View Item 

Show simple item record

Reverse geroscience: how does exposure to early diseases accelerate the age‐related decline in health?

dc.contributor.authorKohanski, Ronald A.
dc.contributor.authorDeeks, Steven G.
dc.contributor.authorGravekamp, Claudia
dc.contributor.authorHalter, Jeffrey B.
dc.contributor.authorHigh, Kevin
dc.contributor.authorHurria, Arti
dc.contributor.authorFuldner, Rebecca
dc.contributor.authorGreen, Paige
dc.contributor.authorHuebner, Robin
dc.contributor.authorMacchiarini, Francesca
dc.contributor.authorSierra, Felipe
dc.date.accessioned2017-01-10T19:06:19Z
dc.date.available2018-02-01T14:56:11Zen
dc.date.issued2016-12
dc.identifier.citationKohanski, Ronald A.; Deeks, Steven G.; Gravekamp, Claudia; Halter, Jeffrey B.; High, Kevin; Hurria, Arti; Fuldner, Rebecca; Green, Paige; Huebner, Robin; Macchiarini, Francesca; Sierra, Felipe (2016). "Reverse geroscience: how does exposure to early diseases accelerate the age‐related decline in health?." Annals of the New York Academy of Sciences 1386(1): 30-44.
dc.identifier.issn0077-8923
dc.identifier.issn1749-6632
dc.identifier.urihttps://hdl.handle.net/2027.42/135360
dc.publisherWiley Periodicals, Inc.
dc.publisherAgency for Healthcare Research and Quality
dc.subject.otherdiabetes
dc.subject.otherHIV
dc.subject.othercancer
dc.subject.otheraging
dc.subject.othergeroscience
dc.subject.otherAIDS
dc.titleReverse geroscience: how does exposure to early diseases accelerate the age‐related decline in health?
dc.typeArticleen_US
dc.rights.robotsIndexNoFollow
dc.subject.hlbsecondlevelScience (General)
dc.subject.hlbtoplevelScience
dc.description.peerreviewedPeer Reviewed
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/135360/1/nyas13297.pdf
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/135360/2/nyas13297_am.pdf
dc.identifier.doi10.1111/nyas.13297
dc.identifier.sourceAnnals of the New York Academy of Sciences
dc.identifier.citedreferenceHalter, J.B. 2011. Aging and insulin secretion. In Handbook of the Biology of Aging. 7th ed. E.J. Masoro & S.N. Austad, Eds.: 373 – 384. Elsevier Inc.
dc.identifier.citedreferenceChang, A.M. et al. 2006. Impaired beta‐cell function in human aging: response to nicotinic acid‐induced insulin resistance. J. Clin. Endocrinol. Metab. 91: 3303 – 3309.
dc.identifier.citedreferenceChang, A.M. & J.B. Halter. 2003. Aging and insulin secretion. Am. J. Physiol. Endocrinol. Metab. 284: E7 – E12.
dc.identifier.citedreferenceBrownlee, M. 2005. The pathobiology of diabetic complications: a unifying mechanism. Diabetes 54: 1615 – 1625.
dc.identifier.citedreferenceCraft, S. 2009. The role of metabolic disorders in Alzheimer disease and vascular dementia: two roads converged. Arch. Neurol. 66: 300 – 305.
dc.identifier.citedreferenceBiessels, G.J. et al. 2006. Risk of dementia in diabetes mellitus: a systematic review. Lancet Neurol. 5: 64 – 74.
dc.identifier.citedreferenceGudala, K. et al. 2013. Diabetes mellitus and risk of dementia: a meta‐analysis of prospective observational studies. J. Diabetes Investig. 4: 640 – 650.
dc.identifier.citedreferenceCheng, G. et al. 2012. Diabetes as a risk factor for dementia and mild cognitive impairment: a meta‐analysis of longitudinal studies. Intern. Med. J. 42: 484 – 491.
dc.identifier.citedreferenceCooper, C. et al. 2015. Modifiable predictors of dementia in mild cognitive impairment: a systematic review and meta‐analysis. Am. J. Psychiatry 172: 323 – 334.
