1994 Fiscal Year Final Research Report Summary
Effect of Pathogen Status on the Manifestation of Accelerated Senescence and Murine Senile Amyloidosis in Senescence Accelerated Mouse (SAM)
Project/Area Number |
05834005
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
老化(加齢)
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Research Institution | Fukui Medical School |
Principal Investigator |
NAIKI Hironobu Fukui Medical Sch., Fac.of Medicine Lecturer, 医学部, 講師 (10227704)
|
Co-Investigator(Kenkyū-buntansha) |
NAKAKUKI Kazuya Fukui Medical Sch., Fac.of Medicine Professor, 医学部, 教授 (90024629)
HOSONO Masamichi Kyoto Univ., Chest Dis.Res.Inst.Associate Professor, 胸部疾患研究所, 助教授 (90107433)
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Project Period (FY) |
1993 – 1994
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Keywords | Regulation of ageing / Pathogen status / Senescence accelerated mouse (SAM) / Immunological function / Murine senile amyloidosis |
Research Abstract |
We investigated the effect of pathogen status on the manifestation of accelerated senescence and murine senile amyloidosis (AApoAII amyloidosis) , using 2 to 11-month-old SAMPX maintained both in conventional and in specific pathogen free (SPF) conditions. Age-related manifestation of accelerated senescence as measured by the grading score system, was significantly suppressed in the SPF group as compared to the conventional group. Manifestation of accelerated senescence was significantly higher in the male group than in the female group. In the 6-month-old conventional group, mild gastrointestinal AApoAII amyloidosis was observed in 33% of mice. In the 11-month-old conventional group, systemic AApoAII amyloidosis involving the spleen and liver was observed in 100% of mice. However, in the SPF group, no AApoAII amyloidosis was observed in any age of mice. Thus, the environmental factors are critical in the pathogenesis of accelerated senscence and AApoAII amyloidosis.
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