We appreciate donations for our ALS research!

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The unique research techniques we have developed for the study of motor neurons hold the potential to significantly contribute to the elucidation of two crucial issues in ALS. We seek support to expedite these studies.

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1. In ALS, aggregates of proteins (clumps, or "aggregates") accumulate in the affected motor neurons, a phenomenon not observed in normal cells. By deeply understanding the mechanism behind the accumulation of these aggregates, we aim to pinpoint the root cause of ALS. This will facilitate the development of methods to clearly identify therapeutic targets and protect motor neurons.

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2. ALS exhibits a characteristic where larger motor neurons, responsible for producing strong body movements, are more susceptible to damage. By understanding the characteristics of larger motor neurons that make them vulnerable in ALS, we aim to develop methods to protect motor neurons from ALS.

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To make donations to our ALS research, please contact Kazuhide Asakawa (Email: kasakawa[a]nig.ac.jp) (please replace [a] with @).

April 7, 2023

Kazuhide Asakawa

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Research Grants that have supported our ALS research:

AMED-PRIME, Grants-in-Aid for Scientific Research, Chugai Pharmaceutical Science Foundation Research Grant, Naito Memorial Scientific Research Encouragement Fund, Uehara Memorial Life Science Foundation Research Grant, 4th Serika Fund Award Research Grant, Brain Science Promotion Foundation Research Grant, Optical Science and Technology Foundation Research Grant, "Yoshio Kode Fund" Research Encouragement Fund, Kato Memorial Intractable Disease Research Grant, 1st Serika Fund Award Research Grant, "Vivid Life" ALS Research Grant, Takeda Scientific Promotion Foundation Medical Research Encouragement, and Daiichi Sankyo Life Science Research Promotion Foundation Research Grant.

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Key Research Achievements:

1. Asakawa K*, Handa H, Kawakami K. In Vivo Optogenetic Phase Transition of an Intrinsically Disordered Protein. Methods in Molecular Biology (2024) 2707:257-264. doi: 10.1007/978-1-0716-3401-1_17. (*Correspondence)

2. Asakawa K*, Handa H, Kawakami K*. Dysregulated TDP-43 proteostasis perturbs excitability of spinal motor neurons during brainstem-mediated fictive locomotion in zebrafish. Development, Growth & Differentiation (2023) doi: 10.1007/978-1-0716-3401-1_17. (*Correspondence)

3. Asakawa K*, Handa H, Kawakami K. Optogenetic phase transition of TDP-43 in spinal motor neurons of zebrafish larvae. Journal of Visualized Experiments (2022) 180 doi: 10.3791/62932. (*Correspondence)

4. Asakawa K*, Handa H, and Kawakami K*. Optogenetic modulation of TDP-43 oligomerization accelerates ALS-related pathologies in the spinal motor neurons. Nature Communications (2020) 11:1004 (*Co-correspondence)

5. Asakawa K* and Kawakami K*. Protocadherin-mediated cell repulsion controls the central topography and efferent projections of the abducens nucleus. Cell Reports (2018) 24:1562-1572 (*Co-correspondence)

6. Asakawa K*, Gembu A and Kawakami K*. Cellular dissection of the spinal cord motor column by BAC transgenesis and gene trapping in zebrafish. Frontiers in Neural Circuits (2013) 7:100. (*Co-correspondence)

7. Asakawa K, Higashijima S, and Kawakami K. An mnr2b/hlxb9lb enhancer trap line that labels spinal and abducens motor neurons in zebrafish. Developmental Dynamics (2012) 241: 327-332.

8. Asakawa K, Suster ML, Mizusawa K, Nagayoshi S, Kotani T, Urasaki A, Kishimoto Y, Hibi M and Kawakami K. Genetic dissection of neural circuits by Tol2 transposon-mediated Gal4 gene and enhancer trapping in zebrafish. Proc Natl Acad Sci U S A (2008) 105:1255-1260.