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              "content": "Here are the studies that include rapamycin:\n\n1. **Yin L, Ye S, Chen Z, Zeng Y (2012)**: \"Rapamycin preconditioning attenuates transient focal cerebral ischemia/reperfusion injury in mice\" [1].\n2. **Spilman P, Podlutskaya N, Hart MJ, Debnath J, Gorostiza O, Bredesen D, Richardson A, Strong R, Galvan V (2010)**: \"Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease\" [1].\n3. **Anisimov VN, Zabezhinski MA, Popovich IG, Piskunova TS, Semenchenko AV, Tyndyk ML, Yurova MN, Rosenfeld SV, Blagosklonny MV (2011)**: \"Rapamycin increases lifespan and inhibits spontaneous tumorigenesis in inbred female mice\" [2].\n4. **Lamming DW, Ye L, Katajisto P, Goncalves MD, Saitoh M, Stevens DM, et al. (2012)**: \"Rapamycin-induced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity\" [5].\n5. **Tataranni T, Biondi G, Cariello M, Mangino M, Colucci G, Rutigliano M, et al. (2011)**: \"Rapamycin-induced hypophosphatemia and insulin resistance are associated with mTORC2 activation and klotho expression\" [5].\n6. **Wilkinson JE, Burmeister L, Brooks SV, Chan CC, Friedline S, Harrison DE, et al. (2012)**: \"Rapamycin slows aging in mice\" [7].\n7. **Reihl K, Seals D, Henson G, LaRocca T, Magerko K, Bosshardt G, et al. (2013)**: \"Dietary rapamycin selectively improves arterial function in old mice\" [7].\n8. **Miller RA, Harrison DE, Astle CM, Fernandez E, Flurkey K, Han M, et al. (2014)**: \"Rapamycin-mediated lifespan increase in mice is dose and sex dependent and metabolically distinct from dietary restriction\" [10].\n\nThese studies cover a range of topics including the effects of rapamycin on cerebral ischemia, Alzheimer's disease, lifespan extension, insulin resistance, aging, and arterial function.",
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              "text": "168. Yin L, Ye S, Chen Z, Zeng Y . Rapamycin preconditioning attenuates tran-\nsient focal cerebral ischemia/reperfusion injury in mice. Int J Neurosci. 2012;122:748756. doi: 10.3109/00207454.2012.721827\n 169. Spilman P, Podlutskaya N, Hart MJ, Debnath J, Gorostiza O, Bredesen \nD, Richardson A, Strong R, Galvan V . Inhibition of mTOR by rapamy-cin abolishes cognitive deficits and reduces amyloid-beta levels in a \nmouse model of Alzheimers disease. PLoS One. 2010;5:e9979. doi: \n10.1371/journal.pone.0009979",
              "title": "2018 -  Mechanisms of Vascular Aging.pdf",
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              "text": "Anisimov VN, Zabezhinski MA, Popovich IG, Piskunova TS,\nSemenchenko AV, Tyndyk ML, Yurova MN, Rosenfeld SV,Blagosklonny MV (2011b) Rapamycin increases lifespan and\ninhibits spontaneous tumorigenesis in inbred female mice. Cell\nCycle 10:42304236\nAugustine JJ, Bodziak KA, Hricik DE (2007) Use of sirolimus in\nsolid organ transplantation. Drugs 67:369391\nBannister CA, Holden SE, Jenkins-Jones S, Morgan CL, Halcox JP,",
              "title": "2016 - The dog aging project translational geroscience in companion.pdf",
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              "text": "ACCEPTED MANUSCRIPTACCEPTED MANUSCRIPT\nmTOR complex 2 (mTORC2), the less clearly identified  and less sensitive to rapamycin. Most information to \ndate on the r ole of mTOR has studied the insulin/nutrient signaling via the mTORC1 and significantly less in \nknown about the role of mTORC2 ( in this review, future references measure either mTORC1 or general mTOR \nactivity )[251]. Earlier this decade studies showed that decreasing TOR signaling, genetically or with rapamycin,",
              "title": "2015 - Cellular and Molecular Biology of Aging Endothelial Cells.pdf",
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              "text": "Harrison, D.E., Strong, R., Sharp, Z.D., Nelson, J.F., Astle, C.M., Flurkey, K.,Nadon, N.L., Wilkinson, J.E., Frenkel, K., Carter, C.S., et al. (2009). Rapamycin\nCell148, January 20, 2012 2012 Elsevier Inc. 55",
              "title": "2012 - Aging, Rejuvenation, and Epigenetic.pdf",
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              "text": "96. Lamming DW, Ye L, Katajisto P, Goncalves MD, Saitoh M, Stevens DM, etal. Rapamycin- \ninduced insulin resistance is mediated by mTORC2 loss and uncoupled from longevity. \nScience. 2012;335:163843.\n 97. Tataranni T, Biondi G, Cariello M, Mangino M, Colucci G, Rutigliano M, etal. Rapamycin- \ninduced hypophosphatemia and insulin resistance are associated with mTORC2 activation \nand klotho expression. Am J Transplant. 2011;11(8):165664.",
              "title": "2020 - Clinical Genetics and Genomics of Aging.pdf",
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              "text": "ing these aspects in future studies on the effects of resveratrol could help to study in \ngreater depth the mechanisms of action of this compound [56].\n Rapamycin\nRapamycin is a macrolide isolated from Streptomyces hygroscopicus, a bacteria \nfrom Pascua Island (Rapa Nui). It has functions as an antibiotic, an immune sup-\npressant drug, and it is also proposed as a CRM.After the first studies, it was found \nthat rapamycin could induce the extension of the replicative life of yeast through the",