dc.identifier.citedreferenceTakeda, S. et al. 2010. Diabetes‐accelerated memory dysfunction via cerebrovascular inflammation and Aβ deposition in an Alzheimer mouse model with diabetes. Proc. Natl. Acad. Sci. U.S.A. 107: 7036 – 7041.
dc.identifier.citedreferenceBaker, L.D. et al. 2011. Insulin resistance and Alzheimer‐like reductions in regional cerebral glucose metabolism for cognitively normal adults with prediabetes or early type 2 diabetes. Arch. Neurol. 68: 51 – 57.
dc.identifier.citedreferenceLuke, E. et al. 2016. Complex mechanisms linking neurocognitive dysfunction to insulin resistance and other metabolic dysfunction. Version 2. F1000Res. 5: 353.
dc.identifier.citedreferenceFrom, A.M. et al. 2009. Changes in diastolic dysfunction in diabetes mellitus over time. Am. J. Cardiol. 103: 1463 – 1466.
dc.identifier.citedreferenceHuebschmann, A.G. et al. 2011. Exercise attenuates the premature cardiovascular aging effects of type 2 diabetes mellitus. Vasc. Med. 16: 378 – 390.
dc.identifier.citedreferenceDai, D.F. et al. 2012. Mitochondria and cardiovascular aging. Circ. Res. 110: 1109 – 1124.
dc.identifier.citedreferenceNorth, B.J. & D.A. Sinclair. 2012. The intersection between aging and cardiovascular disease. Circ. Res. 110: 1097 – 1108.
dc.identifier.citedreferencePanes, J. et al. 1996. Diabetes exacerbates inflammatory responses to ischemia–reperfusion. Circulation 93: 161 – 167.
dc.identifier.citedreferenceSalas, A. et al. 1998. Mechanisms responsible for enhanced inflammatory response to ischemia–reperfusion in diabetes. Am. J. Physiol. 275: H1773 – H1781.
dc.identifier.citedreferenceWang, Q. et al. 2014. Myeloperoxidase deletion prevents high‐fat diet‐induced obesity and insulin resistance. Diabetes 63: 4172 – 4185.
dc.identifier.citedreferenceValerio, A. et al. 2006. TNF‐α downregulates eNOS expression and mitochondrial biogenesis in fat and muscle of obese rodents. J. Clin. Invest. 116: 2791 – 2798.
dc.identifier.citedreferenceKim, F. et al. 2008. Vascular inflammation, insulin resistance, and reduced nitric oxide production precede the onset of peripheral insulin resistance. Arterioscler. Thromb. Vasc. Biol. 28: 1982 – 1988.
dc.identifier.citedreferenceKubes, P. et al. 1991. Nitric oxide: an endogenous modulator of leukocyte adhesion. Proc. Nat. Acad. Sci. U.S.A. 88: 4651 – 4655.
dc.identifier.citedreferenceSatriano, J.H. et al. 2010. Transition of kidney tubule cells to a senescent phenotype in early experimental diabetes. Am. J. Physiol. Cell Physiol. 299: C374 – C380.
dc.identifier.citedreferenceWu, J.R. et al. 2010. Induction of diabetes in aged C57B6 mice results in severe nephropathy. Am. J. Pathol. 176: 2163 – 2176.
dc.identifier.citedreferenceLi, F. et al. 2013. Autophagy attenuates diabetic glomerular damage through protection of hyperglycemia‐induced podocyte damage. PLoS One 8: e60546.
dc.identifier.citedreferencePatschan, D.K. et al. 2014. eEOC‐mediated modulation of endothelial autophagy, senescence, and EnMT in murine diabetic nephropathy. Am. J. Physiol. Renal Physiol. 307: F686 – F694.
dc.identifier.citedreferenceYang, H.‐C. et al. 2011. Cells derived from young bone marrow alleviate renal aging. J. Am. Soc. Nephrol. 22: 2028 – 2036.
dc.identifier.citedreferenceMiao, F. et al. 2014. Evaluating the role of epigenetic histone modifications in the metabolic memory of type 1 diabetes. Diabetes 63: 1748 – 1762.
