Mitochondrial dysfunction in platelets and hippocampi of senescence-accelerated mice |
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Authors: | Jie Xu Chun Shi Qi Li Jiajia Wu E. Lucy Forster David T. Yew |
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Affiliation: | (1) Department of Anatomy, Zhongshan School of Medicine, Sun Yat-Sen University Guangzhou, Guangdong, 510080, China;(2) Department of Anatomy, The Chinese University of Hong Kong, Shatin, New Territories Hong Kong |
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Abstract: | Senescence-accelerated mice (SAM) strains are useful models to understand the mechanisms of age-dependent degeneration. In this study, measurements of the mitochondrial membrane potential (Δψm) of platelets and the Adenosine 5′-triphosphate (ATP) content of hippocampi and platelets were made, and platelet mitochondria were observed in SAMP8 (faster aging mice) and SAMR1 (aging resistant control mice) at 2, 6 and 9 months of age. In addition, an Aβ-induced (Amyloid beta-protein) damage model of platelets was established. After the addition of Aβ, the Δψm of platelets of SAMP8 at 1and 6 months of age were measured. We found that platelet Δψm, and hippocampal and platelet ATP content of SAMP8 mice decreased at a relatively early age compared with SAMR1. The platelets of 6 month-old SAMP8 showed a tolerance to Aβ-induced damages. These results suggest that mitochondrial dysfunction might be one of the mechanisms leading to age-associated degeneration in SAMP mice at an early age and the platelets could serve as a biomarker for detection of mitochondrial function and age related disease. |
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Keywords: | Aging Adenosine 5′ -triphosphate Mitochondria Mitochondrial membrane potential Senescence-accelerated mice |
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