Neuroimmunology, Pathophysiology of glial cells

1975

Graduated from Gifu University, School of Medicine

1983

MD degree (Nagoya University)

1983-1986

Post-doctoral fellow at Dept. Neurol, University of Pennsylvania

1987

Dept. Neurol., Fujita Health Univerisity, Assist. Professor

1995

Dept. Neurol., Nara Medical University, Assoc. Professor

2001

Dept. Neuroimmunol., RIEM, Nagoya University, Professor

Immunological therapy against neurological diseases

In the previous studies, we have found that the most toxic agent from activated microglia was glutamate, which disturbed mitochondrial respiratory chain to induce neuronal dysfunction toward cell death. We also have shown that glutamate production by activated microglia is very unique. They produce glutamate via glutaminase using extracellular glutamine as a substrate, and release it through gap-junction, but not through glutamate transporters. Thus, it is possible that the blockage of glutaminase or gap-junction by a specific inhibitors may reduce production of glutamate, and subsequently reduce neuronal damage caused by activated microglia.

We, thus, plan to investigate whether glutaminase inhibitors or gap-junction inhibitors, or their related products ameliorate clinical signs of the animal models of neurodegenerative disorders, such as Alzheimer’s disease (APP and PS transgenic mice), amyotrophic lateral sclerosis (SOD1 transgenic mice), or multiple sclerosis (experimental autoimmune encephalomyelitis). These studies may give us clues to treat these neurodegenerative disorders.

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1992 Research Award for intractable neurological disease, “Basic and clinical studies on multiple sclerosis” from Aichi Medical Association.
1996 Research Award from the Naito Foundation, “The mechanisms and treatment for neurological disorders caused by immune-mediated and virus-induced mechanisms.”