              "title": "2020 - Clinical Genetics and Genomics of Aging.pdf",
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              "text": "[257] Wilkinson JE, Burmeister L, Brooks SV, Chan CC, Friedline S, Harrison DE, et al. Rapamycin slows \naging in mi ce. Aging Cell. 2012;11:675 -82. \n[258] Selman C, Tullet JM, Wieser D, Irvine E, Lingard SJ, Choudhury AI, et al. Ribosomal protein S6 kinase 1 \nsignaling regulates mammalian life span. Science. 2009;326:140 -4. \n[259] Reihl K, Seals D, Henson G, LaRocca T, Mag erko K, Bosshardt G, et al. Dietary rapamycin selectively \nimproves arterial function in old mice. FASEB Journal. 2013;27:1194.17.",
              "title": "2015 - Cellular and Molecular Biology of Aging Endothelial Cells.pdf",
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              "text": "29. Wilkinson JE, Burmeister L, Brooks SV, Chan C-C, Friedline S, Harrison DE,\net al. Rapamycin slows aging in mice. Aging Cell. 2012;11:675 82.\n30. Lamming DW, Ye L, Katajisto P, Goncalves MD, Saitoh M, Stevens DM, et al.\nRapamycin-induced insulin resistance is mediated by mTORC2 loss and\nuncoupled from longevity. Science. 2012;335:1638 43.\n31. Zampieri M, Ciccarone F, Calabrese R, Franceschi C, Brkle A, Caiafa P.\nReconfiguration of DNA methylation in aging. Mech Ageing Dev. 2015;151:60 70.",
              "title": "2017 - Epigenetic aging signatures in mice livers.pdf",
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              "text": "files [55, 62]. Of note, rapamycin in particular appears to\ninduce additional changes u nrelated to age-associated\nchanges. While both CR and rapamycin induced these\nnon-age-related effects, this effect was much more marked\nfor rapamycin. These non age-related epigenetic changes\ninclude gains of methylation at genes, enhancers and CpG\nislands and losses of methylation at genes and enhancers.\nConceivably, such non age-related effects of rapamycin in",
              "title": "2017 - Diverse interventions that extend mouse.pdf",
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              "text": "23\n 94. Chakrabarti P, English T, Shi J, Smas CM, Kandror KV .Mammalian target of rapamycin \ncomplex 1 suppresses lipolysis, stimulates lipogenesis, and promotes fat storage. Diabetes. \n2010;59:77581.\n 95. Miller RA, Harrison DE, Astle CM, Fernandez E, Flurkey K, Han M, et al. Rapamycin- \nmediated lifespan increase in mice is dose and sex dependent and metabolically distinct from \ndietary restriction. Aging Cell. 2014;13:46877.",
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              "content": "Mapping gene loci that control aging in humans is challenging due to several factors:\n\n1. **Complexity of the Phenotype**: Aging is one of the most complex phenotypes, involving multiple genes that mediate the process through numerous different pathophysiological processes and diseases [4]. This complexity makes it difficult to pinpoint specific gene loci that control aging.\n\n2. **Genetic Diversity and Environmental Heterogeneity**: Human longevity studies face inherent problems such as high degrees of environmental heterogeneity and genetic diversity, which complicate the identification of consistent genetic markers [7].\n\n3. **Rare vs. Common Variants**: Finding common genetic variants that account for the entire genetic component of human lifespan variability has proven difficult. If rare variants explain most of the genetic variation in aging among humans, new genotyping techniques and analysis methods are required to identify these genes and pathways [2], [3].\n\n4. **Numerous Loci Involved**: More than 1000 loci exhibit age-dependent changes in gene expression, but not all of these loci are causally involved in aging. The sheer number of loci to sort out presents a substantial problem [6].\n\n5. **Lack of Consistent Associations**: Common variants within genes involved in aging pathways have not been consistently associated with lifespan in humans, indicating the complexity and variability of the genetic factors involved [10].\n\nThese factors collectively contribute to the difficulty in mapping gene loci that control aging in humans.",
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              "text": "that is differentiated at hundreds of loci. Many ofthe loci that control aging in Drosophila will not have\nthe same effect on human aging. On the other hand,we expect that other loci will work in a parallelmanner in humans. We have no way of knowing a\npriori which group any particular locus will belong\nin. Thus, the individual mutants that increase\nDrosophila lifespan may or may not come from loci",
              "title": "2002 - Pharmacology, Genomics, and the Evolutionary Biology.pdf",