dc.identifier.citedreferenceMartin‐Montalvo, A. et al. 2013. Metformin improves healthspan and lifespan in mice. Nat. Commun. 4: 2192.
dc.identifier.citedreferenceHarrison, D.E. et al. 2014. Acarbose, 17‐α‐estradiol, and nordihydroguaiaretic acid extend mouse lifespan preferentially in males. Aging Cell 13: 273 – 282.
dc.identifier.citedreferenceHodes, R.J. et al. 2016. Disease drivers of aging. Ann. N.Y. Acad. Sci. 1386: 45 – 68.
dc.identifier.citedreferenceGerteis, J. et al. 2014. Multiple Chronic Conditions Chartbook. AHRQ Publications No. Q14‐0038. Rockville, MD: Agency for Healthcare Research and Quality.
dc.identifier.citedreferenceBarnes, P.J. et al. 2015. Mechanisms of development of multimorbidity in the elderly. Eur. Respir. J. 45: 790 – 806.
dc.identifier.citedreferenceJohnson, T.E. 2013. 25 years after age‐1: genes, interventions and the revolution in aging research. Exp. Gerontol. 48: 640 – 643.
dc.identifier.citedreferenceLongo, V.D. et al. 2015. Interventions to slow aging in humans: are we ready ? Aging Cell 14: 497 – 510.
dc.identifier.citedreferenceSierra, F. 2016. The emergence of geroscience as an interdisciplinary approach to the enhancement of health span and life span. Cold Spring Harb. Perspect. Med. 6: a025163.
dc.identifier.citedreferenceAustad, S.N. 2016. The geroscience hypothesis: is it possible to change the rate of aging ? In Advances in Geroscience. F. Sierra & R. Kohanski, Eds.: 1 – 36. Springer.
dc.identifier.citedreferenceLópez‐Otín, C. et al. 2013. The hallmarks of aging. Cell 153: 1194 – 1217.
dc.identifier.citedreferenceBurch, J.B. et al. 2014. Advances in geroscience: impact on healthspan and chronic disease. J. Gerontol. A. Biol. Sci. Med. Sci. 69 ( Suppl. 1 ): S1 – S3.
dc.identifier.citedreferenceLópez‐Otín, C. et al. 2016. Metabolic control of longevity. Cell 166: 802 – 821.
dc.identifier.citedreferenceKennedy, B.K. et al. 2014. Geroscience: linking aging to chronic disease. Cell 159: 709 – 713.
dc.identifier.citedreferenceOeffinger, K.C. et al. 2006. Chronic health conditions in adult survivors of childhood cancer. N. Engl. J. Med. 355: 1572 – 1582.
dc.identifier.citedreferenceMohile, S.G. et al. 2009. Association of a cancer diagnosis with vulnerability and frailty in older Medicare beneficiaries. J. Natl. Cancer Inst. 101: 1206 – 1215.
dc.identifier.citedreferenceMiller, C.J. et al. 2014. Adjudicated morbidity and mortality outcomes by age among individuals with HIV infection on suppressive antiretroviral therapy. PLoS One 9: e95061.
dc.identifier.citedreferenceDeeks, S.G. & A.N. Phillips. 2009. HIV infection, antiretroviral treatment, ageing, and non‐AIDS related morbidity. BMJ 338: a3172.
dc.identifier.citedreferenceMorley, J.E. 2008. Diabetes and aging: epidemiological overview. Clin. Geriatr. Med. 24: 395 – 405.
dc.identifier.citedreferenceBarzilai, N. et al. 2012. The critical role of metabolic pathways in aging. Diabetes 61: 1315 – 1322.
dc.identifier.citedreferenceSmith, B.D. et al. 2009. Future of cancer incidence in the United States: burdens upon an aging, changing nation. J. Clin. Oncol. 27: 2758 – 2765.
dc.identifier.citedreferenceParry, C. et al. 2011. Cancer survivors: a booming population. Cancer Epidemiol. Biomarkers Prev. 20: 1996 – 2005.
