|Associate Professor||MORI Masayuki|
|Assistant Professor||SAWASHITA Jinko|
E-mail ： keiichih(at)shinshu-u.ac.jp
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The long-term goal of research in our laboratory is to understand senescence of organism, and age-associated diseases. Above all, we are interested in amyloidosis. The amyloidoses constitute a large group of diseases including Alzheimer disease and prion diseases. All forms of amyloidosis are caused by an alteration in the conformation and metabolism of several physiological proteins into pathological insoluble fibrils (amyloid fibrils) which, under particular conditions, deposit extracellularly in various tissues. The key in finding a cure and preventive measures for amyloidosis is, therefore, to clarify the mechanisms of amyloid fibril formation, and of deposition to specific organs and tissues. To achieve this goal, we employ molecular genetic and biochemical techniques as well as various spontaneous, transgenic, and knockout mouse models.
We are engaged in the studies for other age-associated diseases and common diseases as well. We utilize senescence-accelerated mouse (SAM) strains, which are the models for accelerated senescence and various age-associated diseases. We also specialize in molecular cloning of the causative genes in animal models for hereditary diseases. In addition, we study the effects of exercise on common diseases in humans, such as obesity, hypertension, and dislipidemia. Specific research interests include:
*Molecular biology of amyloidosis with special interest in the mechanisms for transmission of amyloidosis
*Molecular genetic mechanisms of senescence and lifespan by using senescence-accelerated mouse (SAM) strains
*Molecular cloning of the causative genes in mouse and rat models for hereditary diseases
*Molecular genetic basis of the therapeutic and preventive effects of exercise regimens on age-associated diseases in elderly people in conjunction with ”Matsumoto city Jukunen Taiiku Daigaku” health promotion program
*Anti-aging effects of chemicals, antioxidants, and supplements
1. Mori M, Gotoh S, Taketani S, Hiai H, Higuchi K. (2013) Hereditary cataract of the Nakano mouse: Involvement of a hypomorphic mutation in the coproporphyrinogen oxidase gene. Exp Eye Res 112C: 45-50.
2. Luo H, Higuchi K, Matsumoto K, Mori M. (2013) An interleukin-33 gene polymorphism is a modifier for eosinophilia in rats. Genes Immun 14(3): 192-197.
3. Chen L, Une Y, Higuchi K, Mori M. (2012) Cheetahs have 4 serum amyloid A genes evolved through repeated duplication events. J Hered 103(1): 115-29.
4. Wall JS, Richey T, Stuckey A, Donnell R, Macy S, Martin EB, Williams A, Higuchi K, Kennel SJ. (2012) In vivo molecular imaging of peripheral amyloidosis using heparin-binding peptides. Proc Natl Acad Sci U S A 108(34): E586-94.
5. Wang Y, Sawashita J, Qian J, Zhang B, Fu X, Tian G, Chen L, Mori M, Higuchi K. (2011) ApoA-I deficiency in mice is associated with redistribution of apoA-II and aggravated AApoAII amyloidosis. J Lipid Res 52(8): 1461-70.
6. Imanishi H, Yokota M, Mori M, Shimizu A, Nakada K, Hayashi J. (2011) Nuclear but not mitochondrial DNA involvement in respiratory complex I defects found in Senescence-Accelerated Mouse Strain, SAMP8. Exp Anim 60(4): 397-404.
7. Tomozawa H, Nishio A, Higuchi K, Matsumoto K, Mori M. (2011) Genes for difference in eosinophilic phenotype between MES and BN.MES-Cyba(mes) rats are on chromosomes 9, 5, and 1. Exp Anim 60(2): 151-60.
8. Schmelzer C, Okun J, Haas D, Higuchi K, Sawashita J, Mori M, Döring F. (2010) The reduced form of Coenzyme Q10 mediates distinct effects on cholesterol metabolism at the transcriptional and metabolite level in SAMP1 mice. IUBMB Life 62(11): 812-8.
9. Qian J, Yan J, Ge F, Zhang B, Fu X, Tomozawa H, Sawashita J, Mori M, Higuchi K. (2010) Mouse senile amyloid fibrils deposited in skeletal muscle exhibit amyloidosis-enhancing activity. PLoS Pathogens 6(5): e1000914.