Mitochondrial dysfunction in platelets and hippocampi of senescence-accelerated mice.

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 (Deltapsi(m)) 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 Abeta-induced (Amyloid beta-protein) damage model of platelets was established. After the addition of Abeta, the Deltapsi(m) of platelets of SAMP8 at 1 and 6 months of age were measured. We found that platelet Deltapsi(m), 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 Abeta-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.