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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: Mechanisms of aging in senescence-accelerated mice . | Research Open Access Mechanisms of aging in senescence-accelerated mice Todd A Carter Jennifer A Greenhall Shigeo Yoshida Sebastian Fuchs Robert Helton Anand Swarooph David J Lockhart and Carrolee Barlow Addresses The Salk Institute for Biological Studies La Jolla CA 92037 USA. Department of Ophthalmology and Visual Sciences University of Michigan Ann Arbor MI 48105 USA. Department of Human Genetics University of Michigan Ann Arbor MI 48105 USA. Ambit Biosciences San Diego CA 92121 USA. Current address BrainCells Inc. 10835 Road to the Cure San Diego CA 92121 USA. These authors contributed equally to this work. Correspondence Carrolee Barlow. E-mail cbarlow@braincellsinc.com Published I June 2005 Genome Biology 2005 6 R48 doi I0.I 186 gb-2005-6-6-r48 The electronic version of this article is the complete one and can be found online at http genomebiology.com 2005 6 6 R48 Received 16 December 2004 Revised 9 March 2005 Accepted 5 May 2005 2005 Carter et al. licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Background Progressive neurological dysfunction is a key aspect of human aging. Because of underlying differences in the aging of mice and humans useful mouse models have been difficult to obtain and study. We have used gene-expression analysis and polymorphism screening to study molecular senescence of the retina and hippocampus in two rare inbred mouse models of accelerated neurological senescence SAMP8 and SAMP10 that closely mimic human neurological aging and in a related normal strain SAMR1 and an unrelated normal strain C57BL 6J . Results The majority of age-related gene expression changes were strain-specific with only a few common pathways found for normal and accelerated neurological aging. Polymorphism .
