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JST Press Release

November 14, 2014
Japan Science and Technology Agency (JST)
5-3, Yonbancho, Chiyoda-ku, Tokyo 102-8666

Elucidation of the mechanism of neuronal degeneration in multiple sclerosis.
- The hope in the development of novel therapeutics for nervous diseases -

Multiple sclerosis (MS) is a chronic disease with inflammatory demyelination in the central nervous system. As the pathological changes are distributed in broad area including the cerebrum, the optic nerve, and the spinal cord, MS shows multiple neurological symptoms. Relapse of MS is induced by inflammation, and it is believed that exacerbation of the symptoms is due to irreversible changes of neural network. The molecular mechanisms about this irreversible process have been largely unknown. In this research, we investigated that RGMa expressed on helper T cells induces neuronal death and axonal degeneration. Furthermore, we clearly showed that administration of anti-RGMa neutralizing antibody in mice model of MS improved the neurological symptoms and pathological changes. These findings indicate that anti-RGMa neutralizing antibody is useful for the treatment of MS as intractable disease.

Researcher Information

JST CREST Basic Research Programs
Research Area “Elucidation of the Principles of Formation and Function of the Brain Neural Network and Creation of Control Technologies.”
Research Theme “Elucidation of mechanisms of neural network reorganization and functional recovery after brain injury.”

Journal Information

Tanabe S and Yamashita T. “Repulsive guidance molecule-a is involved in Th17 cell-induced neurodegeneration in autoimmune encephalomyelitis”. Cell Reports, Published Online November 13, 2014, doi: 10.1016/j.celrep.2014.10.038.


[About Research]
Toshihide Yamashita, M.D., Ph.D.
Professor, Graduate School of Medicine, Osaka Univ.
URL: http://www.med.osaka-u.ac.jp/pub/molneu/index_e.html

[About Program]
Takafumi Kawaguchi
Life Innovation Group, Department of Innovation Research, JST
URL: http://www.jst.go.jp/kisoken/crest/en/index.html


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