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Journal articles on the topic 'Ageing-related'

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Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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1

Minton, Kirsty. "Inflammasome-related ageing." Nature Reviews Immunology 17, no. 2 (January 23, 2017): 77. http://dx.doi.org/10.1038/nri.2017.3.

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2

Safarova, G., L. Kozlov, O. Mikhailova, and A. Safarova. "POPULATION AGEING AND AGEING-RELATED POLICIES IN RUSSIA." Innovation in Aging 1, suppl_1 (June 30, 2017): 1090. http://dx.doi.org/10.1093/geroni/igx004.3998.

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3

Jung, Hwa Jin, and Yousin Suh. "Circulating miRNAs in Ageing and Ageing-Related Diseases." Journal of Genetics and Genomics 41, no. 9 (September 2014): 465–72. http://dx.doi.org/10.1016/j.jgg.2014.07.003.

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4

Kuro-o, Makoto. "Ageing-related receptors resolved." Nature 553, no. 7689 (January 2018): 409–10. http://dx.doi.org/10.1038/d41586-017-09032-4.

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5

Muñoz, Gtaciela E., and C. P. Sotomayor. "Ageing-related changes inMycoplasma canadensemembranes." Journal of Applied Bacteriology 72, no. 1 (January 1992): 51–56. http://dx.doi.org/10.1111/j.1365-2672.1992.tb04881.x.

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6

Fu, Zhiling, Jin Zhang, and Yan Zhang. "Role of Molecular Hydrogen in Ageing and Ageing-Related Diseases." Oxidative Medicine and Cellular Longevity 2022 (March 18, 2022): 1–17. http://dx.doi.org/10.1155/2022/2249749.

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Ageing is a physiological process of progressive decline in the organism function over time. It affects every organ in the body and is a significant risk for chronic diseases. Molecular hydrogen has therapeutic and preventive effects on various organs. It has antioxidative properties as it directly neutralizes hydroxyl radicals and reduces peroxynitrite level. It also activates Nrf2 and HO-1, which regulate many antioxidant enzymes and proteasomes. Through its antioxidative effect, hydrogen maintains genomic stability, mitigates cellular senescence, and takes part in histone modification, telomere maintenance, and proteostasis. In addition, hydrogen may prevent inflammation and regulate the nutrient-sensing mTOR system, autophagy, apoptosis, and mitochondria, which are all factors related to ageing. Hydrogen can also be used for prevention and treatment of various ageing-related diseases, such as neurodegenerative disorders, cardiovascular disease, pulmonary disease, diabetes, and cancer. This paper reviews the basic research and recent application of hydrogen in order to support hydrogen use in medicine for ageing prevention and ageing-related disease therapy.
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7

Davies, M. "Comparative ageing and age-related disease." European Geriatric Medicine 5, no. 3 (June 2014): 147–48. http://dx.doi.org/10.1016/j.eurger.2014.03.004.

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8

Bellantuono, Ilaria, and Paul K. Potter. "Modelling ageing and age-related disease." Drug Discovery Today: Disease Models 20 (2016): 27–32. http://dx.doi.org/10.1016/j.ddmod.2017.07.005.

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9

Duchac, Alexander. "Ageing related events at nuclear power plants." Natural Science 05, no. 01 (2013): 31–37. http://dx.doi.org/10.4236/ns.2013.51005.

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10

Navarro-Pardo, Esperanza, Ferran Suay, and Mike Murphy. "Ageing: Not only an age-related issue." Mechanisms of Ageing and Development 199 (October 2021): 111568. http://dx.doi.org/10.1016/j.mad.2021.111568.

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11

Liu, Jun-Ping. "Molecular mechanisms of ageing and related diseases." Clinical and Experimental Pharmacology and Physiology 41, no. 7 (July 2014): 445–58. http://dx.doi.org/10.1111/1440-1681.12247.

