名古屋大学 · Medicine
마사히사 카츠노 교수의 연구실은 신경퇴행성 질환, 특히 스플라인 및 브라질성 근위축증(SBMA)의 발병 기전을 규명하는 데 초점을 맞추고 있습니다. 주로 아依然是성 호르몬 수용체와 폴리글루타민 확장 단백질이 신경세포 기능에 미치는 영향을 분자생물학적·신경병리학적 접근으로 연구하고 있으며, 열충격 단백질 유도제 및 호르몬 조절 치료 전략의 유효성도 함께 탐색하고 있습니다. 특히 동물 모델과 임상 연구를 융합한 번역 의학적 연구가 특징입니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Spinal and bulbar muscular atrophy (SBMA) is an adult-onset motor neuron disease caused by the expansion of a trinucleotide CAG repeat encoding the polyglutamine tract in the first exon of the androgen receptor gene (AR). The pathogenic, polyglutamine-expanded AR protein accumulates in the cell nucleus in a ligand-dependent manner and inhibits transcription by interfering with transcriptional factors and coactivators. Heat-shock proteins (HSPs) are stress-induced chaperones that facilitate the r
Abstract Objective Spinal and bulbar muscular atrophy (SBMA) is a hereditary motor neuron disease caused by the expansion of a polyglutamine tract in the androgen receptor (AR). Animal studies have shown that the pathogenesis of SBMA is dependent on serum testosterone level. This study is aimed at evaluating the efficacy and safety of androgen deprivation by leuprorelin acetate in patients with SBMA. Methods Fifty SBMA patients underwent subcutaneous injections of leuprorelin acetate or placebo
Spinal and bulbar muscular atrophy (SBMA) is a hereditary neurodegenerative disease caused by an expansion of a trinucleotide CAG repeat encoding the polyglutamine tract in the androgen receptor (AR) gene. To elucidate the pathogenesis of polyglutamine-mediated motor neuron dysfunction, we investigated histopathological and biological alterations in a transgenic mouse model of SBMA carrying human pathogenic AR. In affected mice, neurofilaments and synaptophysin accumulated at the distal motor ax
