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Koji Yamanaka Lab.

Department of Neuroscience and Pathobiology, RIEM, Nagoya University

Introduction

This laboratory has started since 2013. Our mission is to uncover the mechanisms of neurodegenerative disorder, motor neuron disease, to develop the viable therapy.

TRIF-ALS-Astrocyte

Apr. 6, 2018: We reported that innate immune TRIF pathway plays an important role in protecting a microenvironment surrounding motor neurons by eliminating aberrantly activated astrocytes. (Komine et al. Cell Death Diff)

group photo

Apr. 6, 2018: New members joined our laboratory.

CysCvivo

Jan. 11, 2018: We reported that CysC ameliorated disease in SOD1-linked ALS model mice. (Watanabe et al. J Neurochem)

Nishino and Yamanaka

Nov. 17, 2017: Mr. Nishino won a Medical Student Research Award of Nagoya University 2017.

An extension lecuture

Oct. 21, 2017: We held an extention lecuture of RIEM 2017 entitled as "Efforts to overcome neurodegenerative diseases".

Our Recent Activities

2018/4/6

Our paper in Cell Death & Differentiation is now in press:

Our research(TRIF-ALS)

We revealed for the first time that the innate immune TRIF pathway is involved in eliminating aberrantly activated astrocytes to maintain the microenvironment surrounding motor neurons in ALS mice. The current study reveals the new roles of innate immunity in ALS pathomechanism and provides a clue to develop a new therapeutic approach for protecting ALS motor neurons.

Open Access
Komine O, Yamashita H, Fujimori-Tonou N, Koike M, Jin S, Moriwaki Y, Endo F, Watanabe S, Uematsu S, Akira S, Uchiyama Y, Takahashi R, Misawa H, Yamanaka K
Outer link Innate immune adaptor TRIF deficiency accelerates disease progression of ALS mice with accumulation of aberrantly activated astrocytes.
Cell Death & Differentiation in press doi:10.1038/s41418-018-0098-3.

Outer link Press Release from Nagoya University

2018/1/12

Our review of the multiple roles of astrocytes in ALS pathology is now in press in Neuroscience Research:

Open Access
Yamanaka K, Komine O
Outer link The multi-dimensional roles of astrocytes in ALS.
Neuroscience Research 126: 31-38, 2018.

Our collaborative papers are now in press as below:

Watanabe-Matsumoto S, Moriwaki Y, Okuda T, Ohara S, Yamanaka K, Abe Y, Yasui M, Misawa H
Outer link Dissociation of blood-brain barrier disruption and disease manifestation in an aquaporin-4-deficient mouse model of amyotrophic lateral sclerosis.
Neuroscience Research in press, 2017.

Open Access
Yamasaki T, Deki-Arima N, Kaneko A, Miyamura N, Iwatsuki M, Matsuoka M, Fujimori-Tonou N, Okamoto-Uchida Y, Hirayama J, Marth JD, Yamanashi Y, Kawasaki H, Yamanaka K, Penninger JM, Shibata S, Nishina H
Outer link Age-dependent motor dysfunction due to neuron-specific disruption of stress-activated protein kinase MKK7.
Scientific Reports 7: 7348, 2017.

2018/1/11

Our papar is now in press in Journal of Neurochemistry:

CysCvivo

We demonstrated that cystatin C, a major component of Bunina bodies in sporadic ALS, extended survival time of SOD1-linked ALS model mice (+9.6 days; +6.48 % of total), probably via AMP-activated kinase (AMPK) mediated pathways. Our data suggest that cystatin C may be a novel therapeutic candidate for ALS.

Open Access
Watanabe S, Komine O, Fumito E, Wakasugi K, Yamanaka K
Outer link Intracerebroventricular administration of Cystatin C ameliorates disease in SOD1-linked amyotrophic lateral sclerosis mice.
Journal of Neurochemistry in press.

2018/1/10

Our members gave presentations in the symposium or meeting listed below:

  • 2017/12/6-9 Conbio2017 (Kobe, Japan) - Speaker: Prof. Yamanaka, & Dr. Watanabe
  • 2017/12/8-10 28th International Symposium on ALS/MND (Boston, USA) - Speaker: Prof. Yamanaka, & Dr. Endo

2017/11/22

Prof. Yamanaka gave presentations in the symposium or meeting listed below:

  • 9/7 60th Anuual Meeting of the Japanese Society for Neurochemistry (Sendai, Japan)
  • 9/19 23rd World Congress of Neurology (WCN) (with 58th Annual Meeting of the Japanese Society of Neurology) (Kyoto, Japan)
    Mr. Nishino also gave his presentation in theis meeting.
  • 9/28 47th Annual Meeting of the Japanese Society of Neuropsychopharmacology (with 39th Annual Meeting of the Japanese Society of Biological Psychiatry) (Sapporo, Japan)
  • 10/6 29th Annual Meeting of the Japanese Society for Neurochemistry (Sapporo, Japan)

2017/11/17

Mr. Nishino won a Medical Student Research Award of Nagoya University 2017.

Nihsino and Yamanaka

2017/11/9

Our collaborative work with Nagoya City University (Drs. Tsuiji & Hattori) is now in press in Scientific Reports:

We analysed age-dependent changes in TDP-43 transgenic mice, and found the accumulation of abundant poly-ubiquitinated, interneuron-specific protein aggregates in the hippocampus of the aged mice. Our results indicate that interneuron degeneration, which occurs upon aging, may be related to the impaired memory of TDP-43 transgenic mice.

Open Access
Tsuiji H, Inoue I, Takeuchi M, Furuya A, Yamakage Y, Watanabe S, Koike M, Hattori M, Yamanaka K
link to other site TDP-43 accelerates age-dependent degeneration of interneurons.
Scientific Reports 7: 14972, 2017.

link to other site Prese release from Nagoya University

2017/10/23

We held an extention lecuture of RIEM 2017 entitled as "Efforts to overcome neurodegenerative diseases".

A large number of audience came to our lecuture in spite of bad weather, a typhoon.
The lecturers presented interesting and useful information about research/nursing on neurodegenrative diseases such as ALS.
We deeply thank all the lectures for their great presentation, and also thank all the audience.

Lecturers Scence in the discussion Presentation by Prof. Yamanaka

(1st) Group photo of the lecuturers. Drs. Ikuko Aiba (Higashi-Nagoya National Hospital), Yasumasa Kokubo (Mie Univ.), Hideyuki Okano (Keio Univ.), and Koji Yamanaka (Nagoya Univ.) from the left.
(2nd) A scene in the discussion.
(3rd) A scene in the lecuture by Dr. Yamanaka.

2017/10/2

Mr. Kidou & Mr. Inami joined our laboratory. See our members page.

2017/6/1

Ms. Matsuoka joined our laboratory.

2017/4/27

Members page was up-dated.