論文 - 勝野　雅央

Geranylgeranylacetone ameliorates ischemic acute renal failure via induction of Hsp70. 査読有り

Suzuki S, Maruyama S, Sato W, Morita Y, Sato F, Miki Y, Kato S, Katsuno M, Sobue G, Yuzawa Y, Matsuo S.

Kidney Int   67 巻   頁： 2210-2220   2005年

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Clinical and electrophysiologic correlates of IVIg responsiveness in CIDP. 査読有り

Iijima M, Yamamoto M, Hirayama M, Tanaka F, Katsuno M, Mori K, Koike H, Hattori N, Arimura K, Nakagawa M, Yoshikawa H, Hayasaka K, Onodera O, Baba M, Yasuda H, Saito T, Nakazato M, Nakashima K, Kira J, Kaji R, Oka N, Sobue G.

Neurology   64 巻   頁： 1471-1475   2005年

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Gene expression profile of spinal motor neurons in sporadic amyotrophic lateral sclerosis. 査読有り

Jiang YM, Yamamoto M, Kobayashi Y, Yoshihara T, Liang Y, Terao S, Takeuchi H, Ishigaki S, Katsuno M, Adachi H, Niwa J, Tanaka F, Doyu M, Yoshida M, Hashizume Y, Sobue G.

Ann Neurol   57 巻   頁： 236-251   2005年

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Multiple regional 1H-MR spectroscopy in multiple system atrophy: NAA/Cr reduction in pontine base as a valuable diagnostic marker. 査読有り

Watanabe H, Fukatsu H, Katsuno M, Sugiura M, Hamada K, Okada Y, Hirayama M, Ishigaki T, Sobue G.

J Neurol Neurosurg Psychiatry   75 巻   頁： 103-109   2004年

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Polyglutamine diminishes VEGF; passage to motor neuron death? 招待有り 査読有り

Katsuno M, Sobue G.

Neuron   41 巻   頁： 677-679   2004年

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担当区分：筆頭著者   記述言語：英語  

Sweet relief for Huntington disease. 招待有り 査読有り

Katsuno M, Adachi H, Sobue G.

Nat Med   10 巻   頁： 123-124   2004年

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担当区分：筆頭著者   記述言語：英語  

Spinal and bulbar muscular atrophy: ligand-dependent pathogenesis and therapeutic perspectives. 招待有り 査読有り

Katsuno M, Adachi H, Tanaka F, Sobue G.

J Mol Med   82 巻   頁： 298-307   2004年

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担当区分：筆頭著者   記述言語：英語  

Sodium butyrate ameliorates phenotypic expression in a transgenic mouse model of spinal and bulbar muscular atrophy. 査読有り

Minamiyama M, Katsuno M, Adachi H, Waza M, Sang C, Kobayashi Y, Tanaka F, Doyu M, Inukai A, Sobue G.

Hum Mol Genet   13 巻   頁： 1183-92   2004年

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Spinal and bulbar muscular atrophy (SBMA) is an inherited motor neuron disease caused by the expansion of a polyglutamine (polyQ) tract within the androgen receptor. Unifying mechanisms have been implicated in the pathogenesis of polyQ-dependent neurodegenerative diseases including SBMA, Huntington disease and spinocerebellar ataxias. It has been suggested that mutant protein containing polyQ inhibits histone acetyltransferase activity, resulting in transcriptional dysfunction and subsequent neuronal dysfunction. Histone deacetylase (HDAC) inhibitors alleviate neurological phenotypes in fly and mouse models of polyQ disease, although the therapeutic effect is limited by the toxicity of these compounds. We studied the therapeutic effects of sodium butyrate (SB), an HDAC inhibitor, in a transgenic mouse model of SBMA. Oral administration of SB ameliorated neurological phenotypes as well as increased acetylation of nuclear histone in neural tissues. These therapeutic effects, however, were seen only within a narrow range of SB dosage. Our results indicate that SB is a possible therapeutic agent for SBMA and other polyQ diseases, although an appropriate dose should be determined for clinical application.