{ "titles": [ "2012 - Genome-Environment Interactions That Modulate.pdf", "2001 - Demography in the age of genomics.pdf", "2020 - Protecting the Aging Genome.pdf", "2020 - Clinical Genetics and Genomics of Aging.pdf", "2018 - Spontaneous DNA damage to the nuclear genome promotes senescence.pdf", "2009 - The Human Ageing Genomic Resources online.pdf", "2009 - Adaptation, aging, and genomic information.pdf", "2012 - Genome-Environment Interactions That Modulate.pdf", "2009 - MicroRNAs in C. elegans Aging Molecular Insurance for Robustness.pdf", "2002 - Pharmacology, Genomics, and the Evolutionary Biology.pdf" ], "extraction_id": [ "68b12e10-d643-570a-aa63-eda62de81928", "e3014138-3d5b-58bc-a1a5-5ac6f04cac1c", "e5067ce2-69a6-5433-bed4-b95daeaa691e", "822571e2-b05d-5e17-9eaa-431151851111", "005e73b5-7a93-53ff-946c-735fb4588de5", "7ada6b55-99c2-5e20-bf96-d153f927256c", "c2a8f947-44f2-5100-99e5-9c3a2f1284e9", "8650652a-1765-563b-a98e-2e9336bcf29a", "c8d6f90d-a25c-590a-a546-4500df09aa28", "6c9e1997-bfe6-5708-a476-07c833eed8fa" ], "document_id": [ "b1a1997c-e9df-5dc0-9d12-a3977d0c64ec", "0f07fa43-feb6-5656-b7e7-b8faa86f5623", "bb774030-2570-5596-b2ab-b8f57ff81086", "62b635c3-040e-512a-b016-6ef295308a1e", "08be7274-78a3-5e93-9e8c-3d4f6dbeacf9", "e43cd3b6-ad8e-5422-ba7c-ceb6e66cc529", "54a993af-b86b-5cc3-a04b-bab03c244534", "b1a1997c-e9df-5dc0-9d12-a3977d0c64ec", "dff49223-ac74-5419-a190-a0c7f43a5ee5", "1bc636a3-6ce0-5fea-b549-0dae90a78f1b" ], "id": [ "chatcmpl-AIFlT2nob40QrExWjGMMqZ4fSc8yC", "78733c6a-d870-5154-9128-eb66291fa967", "9da7c5dc-0deb-577c-bb22-83f987bd76dd", "3c636897-c47e-505d-9203-306124b73e0e", "265126e3-2a4d-518f-93cf-21a201747eef", "dcc13291-f18b-5094-83b6-4609322bc242", "1c4286b6-ede2-568b-9c18-b1e99ede17a6", "2c5241f1-1655-5e36-a787-b966767b2534", "f20fd517-5f05-53ca-93a5-916bc891ad92", "69681eeb-6629-5091-b2b4-b4444e570913", "5d8cc04f-7e13-5dbc-80c2-a35643954e9a" ], "contexts": [ "need to develop approaches and therapies targeting theaging process and age-related diseases (Butler et al.,2008). Delaying the process of aging, even slightly,would have profound social, medical and economic ben-efits (Olshansky et al., 2006; Butler et al., 2008). Forexample, slowing aging by a mere 7 years would cutmortality of age-related diseases by half at every age.Therefore, the potential benefits from research on thebasic biology and genetics of aging are unparalleled interms of improving quality", "raises the possibility of therapies to slow aging. Therefore the discoveryof a gerontogene with even very rare mutations that increased longevitywould cause speculation about future trends in mortality. However, thediscovery of such a gene would be relevant only to long-term (and, there-fore, very speculative) projections. Prospective Epidemiologic Surveys that Include Genetic Information Some epidemiologic cohort studies of populations have collected", "Interestingly, when senescent cells are abolished either through genetic manipulation or via senolytic drugs, biological aging is signicantly halted in mice [ 53,54]. Therefore, trials are now under way to test the ability of senolytics to postpone age-associated pathologies in humans [ 55]. Notably, multi- ple drugs are being pursued that either directly or indirectly impact DNA repair or the consequenceof DNA damage. Future Prospects: Developing Interventions through DNA Repair", "5. Goldman DP, etal. Substantial health and economic returns from delayed aging may warrant a new focus for medical research. Health Aff (Millwood). 2013;32(10):1698705. 6. Esplin ED, Oei L, Snyder MP.Personalized sequencing and the future of medicine: discov- ery, diagnosis and defeat of disease. Pharmacogenomics. 2014;15(14):177190. 