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12

Muñoz, Gtaciela E., and C. P. Sotomayor. "Ageing-related changes in Mycoplasma canadense membranes." Journal of Applied Microbiology 72, no. 1 (January 1992): 51–56. http://dx.doi.org/10.1111/j.1365-2672.1992.tb05186.x.

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13

Grundy, Emily. "Ageing: Age-Related Change in Later Life." Population Studies 45, no. 1 (March 1991): 133–56. http://dx.doi.org/10.1080/0032472031000145936.

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14

Koch, Melissa, Paul Stolee, Maggie MacNeil, Jacobi Elliott, Plinio Morita, Ayse Kuspinar, and Don Juzwishin. "Innovation processes for ageing-related health technologies." Healthcare Management Forum 34, no. 1 (July 8, 2020): 34–42. http://dx.doi.org/10.1177/0840470420936715.

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Innovative technologies offer potential benefits for the health and care needs of an ageing population, but the processes by which these innovations are developed and implemented are not well understood. As part of a Canadian research network focused on ageing and technology, we explored how technologies currently being developed to support older adults and their caregivers fare through the processes of innovation. We conducted a multiple case study focused on development of four technology products. Interviews were conducted with project members (n = 8) during site visits to the locations of the four cases, as well as with other key informants (n = 12). Directed coding, guided by the Accelerating Diffusion of Proven Technologies for Older Adults (ADOPT) model was used to analyse the data. Findings illustrate the complexities of innovation processes, including the challenges in developing a business case as well as benefits of a collaborative network.
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15

Grundy, Emily. "Ageing: Age-Related Change in Later Life." Population Studies 45, sup1 (January 1991): 133–56. http://dx.doi.org/10.1080/14774747.1991.11878503.

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16

Algarni, F. S., D. P. Gross, A. Senthilselvan, and M. C. Battie. "Ageing workers with work-related musculoskeletal injuries." Occupational Medicine 65, no. 3 (March 10, 2015): 229–37. http://dx.doi.org/10.1093/occmed/kqu213.

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17

Krisko, Anita, and Miroslav Radman. "Protein damage, ageing and age-related diseases." Open Biology 9, no. 3 (March 2019): 180249. http://dx.doi.org/10.1098/rsob.180249.

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Ageing is considered as a snowballing phenotype of the accumulation of damaged dysfunctional or toxic proteins and silent mutations (polymorphisms) that sensitize relevant proteins to oxidative damage as inborn predispositions to age-related diseases. Ageing is not a disease, but it causes (or shares common cause with) age-related diseases as suggested by similar slopes of age-related increase in the incidence of diseases and death. Studies of robust and more standard species revealed that dysfunctional oxidatively damaged proteins are the root cause of radiation-induced morbidity and mortality. Oxidized proteins accumulate with age and cause reversible ageing-like phenotypes with some irreversible consequences (e.g. mutations). Here, we observe in yeast that aggregation rate of damaged proteins follows the Gompertz law of mortality and review arguments for a causal relationship between oxidative protein damage, ageing and disease. Aerobes evolved proteomes remarkably resistant to oxidative damage, but imperfectly folded proteins become sensitive to oxidation. We show that α-synuclein mutations that predispose to early-onset Parkinson's disease bestow an increased intrinsic sensitivity of α-synuclein to in vitro oxidation. Considering how initially silent protein polymorphism becomes phenotypic while causing age-related diseases and how protein damage leads to genome alterations inspires a vision of predictive diagnostic, prognostic, prevention and treatment of degenerative diseases.
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18

Kanigur Sultuybek, Gönül, Tugba Soydas, and Guven Yenmis. "NF‐κB as the mediator of metformin's effect on ageing and ageing‐related diseases." Clinical and Experimental Pharmacology and Physiology 46, no. 5 (March 12, 2019): 413–22. http://dx.doi.org/10.1111/1440-1681.13073.

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19

Rossiello, Francesca, Diana Jurk, João F. Passos, and Fabrizio d’Adda di Fagagna. "Telomere dysfunction in ageing and age-related diseases." Nature Cell Biology 24, no. 2 (February 2022): 135–47. http://dx.doi.org/10.1038/s41556-022-00842-x.

