Aging, inflammation and the environment
TLDR
It is pointed out that longitudinal studies with a life course approach are needed to gain further mechanistic insight on the processes that lead to functional decline with aging, and the role played by inflammation and environmental challenges.About:
This article is published in Experimental Gerontology.The article was published on 2018-05-01 and is currently open access. It has received 238 citations till now. The article focuses on the topics: Cognitive decline.read more
Citations
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Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty
Luigi Ferrucci,Elisa Fabbri +1 more
TL;DR: Whether therapies to modulate inflammageing can reduce the age-related decline in health is discussed, and the hypothesis that inflammation affects CVD, multimorbidity, and frailty is supported by mechanistic studies but requires confirmation in humans.
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Ageing as a risk factor for neurodegenerative disease.
Yujun Hou,Xiuli Dan,Mansi Babbar,Yong Wei,Steen G. Hasselbalch,Deborah L. Croteau,Vilhelm A. Bohr,Vilhelm A. Bohr +7 more
TL;DR: Hallmarks of ageing — genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication — correlate with susceptibility to neurodegenerative disease.
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Facing up to the global challenges of ageing.
TL;DR: Interventions, including changes to lifestyle and medical innovations, are needed to prevent disease and increase late-life health in humans.
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Measuring biological aging in humans: A quest.
Luigi Ferrucci,Marta Gonzalez-Freire,Elisa Fabbri,Elisa Fabbri,Eleanor M. Simonsick,Toshiko Tanaka,Zenobia A. Moore,Shabnam Salimi,Felipe Sierra,Rafael de Cabo +9 more
TL;DR: Current research focuses on measuring the pace of aging to identify individuals who are “aging faster” to test and develop interventions that could prevent or delay the progression of multimorbidity and disability with aging.
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Redefining Chronic Inflammation in Aging and Age-Related Diseases: Proposal of the Senoinflammation Concept.
Hae Young Chung,Dae Hyun Kim,Eun Kyeong Lee,Ki Wung Chung,Sangwoon Chung,Bonggi Lee,Arnold Y. Seo,Jae Heun Chung,Young Suk Jung,Eunok Im,Jaewon Lee,Nam Deuk Kim,Yeon Ja Choi,Dong Soon Im,Byung Pal Yu +14 more
TL;DR: This review discusses newly emerging data on multi-phase inflammatory networks and proinflammatory pathways as they relate to aging and provides a schema highlighting the important and ever-increasing roles of proinflammatory senescence-associated secretome, inflammasome, ER stress, TLRs, and microRNAs, which support the senoinflammation concept.
References
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The Hallmarks of Aging
TL;DR: Nine tentative hallmarks that represent common denominators of aging in different organisms are enumerated, with special emphasis on mammalian aging, to identify pharmaceutical targets to improve human health during aging, with minimal side effects.
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The pro- and anti-inflammatory properties of the cytokine interleukin-6
TL;DR: It turns out that regenerative or anti-inflammatory activities of interleukin-6 are mediated by classic signaling whereas pro-inflammatory responses of interLEukin -6 are rather mediated by trans-signaling.
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Chronic Inflammation (Inflammaging) and Its Potential Contribution to Age-Associated Diseases
TL;DR: The session on inflammation of the Advances in Gerosciences meeting held at the National Institutes of Health/National Institute on Aging in Bethesda on October 30 and 31, 2013 was aimed at defining these important unanswered questions about inflammaging.
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Longitudinal Effects of Aging on Serum Total and Free Testosterone Levels in Healthy Men
TL;DR: Observations of health factor independent, age-related longitudinal decreases in T and free T, resulting in a high frequency of hypogonadal values, suggest that further investigation of T replacement in aged men, perhaps targeted to those with the lowest serum T concentrations, are justified.
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Premature ageing in mice expressing defective mitochondrial DNA polymerase
Aleksandra Trifunovic,Anna Wredenberg,Maria Falkenberg,Johannes N. Spelbrink,Anja T. Rovio,Carl E.G. Bruder,Mohammad Bohlooly-Y,Sebastian Gidlöf,Anders Oldfors,Rolf Wibom,Jan Törnell,Howard T. Jacobs,Nils-Göran Larsson +12 more
TL;DR: The results provide a causative link between mtDNA mutations and ageing phenotypes in mammals by creating homozygous knock-in mice that express a proof-reading-deficient version of PolgA, the nucleus-encoded catalytic subunit of mtDNA polymerase.