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Redox system expression in the motor neurons in amyotrophic lateral sclerosis (ALS): immunohistochemical studies on sporadic ALS, superoxide dismutase 1 (SOD1)-mutated familial ALS, and SOD1-mutated ALS animal models.
Kato S, Kato M, Abe Y, Matsumura T, Nishino T, Aoki M, Itoyama Y, Asayama K, Awaya A, Hirano A, Ohama E. Kato S, et al. Among authors: asayama k. Acta Neuropathol. 2005 Aug;110(2):101-12. doi: 10.1007/s00401-005-1019-3. Epub 2005 Jun 28. Acta Neuropathol. 2005. PMID: 15983830
Astrocytic hyaline inclusions contain advanced glycation endproducts in familial amyotrophic lateral sclerosis with superoxide dismutase 1 gene mutation: immunohistochemical and immunoelectron microscopical analyses.
Kato S, Horiuchi S, Nakashima K, Hirano A, Shibata N, Nakano I, Saito M, Kato M, Asayama K, Ohama E. Kato S, et al. Among authors: asayama k. Acta Neuropathol. 1999 Mar;97(3):260-6. doi: 10.1007/s004010050983. Acta Neuropathol. 1999. PMID: 10090673
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.
Kato S, Nakashima K, Horiuchi S, Nagai R, Cleveland DW, Liu J, Hirano A, Takikawa M, Kato M, Nakano I, Sakoda S, Asayama K, Ohama E. Kato S, et al. Among authors: asayama k. Neuropathology. 2001 Mar;21(1):67-81. doi: 10.1046/j.1440-1789.2001.00359.x. Neuropathology. 2001. PMID: 11304045 Review.
532 results