dc.identifier.citedreferenceScher, K.S. & A. Hurria. 2012. Under‐representation of older adults in cancer registration trials: known problem, little progress. J. Clin. Oncol. 30: 2036 – 2038.
dc.identifier.citedreferenceTalarico, L. et al. 2004. Enrollment of elderly patients in clinical trials for cancer drug registration: a 7‐year experience by the US Food and Drug Administration. J. Clin. Oncol. 22: 4626 – 4631.
dc.identifier.citedreferenceHurria, A. et al. 2016. Validation of a prediction tool for chemotherapy toxicity in older adults with cancer. J. Clin. Oncol. 34: 2366 – 2371.
dc.identifier.citedreferenceExtermann, M. et al. 2012. Predicting the risk of chemotherapy toxicity in older patients: the Chemotherapy Risk Assessment Scale for High‐Age Patients (CRASH) score. Cancer 118: 3377 – 3386.
dc.identifier.citedreferencePinder, M.C. et al. 2007. Congestive heart failure in older women treated with adjuvant anthracycline chemotherapy for breast cancer. J. Clin. Oncol. 25: 3808 – 3815.
dc.identifier.citedreferenceLichtman, S.M. et al. 2012. Paclitaxel efficacy and toxicity in older women with metastatic breast cancer: combined analysis of CALGB 9342 and 9840. Ann. Oncol. 23: 632 – 638.
dc.identifier.citedreferenceMulrooney, D.A. et al. 2009. Cardiac outcomes in a cohort of adult survivors of childhood and adolescent cancer: retrospective analysis of the Childhood Cancer Survivor Study cohort. BMJ 339: b4606.
dc.identifier.citedreferenceBaker, F. et al. 2003. Health‐related quality of life of cancer and noncancer patients in Medicare managed care. Cancer 97: 674 – 681.
dc.identifier.citedreferenceKeating, N.L. et al. 2005. Physical and mental health status of older long‐term cancer survivors. J. Am. Geriatr. Soc. 53: 2145 – 2152.
dc.identifier.citedreferenceReeve, B.B. et al. 2009. Impact of cancer on health‐related quality of life of older Americans. J. Natl. Cancer Inst. 101: 860 – 868.
dc.identifier.citedreferenceWeaver, K.E. et al. 2012. Mental and physical health‐related quality of life among U.S. cancer survivors: population estimates from the 2010 National Health Interview Survey. Cancer Epidemiol. Biomarkers Prev. 21: 2108 – 2117.
dc.identifier.citedreferenceCourneya, K.S. et al. 2007. Effects of aerobic and resistance exercise in breast cancer patients receiving adjuvant chemotherapy: a multicenter randomized controlled trial. J. Clin. Oncol. 25: 4396 – 4404.
dc.identifier.citedreferenceHornsby, W.E. et al. 2014. Safety and efficacy of aerobic training in operable breast cancer patients receiving neoadjuvant chemotherapy: a phase II randomized trial. Acta Oncol. 53: 65 – 74.
dc.identifier.citedreferenceSegal, R.J. et al. 2009. Randomized controlled trial of resistance or aerobic exercise in men receiving radiation therapy for prostate cancer. J. Clin. Oncol. 27: 344 – 351.
dc.identifier.citedreferencevan Waart, H. et al. 2015. Effect of low‐intensity physical activity and moderate‐ to high‐intensity physical exercise during adjuvant chemotherapy on physical fitness, fatigue, and chemotherapy completion rates: results of the PACES randomized clinical trial. J. Clin. Oncol. 33: 1918 – 1927.
dc.identifier.citedreferenceButtiglieri, S. et al. 2011. The aging effect of chemotherapy on cultured human mesenchymal stem cells. Exp. Hematol. 39: 1171 – 1181.
dc.identifier.citedreferenceSanoff, H.K. et al. 2014. Effect of cytotoxic chemotherapy on markers of molecular age in patients with breast cancer. J. Natl. Cancer Inst. 106: dju057.
dc.identifier.citedreferenceBeeharry, N. & D. Broccoli. 2005. Telomere dynamics in response to chemotherapy. Curr. Mol. Med. 5: 187 – 196.
