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  Identification of gene expression alterations underlying the aging process in mammalsRelated Patent Categories: Chemistry: Molecular Biology And Microbiology, Measuring Or Testing Process Involving Enzymes Or Micro-organisms; Composition Or Test Strip Therefore; Processes Of Forming Such Composition Or Test Strip, Involving Nucleic AcidIdentification of gene expression alterations underlying the aging process in mammals description/claimsThe Patent Description & Claims data below is from USPTO Patent Application 20060068438, Identification of gene expression alterations underlying the aging process in mammals. Brief Patent Description - Full Patent Description - Patent Application Claims
CROSS-REFERENCE TO RELATED APPLICATION [0001] This application claims priority to 60/277,382, filed Mar. 19, 2001 and incorporated by reference herein. BACKGROUND OF THE INVENTION [0003] A common feature of most multicellular organisms is the progressive and irreversible physiological decline that characterizes senescence. Although genetic and environmental factors can influence the aging process, the molecular basis of senescence remains unknown. Postulated mechanisms include cumulative damage to DNA leading to genomic instability, epigenetic alterations that lead to altered gene expression patterns, telomere shortening in replicative cells, oxidative damage to critical macromolecules and nonenzymatic glycation of long-lived proteins (S. M. Jazwinski, Science 273:54,1996; G. M. Martin, et al., Nature Gen. 13:25, 1996; F. B. Johnson, et al., Cell 96:291, 1996; K. B. Beckman and B. N. Ames, Physiol. Revs. 78:547, 1998). Factors which contribute to the difficulty of elucidating mechanisms and testing interventions include the complexity of organismal senescence and the lack of molecular markers of biological age (biomarkers). Aging is complex in that underlying mechanisms in tissues with limited regenerative capacities (e.g., skeletal and cardiac muscle, brain), which are composed mainly of postmitotic (non-dividing) cells, may differ markedly from those operative in proliferative tissues. Accordingly, approaches which provide a global assessment of senescence in specific tissues would greatly increase understanding of the aging process and the possibility of pharmaceutical, genetic or nutritional intervention. [0004] Genetic manipulation of the aging process in multicellular organisms has been achieved in Drosophila, through the over-expression of catalase and Cu/Zn superoxide dismutase (W. C. Orr and R. S. Sohal, Science 263:1128,1994; T. L. Parkes, et al., Nat. Genet. 19:171, 1998), in the nematode C. elegans, through alterations in the insulin receptor signaling pathway (S. Ogg, et al., Nature 389:994, 1997; S. Paradis and G. Ruvkun, Genes Dev. 12:2488-2498, 1998; H. A. Tissenbaum and G. Ruvkun, Genetics 148:703, 1998), and through the selection of stress-resistant mutants in either organism (T. E. Johnson, Science 249:908, 1990; S. Murakami and T. E. Johnson, Genetics 143:1207, 1996; Y. J. Lin, et al., Science 282:943, 1998). In mammals, there has been limited success in the identification of genes that control aging rates. Mutations in the Werner Syndrome locus (WRN) accelerate the onset of a subset of aging-related pathology in humans, but the role of the WRN gene product in the modulation of normal aging is unknown (C. E. Yu, et al., Science 272:258, 1996; D. B. Lombard and L. Guanrente, Trends Genet. 12:283, 1996). [0005] In contrast to the current lack of genetic interventions to retard the aging process in mammals, caloric restriction (CR) appears to slow the intrinsic rate of aging (R. Weindruch and R. L. Walford, The Retardation of Aging and Disease by Dietary Restriction (C C. Thomas, Springfield, Ill., 1988; L. Fishbein, Ed., Biological Effects of Dietary Restriction (Springer-Verlag, New York, 1991; B. P. Yu, Ed., Modulation of Aging Processes by Dietary Restriction (CRC Press, Boca Raton, Fla. 1994). Most studies have involved laboratory rodents which, when subjected to a long-term, 25-50% reduction in calorie intake without essential nutrient deficiency, display delayed onset of age-associated pathological and physiological changes and extension of maximum lifespan. BRIEF DESCRIPTION OF THE SEVERAL VIEWS OF THE DRAWINGS [0006] FIGS. 1-23 are individual bar graphs disclosing the fold change of messages and lines showing signal intensities corresponding to individual sequences in young and old tissue. [0007] FIG. 1 discloses changes in M21050. [0008] FIG. 2 discloses changes in Z49204. [0009] FIG. 3 discloses changes in U49430. [0010] FIG. 4 discloses changes in K02782. [0011] FIG. 5 discloses changes in X58861. [0012] FIG. 6 discloses changes in X66295. [0013] FIG. 7 discloses changes in M22531. [0014] FIG. 8 discloses changes in X67809. [0015] FIG. 9 discloses changes in U19118. [0016] FIG. 10 discloses changes in M64086. [0017] FIG. 11 discloses changes in M63695. [0018] FIG. 12 discloses changes in U39066. [0019] FIG. 13 discloses changes in X92590. [0020] FIG. 14 discloses changes in X56518. [0021] FIG. 15 discloses changes in AA182189. [0022] FIG. 16 discloses changes in X16493. 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