H, Takahashi R, Hyman BT, Shimohama S, Berezovska O, Kinoshita A. N-cadherin-based adhesion enhances Abeta release and decreases Abeta42/40 ratio.J Neurochem. 2009, 108:350-60
3. スカイプとWebカメラを使用した在宅認知症患者とその介護者への支援:保利美也子、久保田正和、木下彩栄 癌と化学療法、35 (1) 46-47. 2008
4. 植村健吾、安藤功一、久保田正和、木下彩栄:gammaセクレターゼとシナプス機能 Cognition & Dementia 7, 46-54 (2008).
5. Uemura, K., Kuzuya, A., Shimozono, Y., Aoyagi., N., Ando, K., Shimohama, S., & Kinoshita, A. GSK3beta activity modifies the localization and function of presenilin1. J Biol.Chem. 282, 15823-32 (2007).
6. Uemura K., Kuzuya, A., Aoyagi, N., Ando, K., Shimozono, Y., Ninomiya, H., Shimohama, S., Kinoshita, A. Amyloid beta inhibits ectodomain shedding of N-cadherin via down-regulation of cell-surface NMDA receptor. Neuroscience 145:5-10 (2007)
7. Uemura, K., Kihara T., Kuzuya, A., Okawa, K., Bito H, Ninomiya H, Sugimoto H, Shimohama S., and Kinoshita, A: Modulation of beta-catenin nuclear signaling via epsilon-cleavage of N-cadherin. Biochem Biophys Res Commun 345:951-8 (2006)
8. Uemura, K., Kihara T, Kuzuya, A., Okawa, K., Sugimoto H, Shimohama S., and Kinoshita, A: Characterization of N-cadherin cleavage by ADAM10 and Presenilin 1. Neurosci Lett.402:278-13 (2006)