dc.identifier.citedreferenceYoon, S.Y. et al. 2007. Telomere length shortening of peripheral blood mononuclear cells in solid‐cancer patients undergoing standard‐dose chemotherapy might be correlated with good treatment response and neutropenia severity. Acta Haematol. 118: 30 – 37.
dc.identifier.citedreferenceDiker‐Cohen, T. et al. 2013. The effect of chemotherapy on telomere dynamics: clinical results and possible mechanisms. Leuk. Lymphoma 54: 2023 – 2029.
dc.identifier.citedreferenceUnryn, B.M. et al. 2006. Acceleration of telomere loss by chemotherapy is greater in older patients with locally advanced head and neck cancer. Clin. Cancer Res. 12: 6345 – 6350.
dc.identifier.citedreferenceFranceschi, C. & J. Campisi. 2010. Chronic inflammation (inflammaging) and its potential contribution to age‐associated diseases. J. Gerontol. A Biol. Sci. Med. Sci. 69 ( Suppl. 1 ): S4 – S9.
dc.identifier.citedreferenceRedon, C.E. et al. 2010. Tumors induce complex DNA damage in distant proliferative tissues in vivo. Proc. Natl. Acad. Sci. U.S.A. 107: 17992 – 17997.
dc.identifier.citedreferenceMantovani, A. et al. 2008. Cancer‐related inflammation. Nature 454: 436 – 444.
dc.identifier.citedreferenceWatt, D.G. et al. 2015. Routine clinical markers of the magnitude of the systemic inflammatory response after elective operation: a systematic review. Surgery 157: 362 – 380.
dc.identifier.citedreferenceKim, J.H. et al. 2014. Mechanisms of radiation‐induced normal tissue toxicity and implications for future clinical trials. Radiat. Oncol. J. 32: 103 – 115.
dc.identifier.citedreferenceVelarde, M.C. et al. 2013. Senescent cells and their secretory phenotype as targets for cancer therapy. Interdiscip. Top. Gerontol. 38: 17 – 27.
dc.identifier.citedreferenceCouzin‐Frankel, J. 2013. Breakthrough of the year 2013. Cancer immunotherapy. Science 342: 1432 – 1433.
dc.identifier.citedreferenceGravekamp, C. 2011. The impact of aging on cancer vaccination. Curr. Opin. Immunol. 23: 555 – 560.
dc.identifier.citedreferenceGravekamp, C. 2009. The importance of the age factor in cancer vaccination at older age. Cancer Immunol. Immunother. 58: 1969 – 1977.
dc.identifier.citedreferenceChandra, D. et al. 2013. Myeloid‐derived suppressor cells have a central role in attenuated Listeria monocytogenes ‐based immunotherapy against metastatic breast cancer in young and old mice. Br. J. Cancer 108: 2281 – 2290.
dc.identifier.citedreferenceCastro, F. et al. Vaccination with Mage‐b DNA induces CD8 T‐cell responses at young but not old age in mice with metastatic breast cancer. Br. J. Cancer 101: 1329 – 1337.
dc.identifier.citedreferenceSuzuki, E. et al. 2005. Gemcitabine selectively eliminates splenic Gr‐1+/CD11b+ myeloid suppressor cells in tumor‐bearing animals and enhances antitumor immune activity. Clin. Cancer Res. 11: 6713 – 6721.
dc.identifier.citedreferenceGabrilovich, D.I. and S. Nagaraj 2009. Myeloid‐derived suppressor cells as regulators of the immune system. Nat. Rev. Immunol. 9: 162 – 174.
dc.identifier.citedreferenceLi, H. et al. 2009. Cancer‐expanded myeloid‐derived suppressor cells induce anergy of NK cells through membrane‐bound TGF‐β1. J. Immunol. 182: 240 – 249.
dc.identifier.citedreferenceSerafini, P. et al. 2008. Myeloid‐derived suppressor cells promote cross‐tolerance in B‐cell lymphoma by expanding regulatory T cells. Cancer Res. 68: 5439 – 5449.