7. Marian AJ.Clinical applications of molecular genetic discoveries. Transl Res. 2016;168:614.", "J.L. Kirkland, Barriers to the Preclinical Development of Therapeutics that Target Aging Mechanisms, J. Gerontol. A Biol. Sci. Med Sci. 71 (11) (2016) 1388 1394 . [2]D.J. Baker, B.G. Childs, M. Durik, M.E. Wijers, C.J. Sieben, J. Zhong, R.A. Saltness, K.B. Jeganathan, G.C. Verzosa, A. Pezeshki, K. Khazaie, J.D. Miller, J.M. van Deursen, Naturally occurringp16(Ink4a)-positive cells shorten healthy lifespan, Nature 530 (7589) (2016) 184 189.", "series of recent breakthroughs, a number of genes capable ofaltering the aging process as a whole or at least to a largedegree have been identified in animal models and even a fewin humans (Finch & Ruvkun, 2001; de Magalhes, 2005; Kenyon,2005). Furthermore, multiple alleles have been examined fortheir association with human exceptional longevity (Vijg & Suh,2005). This is a fascinating and important area of research, yetthere are now so many genes being associated with aging andlongevity that keeping", "pharmaceutical and other interventions for human aging based on research that starts with the genomic information required to sustain adaptation, and thus health, in older fruit flies [36-39]. Naturally, any such genomic short-cut to reverse-engineering the evolution of slowed aging from fruit flies to humans is fraught with potential for error. Such evolutionarily deep orthologies are sure to supply", "century. Manipulation of aging-related genes by diet,lifestyle, and pharmaceuticals could dramatically im-prove human health and could be used to develop drugsagainst age-related diseases such as cancer, heart dis-ease, type 2 diabetes, obesity, and neurodegenerativediseases. The hundreds of aging-related genes and genesrelated to CR already identified offer enormous oppor-tunities for target discovery (Fig. 2). Although aging-related genes cannot be modified in humans, under-standing how these can be", "[7] Hughes, S.E., Evason, K., Xiong, C., Kornfeld, K. Genetic and pharmacological factors that influence reproductive aging in nema- todes. PLoS Genet. 2007 , 3: e25. [8] Vijg, J., Campisi, J. Puzzles, promises and a cure for ageing. Na- ture 2008 , 454: 1065-1071. [9] Rolland, Y., Czerwinski, S., Abellan Van Kan, G., Morley, J.E., Cesari, M., Onder, G., Woo, J., Baumgartner, R., Pillard, F., Boirie, Y., Chumlea, W.M., Vellas, B. Sarcopenia: its assessment, etiol-", "for the aging process during the 20th Century. Thissituation poses a fundamental challenge to anti-aging medicine: how to develop effective therapies for a genomically complex pathology. We propose such astrategy. As a rst step, we recommend the use of modelsystems in which signicant genetic intervention is not proscribed or impractical. Second, we propose that work" ], "answer": "Yes, there are promising anti-aging therapies being developed based on genetic research. Several approaches are being explored: 1. **Senolytic Drugs**: Research has shown that abolishing senescent cells through genetic manipulation or senolytic drugs can significantly halt biological aging in mice. Trials are underway to test the ability of senolytics to postpone age-associated pathologies in humans [3]. 2. **Genetic Discoveries in Aging**: A number of genes capable of altering the aging process have been identified in animal models and even in humans. This area of research is promising as it explores the association of multiple alleles with human exceptional longevity [6]. 3. **Manipulation of Aging-Related Genes**: There is potential in manipulating aging-related genes through diet, lifestyle, and pharmaceuticals to improve human health and develop drugs against age-related diseases such as cancer, heart disease, type 2 diabetes, obesity, and neurodegenerative diseases [8]. These developments indicate that genetic research is paving the way for potential anti-aging therapies.", "question": "Are there any promising anti-aging therapies being developed based on genetic research?" }