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20

Palla, Gergely, Péter Pollner, Judit Börcsök, András Major, Béla Molnár, and István Csabai. "Hierarchy and control of ageing-related methylation networks." PLOS Computational Biology 17, no. 9 (September 17, 2021): e1009327. http://dx.doi.org/10.1371/journal.pcbi.1009327.

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DNA methylation provides one of the most widely studied biomarkers of ageing. Since the methylation of CpG dinucleotides function as switches in cellular mechanisms, it is plausible to assume that by proper adjustment of these switches age may be tuned. Though, adjusting hundreds of CpG methylation levels coherently may never be feasible and changing just a few positions may lead to biologically unstable state. A prominent example of methylation-based age estimators is provided by Horvath’s clock, based on 353 CpG dinucleotides, showing a high correlation (not necessarily causation) with chronological age across multiple tissue types. On this small subset of CpG dinucleotides we demonstrate how the adjustment of one methylation level leads to a cascade of changes at other sites. Among the studied subset, we locate the most important CpGs (and related genes) that may have a large influence on the rest of the sub-system. According to our analysis, the structure of this network is way more hierarchical compared to what one would expect based on ensembles of uncorrelated connections. Therefore, only a handful of CpGs is enough to modify the system towards a desired state. When propagation of the change over the network is taken into account, the resulting modification in the predicted age can be significantly larger compared to the effect of isolated CpG perturbations. By adjusting the most influential single CpG site and following the propagation of methylation level changes we can reach up to 5.74 years in virtual age reduction, significantly larger than without taking into account of the network control. Extending our approach to the whole methylation network may identify key nodes that have controller role in the ageing process.
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21

Waters, M. "Dental Materials in Vivo, Ageing and Related Phenomena." British Dental Journal 195, no. 12 (December 2003): 722. http://dx.doi.org/10.1038/sj.bdj.4810850.

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22

Curcio, Christine A. "Photoreceptor topography in ageing and age-related maculopathy." Eye 15, no. 3 (May 2001): 376–83. http://dx.doi.org/10.1038/eye.2001.140.

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23

Ewa, Sikora. "Ageing and age-related diseases – the common denominator?" Pharmacological Reports 61, no. 6 (November 2009): 1233. http://dx.doi.org/10.1016/s1734-1140(09)70206-3.

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24

Vaiserman, Alexander, Alexander Koliada, Alina Zayachkivska, and Oleh Lushchak. "Curcumin: A therapeutic potential in ageing-related disorders." PharmaNutrition 14 (December 2020): 100226. http://dx.doi.org/10.1016/j.phanu.2020.100226.

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25

Eleftheriou, Christos S., Nikos B. Trakas, and Socrates J. Tzartos. "Cellular ageing related proteins secreted by human fibroblasts." Mutation Research/DNAging 256, no. 2-6 (March 1991): 127–38. http://dx.doi.org/10.1016/0921-8734(91)90006-w.

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26

Bürkle, Alexander, Graziella Caselli, Claudio Franceschi, Erminia Mariani, Paolo Sansoni, Angela Santoni, Giancarlo Vecchio, Jacek M. Witkowski, and Calogero Caruso. "Pathophysiology of ageing, longevity and age related diseases." Immunity & Ageing 4, no. 1 (2007): 4. http://dx.doi.org/10.1186/1742-4933-4-4.

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27

Hess, Thomas M. "Ageing-related influences on personal need for structure." International Journal of Behavioral Development 25, no. 6 (November 2001): 482–90. http://dx.doi.org/10.1080/01650250042000429.