dc.identifier.citedreferenceKroemer, G. et al. 2013. Immunogenic cell death in cancer therapy. Ann. Rev. Immunol. 31: 51 – 72.
dc.identifier.citedreferenceHearps, A. et al. 2016. HIV and aging: parallels and synergistic mechanisms leading to premature disease and functional decline. In Advances in Geroscience. F. Sierra & R. Kohansky, Eds.: 509 – 550. Springer International.
dc.identifier.citedreferenceAlthoff, K.N. et al.; Veterans Aging Cohort Study (VACS). 2015. Comparison of risk and age at diagnosis of myocardial infarction, end‐stage renal disease, and non‐AIDS‐defining cancer in HIV‐infected versus uninfected adults. Clin. Infect. Dis. 60: 627 – 638.
dc.identifier.citedreferenceHigh, K.P. et al.; OAR Working Group on HIV and Aging. 2012. HIV and aging: state of knowledge and areas of critical need for research. A report to the NIH Office of AIDS Research by the HIV and Aging Working Group. J. Acquir. Immune Defic. Syndr. 60 ( Suppl. 1 ): S1 – S18.
dc.identifier.citedreferenceErlandson, K.M. et al. 2014. Functional impairment, disability, and frailty in adults aging with HIV‐infection. Curr. HIV/AIDS Rep. 11: 279 – 290.
dc.identifier.citedreferenceGreene, M. et al. 2015. Geriatric syndromes in older HIV‐infected adults. J. Acquir. Immune Defic. Syndr. 69: 161 – 167.
dc.identifier.citedreferenceSchrack, J.A. et al. 2015. Multicenter AIDS cohort study. Accelerated longitudinal gait speed decline in HIV‐infected older men. J. Acquir. Immune Defic. Syndr. 70: 370 – 376.
dc.identifier.citedreferenceChan, P. et al. 2016. Cognitive impairment and persistent CNS injury in treated HIV. Curr. HIV/AIDS Rep. 13: 209 – 217.
dc.identifier.citedreferenceSaylor, D. et al. 2016. HIV‐associated neurocognitive disorder—pathogenesis and prospects for treatment. Nat. Rev. Neurol. 12: 234 – 248.
dc.identifier.citedreferenceMorgan, E.E. et al. 2012. Synergistic effects of HIV infection and older age on daily functioning. J. Acquir. Immune Defic. Syndr. 61: 341 – 348.
dc.identifier.citedreferenceRodriguez‐Penney, A.T. et al. 2013. Co‐morbidities in persons infected with HIV: increased burden with older age and negative effects on health‐related quality of life. AIDS Patient Care STDS 27: 5 – 16.
dc.identifier.citedreferenceSo‐Armah, K.A. et al; VACS Project Team. 2016. Do biomarkers of inflammation, monocyte activation, and altered coagulation explain excess mortality between HIV infected and uninfected people ? J. Acquir. Immune Defic. Syndr. 72: 206 – 213.
dc.identifier.citedreferenceHearps, A.C. et al. 2014. Inflammatory co‐morbidities in HIV+ individuals: learning lessons from healthy ageing. Curr. HIV/AIDS Rep. 11: 20 – 34.
dc.identifier.citedreferenceSvicher, V. et al. 2014. HIV compartments and reservoirs. Curr. HIV/AIDS Rep. 11: 186 – 194.
dc.identifier.citedreferenceCrowell, T.A. & H. Hatano. 2015. Clinical outcomes and antiretroviral therapy in ‘elite’ controllers: a review of the literature. J. Virus Erad. 1: 72 – 77.
dc.identifier.citedreferenceAppay, V. & D. Sauce. 2016. Assessing immune aging in HIV‐infected patients. Virulence 16: 1 – 10.
dc.identifier.citedreferenceEberhard, J.M. et al. 2016. Partial recovery of senescence and differentiation disturbances in CD8 + T cell effector‐memory cells in HIV‐1 infection after initiation of anti‐retroviral treatment. Clin. Exp. Immunol. 186: 227 – 238.