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              "text": "understanding of molecular mechanisms underlyingthe human ageing process. Like other complexhuman traits, nding common variants that accountfor the entire genetic component of human lifespan\nvariability has proved difcult. If rare variants rather\nthan common variants explain most of the genetic vari-ation in ageing among humans, new genotypingtechniques and new analysis methods must be devel-oped to nd genes and pathways involved in ageing.Next-generation sequencing technologies are faster",
              "title": "2010 - Genetics and genomics of human ageing.pdf",
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              "text": "understanding of molecular mechanisms underlyingthe human ageing process. Like other complexhuman traits, nding common variants that accountfor the entire genetic component of human lifespan\nvariability has proved difcult. If rare variants rather\nthan common variants explain most of the genetic vari-ation in ageing among humans, new genotypingtechniques and new analysis methods must be devel-oped to nd genes and pathways involved in ageing.Next-generation sequencing technologies are faster",
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              "text": "Several explanations are possible for the lack of genome-\nwide signicant ndings. First, mortality is arguably 1 ofthe most complex phenotypes, and several trajectories to-ward extreme old age have been identied (Evert et al.,2003). Multiple genes could mediate the aging process butwould have their effects through numerous different patho-physiological processes and diseases that act as intermediate",
              "title": "2011 - A genome-wide association study of aging.pdf",
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              "text": "effect fundamental mechanisms of aging (14, 16). The drawbacksof such studies include the improbability of picking the right geneto study the myriad of known and unknown genes affecting theprocess of interest (17). The linkage study described heremarkedly improves the efficiency of such association studies bydefining a region likely to contain polymorphism(s) with signif-icant influence on life span.\nAdditional association studies with these families and repli-",
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              "text": "[12]More than 1000\nloci exhibit age-dependent changes in geneexpression (1264 genes). This is a substantialproblem, because not all of these loci will be causally\ninvolved in aging, and there are so many to sort out.\nAn additional application of gene chip technologyis to compare ies with and without a lifespanmodulating physiological treatment. Pletcher et al.",
              "title": "2002 - Pharmacology, Genomics, and the Evolutionary Biology.pdf",
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              "text": "span and have yielded insights into potential biological\npathways and processes related to aging. Despite these\nsuccesses, several problems are inherent in human\nlongevity studies including potentially high degrees ofenvironmental heterogeneity, genetic diversity, and lack of\nbirth matched controls, among others [ 8].\nInbred mouse strains represent a powerful alternative for\nidentifying genes underlying complex trait genes such as\nlongevity [ 9]. Initial mapping approaches include quanti-",
              "title": "2015 - A Chromosome 13 locus is associated with male-specific mortality in mice.pdf",
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              "text": "86\nDespite the progress in elucidating the genetic basis of\nlongevity and aging in many organism models, ranging from\nyeast and nematodes to mice, a large-scale, systematic\napproach for the exploration of aging in humans is still atthe beginning.\n87So far, a variation in the gene coding for\napolipoprotein E ( APOE )88,89and forkhead box O3A gene\n(FOXO3A ) have been consistently associated with longevity\nin various populations.90,91Recently, stress response genes,",
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              "text": "discover core mechanisms of regulation.ANALYSIS OF HUMAN VARIATION IN\nTHE GENETIC CONTROL OF LONGEVITY\nHeritability studies have convincingly demonstrated that at\nleast some fraction of human lifespan is heritable. In tandem,\nlarge-scale genome-wide association studies (GWAS) have\nidentied numerous loci associated with age-related traits\n(Buniello et al., 2019). While genetic studies have functionally\nshown an inverse eect of multiple age-related, disease-",
              "title": "2021 - Footprints in the Sand Deep Taxonomic Comparisons in Vertebrate Genomics to Unveil the Genetic Programs of Human Longevity.pdf",
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              "text": "Kenyon, 2010; Vellai et al., 2003 ). However, in humans,\ncommon variants within genes involved in these pathways\nhave not been consistently associated with lifespan ( Chris-tensen et al., 2006; Kenyon, 2010; Kuningas et al., 2008;\nVijg and Suh, 2005 ).\nThe lack of success in the identication of genes related\nto aging in humans may be due to the complexity of the\nphenotype. One approach to investigate aging and longevity\nis to compare frequencies of genetic variants between no-",
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