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The need for structure construct was examined in relation to adult age using the Personal Need for Structure scale (PNS; M.M. Thompson, M.E. Naccarato, & K. Parker, 1989). The results of a series of confirmatory factor analyses indicated that the two intercorrelated-factor structure of the PNS scale held up well across individuals aged 21 to 85, validating its use for the examination of ageing effects. Structural equation modelling analyses found that ageing was associated with lower levels of physical health and cognitive skill, which in turn were related to higher PNS scores. It was also found, however, that the impact of reductions in these resources on need for structure were counteracted by high levels of social activity and emotional health. The argument is made that ageing-related changes in personal resources impact everyday behaviour through changes in motivation, such as need for structure.
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28

Latorre, Eva, and Lorna W. Harries. "Splicing regulatory factors, ageing and age-related disease." Ageing Research Reviews 36 (July 2017): 165–70. http://dx.doi.org/10.1016/j.arr.2017.04.004.

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29

Sostres, Carlos, Carla Gargallo, and Angel Lanas. "Drug-related damage of the ageing gastrointestinal tract." Best Practice & Research Clinical Gastroenterology 23, no. 6 (December 2009): 849–60. http://dx.doi.org/10.1016/j.bpg.2009.10.006.

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30

Stevanovic, Milena, Andrijana Lazic, Marija Schwirtlich, and Danijela Stanisavljevic Ninkovic. "The Role of SOX Transcription Factors in Ageing and Age-Related Diseases." International Journal of Molecular Sciences 24, no. 1 (January 3, 2023): 851. http://dx.doi.org/10.3390/ijms24010851.

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The quest for eternal youth and immortality is as old as humankind. Ageing is an inevitable physiological process accompanied by many functional declines that are driving factors for age-related diseases. Stem cell exhaustion is one of the major hallmarks of ageing. The SOX transcription factors play well-known roles in self-renewal and differentiation of both embryonic and adult stem cells. As a consequence of ageing, the repertoire of adult stem cells present in various organs steadily declines, and their dysfunction/death could lead to reduced regenerative potential and development of age-related diseases. Thus, restoring the function of aged stem cells, inducing their regenerative potential, and slowing down the ageing process are critical for improving the health span and, consequently, the lifespan of humans. Reprograming factors, including SOX family members, emerge as crucial players in rejuvenation. This review focuses on the roles of SOX transcription factors in stem cell exhaustion and age-related diseases, including neurodegenerative diseases, visual deterioration, chronic obstructive pulmonary disease, osteoporosis, and age-related cancers. A better understanding of the molecular mechanisms of ageing and the roles of SOX transcription factors in this process could open new avenues for developing novel strategies that will delay ageing and prevent age-related diseases.
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31

Carroll, Bernadette, Graeme Hewitt, and Viktor I. Korolchuk. "Autophagy and ageing: implications for age-related neurodegenerative diseases." Essays in Biochemistry 55 (September 27, 2013): 119–31. http://dx.doi.org/10.1042/bse0550119.

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Autophagy is a process of lysosome-dependent intracellular degradation that participates in the liberation of resources including amino acids and energy to maintain homoeostasis. Autophagy is particularly important in stress conditions such as nutrient starvation and any perturbation in the ability of the cell to activate or regulate autophagy can lead to cellular dysfunction and disease. An area of intense research interest is the role and indeed the fate of autophagy during cellular and organismal ageing. Age-related disorders are associated with increased cellular stress and assault including DNA damage, reduced energy availability, protein aggregation and accumulation of damaged organelles. A reduction in autophagy activity has been observed in a number of ageing models and its up-regulation via pharmacological and genetic methods can alleviate age-related pathologies. In particular, autophagy induction can enhance clearance of toxic intracellular waste associated with neurodegenerative diseases and has been comprehensively demonstrated to improve lifespan in yeast, worms, flies, rodents and primates. The situation, however, has been complicated by the identification that autophagy up-regulation can also occur during ageing. Indeed, in certain situations, reduced autophagosome induction may actually provide benefits to ageing cells. Future studies will undoubtedly improve our understanding of exactly how the multiple signals that are integrated to control appropriate autophagy activity change during ageing, what affect this has on autophagy and to what extent autophagy contributes to age-associated pathologies. Identification of mechanisms that influence a healthy lifespan is of economic, medical and social importance in our ‘ageing’ world.
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32

Walters, Hannah, and Lynne Cox. "mTORC Inhibitors as Broad-Spectrum Therapeutics for Age-Related Diseases." International Journal of Molecular Sciences 19, no. 8 (August 8, 2018): 2325. http://dx.doi.org/10.3390/ijms19082325.