dc.identifier.citedreferenceCobos Jiménez, V. et al.; AGEhIV Study Group. 2016. T‐cell activation independently associates with immune senescence in HIV‐infected recipients of long‐term antiretroviral treatment. J. Infect. Dis. 214: 216 – 225.
dc.identifier.citedreferenceXu, M. et al. 2016. Transplanted senescent cells induce an osteoarthritis‐like condition in mice. J. Gerontol. A Biol. Sci. Med. Sci. pii: glw154.
dc.identifier.citedreferenceZhu, Y. et al. 2015. The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs. Aging Cell 14: 644 – 658.
dc.identifier.citedreferenceDeleage, C. et al. 2016. Impact of early cART in the gut during acute HIV infection. JCI Insight 1: e87065.
dc.identifier.citedreferenceWang, H. & D.P. Kotler. 2014. HIV enteropathy and aging: gastrointestinal immunity, mucosal epithelial barrier, and microbial translocation. Curr. Opin. HIV AIDS 9: 309 – 316.
dc.identifier.citedreferenceTrøseid, M. et al. 2014. Microbial translocation and cardiometabolic risk factors in HIV infection. AIDS Res. Hum. Retroviruses 30: 514 – 522.
dc.identifier.citedreferenceMarioni, R.E. et al. 2015. The epigenetic clock is correlated with physical and cognitive fitness in the Lothian Birth Cohort 1936. Int. J. Epidemiol. 44: 1388 – 1396.
dc.identifier.citedreferenceRickabaugh, T.M. et al. 2015. Acceleration of age‐associated methylation patterns in HIV‐1‐infected adults. PLoS One 10: e0119201.
dc.identifier.citedreferenceGross, A.M. et al. 2016. Methylome‐wide analysis of chronic HIV infection reveals five‐year increase in biological age and epigenetic targeting of HLA. Mol. Cell 62: 157 – 168.
dc.identifier.citedreferenceHorvath, S. & A.J. Levine. 2015. HIV‐1 infection accelerates age according to the epigenetic clock. J. Infect. Dis. 212: 1563 – 1573.
dc.identifier.citedreferenceWeinstein, T.L. & X. Li. 2016. The relationship between stress and clinical outcomes for persons living with HIV/AIDS: a systematic review of the global literature. AIDS Care 28: 160 – 169.
dc.identifier.citedreferencePanagiotakopoulos, L. et al. 2015. HIV‐1 proteins accelerate HPA axis habituation in female rats. Physiol. Behav. 150: 8 – 15.
dc.identifier.citedreferenceWillig, A.L. & E.T. Overton. 2016. Metabolic complications and glucose metabolism in HIV infection: a review of the evidence. Curr. HIV/AIDS Rep. 13: 289 – 296.
dc.identifier.citedreferenceHerrin, M. et al. 2016. Weight gain and incident diabetes among HIV‐infected veterans initiating antiretroviral therapy compared with uninfected individuals. J. Acquir. Immune Defic. Syndr. 73: 228 – 236.
dc.identifier.citedreferenceYuh, B. et al. 2015. Weight change after antiretroviral therapy and mortality. Clin. Infect. Dis. 60: 1852 – 1859.
dc.identifier.citedreferenceCalza, L. et al. 2016. Clinical management of dyslipidaemia associated with combination antiretroviral therapy in HIV‐infected patients. J. Antimicrob. Chemother. 71: 1451 – 1465.
dc.identifier.citedreferencePérez‐Matute, P. et al. 2013. Role of mitochondria in HIV infection and associated metabolic disorders: focus on nonalcoholic fatty liver disease and lipodystrophy syndrome. Oxid. Med. Cell. Longev. 2013: 493413.
dc.identifier.citedreferencePayne, B.A. et al. 2015. Mitochondrial DNA mutations in ageing and disease: implications for HIV ? Antivir. Ther. 20: 109 – 120.
dc.identifier.citedreferenceTorres, R.A. & W. Lewis. 2014. Aging and HIV/AIDS: pathogenetic role of therapeutic side effects. Lab. Invest. 94: 120 – 128.
