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The Senescence Accelerated Mouse (SAM) prone 8 (P8) is an animal model for aging which induces dementia. We tried to clarify the intracellular changes of Adenosine Triphosphate (ATP) which is a main cellular energy source, choline which is a precursor molecule biosynthesis for the of acetylcholine and Protein Carbonyl O-Methyltransferase (PCMT) activity which is believed to be involved in the repair of abnormal proteins in cerebral corteges of SAM P8 and R1, mice of 35 weeks old. Relative organ weights of brain, spleen, kidney, testis and heart to body weight in 35 weeks old SAM PS were not significantly different from those of R1 mice. However, decrease in ATP and choline content was observed in the cerebral cortex of SAM PS when compared to those of R1 mice. Statistical significance was observed in choline content(p$lt;0.01). PCMT activities were significantly increased in the cerebral corteges and spleens of SAM PS mice compared to those of normal animals(p$lt;0.01). From these results, decreased energy production and abnormal composition of which has a congenital learning and memory deficit was a similar pathological phenomenons to the changes of human dementia brain. And then, the animal used in this study may be an useful disease model for studying human dementia. Although it is considered that the increase of PCMT activity may related with a neuronal degeneration of cerebral cortex in SAM P8.
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