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Chronological age represents the greatest risk factor for many life-threatening diseases, including neurodegeneration, cancer, and cardiovascular disease; ageing also increases susceptibility to infectious disease. Current efforts to tackle individual diseases may have little impact on the overall healthspan of older individuals, who would still be vulnerable to other age-related pathologies. However, recent progress in ageing research has highlighted the accumulation of senescent cells with chronological age as a probable underlying cause of pathological ageing. Cellular senescence is an essentially irreversible proliferation arrest mechanism that has important roles in development, wound healing, and preventing cancer, but it may limit tissue function and cause widespread inflammation with age. The serine/threonine kinase mTOR (mechanistic target of rapamycin) is a regulatory nexus that is heavily implicated in both ageing and senescence. Excitingly, a growing body of research has highlighted rapamycin and other mTOR inhibitors as promising treatments for a broad spectrum of age-related pathologies, including neurodegeneration, cancer, immunosenescence, osteoporosis, rheumatoid arthritis, age-related blindness, diabetic nephropathy, muscular dystrophy, and cardiovascular disease. In this review, we assess the use of mTOR inhibitors to treat age-related pathologies, discuss possible molecular mechanisms of action where evidence is available, and consider strategies to minimize undesirable side effects. We also emphasize the urgent need for reliable, non-invasive biomarkers of senescence and biological ageing to better monitor the efficacy of any healthy ageing therapy.
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33

Zhong, Hao, Bin Liao, Xiao Dong Wu, Ling Fei Cao, and Paul A. Rometsch. "Development of Al-Mg-Si-(Cu) Alloys for Automotive Body Panels and the Related Ageing Behaviours." Materials Science Forum 879 (November 2016): 279–83. http://dx.doi.org/10.4028/www.scientific.net/msf.879.279.

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In this work, Al-Mg-Si-Cu alloys for automotive body panels were designed and the related ageing behaviours were discussed in detail to help understand natural ageing and pre-ageing, as well as their influence on the subsequent paint-bake response. The clustering behavior of these Al-Mg-Si-Cu alloys in different ageing conditions was investigated by hardness / yield strength and electrical conductivity testing. The microstructure was investigated by using Electron Backscattered Diffraction (EBSD) technique, along with Scanning Electron Microscopy with Backscattered Electron Detector (BSE). The results show that the paint bake response is strongly influenced by the pre-ageing and natural ageing conditions. Both alloys show serrated yielding in a short natural ageing condition. Immediate high-temperature pre-ageing treatments were found to give a promising hardening response during the subsequent artificial ageing/ paint baking at 170oC.
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34

Bucaciuc Mracica, Teodora, Anca Anghel, Catalin Florentin Ion, Corina Violeta Moraru, Robi Tacutu, and Gligor Andrei Lazar. "MetaboAge DB: a repository of known ageing-related changes in the human metabolome." Biogerontology 21, no. 6 (August 12, 2020): 763–71. http://dx.doi.org/10.1007/s10522-020-09892-w.

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Abstract Accumulating metabolomics data is starting to become extremely useful in understanding the ageing process, by providing a snapshot into the metabolic state of tissues and organs, at different ages. Molecular studies of such metabolic variations during “normal” ageing can hence guide lifestyle changes and/or medical interventions aimed at improving healthspan and perhaps even lifespan. In this work, we present MetaboAge, a freely accessible database which hosts ageing-related metabolite changes, occurring in healthy individuals. Data is automatically filtered and then manually curated from scientific articles reporting statistically significant associations of human metabolite variations or correlations with ageing. Up to date, MetaboAge contains 408 metabolites annotated with their biological and chemical information, and more than 1515 ageing-related variations, graphically represented on the website grouped by validation methods, sex and age-groups. The MetaboAge database aims to continually structure the expanding information from the field of metabolomics in relation to ageing, thus making it more accessible for further research in gerontology.
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35

Chmielewski, Piotr Paweł. "Human ageing as a dynamic, emergent and malleable process: from disease-oriented to health-oriented approaches." Biogerontology 21, no. 1 (October 8, 2019): 125–30. http://dx.doi.org/10.1007/s10522-019-09839-w.

