Formation of advanced glycation end-product-modified superoxide dismutase-1 (SOD1) is one of the mechanisms responsible for inclusions common to familial amyotrophic lateral sclerosis patients with SOD1 gene mutation, and transgenic mice expressing human SOD1 gene mutation

Shinsuke Kato, Kenji Nakashima, Seikoh Horiuchi, Ryoji Nagai, Don W. Cleveland, Jian Liu, Asao Hirano, Miki Takikawa, Masako Kato, Imaharu Nakano, Saburo Sakoda, Kohtaro Asayama, Eisaku Ohama

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