dc.identifier.citedreferenceEffros, R.B. 2011. Telomere/telomerase dynamics within the human immune system: effect of chronic infection and stress. Exp. Gerontol. 46: 135 – 140.
dc.identifier.citedreferenceXie, Z. et al. 2015. Early telomerase inactivation accelerates aging independently of telomere length. Cell 160: 928 – 939.
dc.identifier.citedreferenceEspert, L. et al. 2015. Autophagy in Mycobacterium tuberculosis and HIV infections. Front. Cell. Infect. Microbiol. 5: 49.
dc.identifier.citedreferenceDinkins, C. et al. 2015. Roles of autophagy in HIV infection. Immunol. Cell Biol. 93: 11 – 17.
dc.identifier.citedreferenceMenke, A. et al. 2015. Prevalence of and trends in diabetes among adults in the United States, 1988–2012. JAMA 314: 1021 – 1029.
dc.identifier.citedreferenceKirkman, M.S. et al. 2012. Diabetes in older adults: a consensus report. J. Am. Geriatr. Soc. 60: 2342 – 2356.
dc.identifier.citedreferenceBooth, G.L. et al. 2006. Relation between age and cardiovascular disease in men and women with diabetes compared with non‐diabetic people: a population‐based retrospective cohort study. Lancet 368: 29 – 36.
dc.identifier.citedreferenceHalter, J.B. et al. 2014. Diabetes and cardiovascular disease in older adults: current status and future directions. Diabetes 63: 2578 – 2589.
dc.identifier.citedreferenceBarzilai, N. & L. Ferrucci. 2012. Insulin resistance and aging: a cause or a protective response ? J. Gerontol. A Biol. Sci. Med. Sci. 67: 1329 – 1331.
dc.identifier.citedreferenceMaedler, K. et al. 2006. Aging correlates with decreased β‐cell proliferative capacity and enhanced sensitivity to apoptosis: a potential role for Fas and pancreatic duodenal homeobox‐1. Diabetes 55: 2455 – 2462.
dc.identifier.citedreferenceRankin, M. & J. Kushner. 2009. Adaptive β‐cell proliferation is severely restricted with advanced age. Diabetes 58: 1365 – 1372.
dc.identifier.citedreferenceTschen, S.‐I. et al. 2009. Age‐dependent decline in β‐cell proliferation restricts the capacity of β‐cell regeneration in mice. Diabetes 58: 1312 – 1320.
dc.identifier.citedreferenceKrishnamurthy, J. et al. 2006. p16 ink4a induces an age‐dependent decline in islet regenerative potential. Nature 443: 453 – 457.
dc.identifier.citedreferenceSaxena, R. et al. 2007. Genome‐wide association analysis identifies loci for type 2 diabetes and triglyceride levels. Science 316: 1331 – 1336.
dc.identifier.citedreferenceScott, L.J. et al. 2007. A genome‐wide association study of type 2 diabetes in Finns detects multiple susceptibility variants. Science 316: 1341 – 1345.
dc.identifier.citedreferenceSteinthorsdottir, V. et al. 2007. A variant in CDKAL1 influences insulin response and risk of type 2 diabetes. Nat. Genet. 39: 770 – 775.
dc.identifier.citedreferenceZeggini, E. et al. 2007. Replication of genome‐wide association signals in UK samples reveals risk loci for type 2 diabetes. Science 316: 1336 – 1341.
dc.owningcollnameInterdisciplinary and Peer-Reviewed


Files in this item

Name:
nyas13297.pdf
Size:
185.5KB
Format:
PDF
View/Open
Name:
nyas13297_am.pdf
Size:
683.0KB
Format:
PDF
View/Open

Show simple item record

Remediation of Harmful Language

The University of Michigan Library aims to describe library materials in a way that respects the people and communities who create, use, and are represented in our collections. Report harmful or offensive language in catalog records, finding aids, or elsewhere in our collections anonymously through our metadata feedback form. More information at Remediation of Harmful Language.

Accessibility

If you are unable to use this file in its current format, please select the Contact Us link and we can modify it to make it more accessible to you.