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Abstract Over the decades, biogerontology has matured as a scientific discipline. Currently, a number of theoretical frameworks are available to researchers when interpreting empirical data. Despite the great progress that has been made, a comprehensive understanding of biological processes that shape ageing is lacking. Senescence is a dynamic, plastic and highly complex metaphenomenon whose aetiology remains unclear. The paucity of information notwithstanding, some researchers promote ‘anti-ageing’ drugs and formulae every now and again. The rationale behind this concept is that ageing can be reduced to a mixture of biochemical reactions. Furthermore, the distinction between ageing and disease has been questioned on the grounds that ageing is the root of age-related diseases. It has been claimed that disease-oriented approaches can help delay ageing and prevent age-related diseases. Although these methods seem incongruous from an evolutionary standpoint, they become popular amongst the public. Moreover, if ageing is classified as a disease, this situation is likely to be exacerbated. Therefore, it is important to recognise the limitations of these reductionist and disease-oriented approaches. Only holistic and evidence-based strategies might be useful in slowing down ageing and preventing age-related diseases in the future.
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36

Dai, Lu, Leon Schurgers, Paul G. Shiels, and Peter Stenvinkel. "A biomimetic natural sciences approach to understanding the mechanisms of ageing in burden of lifestyle diseases." Clinical Science 135, no. 10 (May 2021): 1251–72. http://dx.doi.org/10.1042/cs20201452.

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Abstract The worldwide landscape of an ageing population and age-related disease brings with it huge socio-economic and public healthcare concerns across nations. Correspondingly, monumental human and financial resources have been invested in biomedical research, with a mission to decode the mechanisms of ageing and how these contribute to age-related disease. Multiple hallmarks of ageing have been identified that are common across taxa, highlighting their fundamental importance. These include dysregulated mitochondrial metabolism and telomeres biology, epigenetic modifications, cell–matrix interactions, proteostasis, dysregulated nutrient sensing, stem cell exhaustion, inflammageing and immuno-senescence. While our understanding of the molecular basis of ageing is improving, it remains a complex and multifactorial process that remains to be fully understood. A key aspect of the shortfall in our understanding of the ageing process lies in translating data from standard animal models to humans. Consequently, we suggest that a ‘biomimetic’ and comparative approach, integrating knowledge from species in the wild, as opposed to inbred genetically homogenous laboratory animals, can provide powerful insights into human ageing processes. Here we discuss some particularities and comparative patterns among several species from the animal kingdom, endowed with longevity or short lifespans and unique metabolic profiles that could be potentially exploited to the understanding of ageing and age-related diseases. Based upon lessons from nature, we also highlight several avenues for renewed focus in the pathophysiology of ageing and age-related disease (i.e. diet-microbiome-health axis, oxidative protein damage, adaptive homoeostasis and planetary health). We propose that a biomimetic alliance with collaborative research from different disciplines can improve our understanding of ageing and age-related diseases with long-term sustainable utility.
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37

Sikora, Ewa, Anna Bielak-Zmijewska, and Grazyna Mosieniak. "Cellular Senescence in Ageing, Age-Related Disease and Longevity." Current Vascular Pharmacology 12, no. 5 (December 18, 2013): 698–706. http://dx.doi.org/10.2174/1570161111666131219094045.

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38

Zglinicki, T., and C. Martin-Ruiz. "Telomeres as Biomarkers for Ageing and Age-Related Diseases." Current Molecular Medicine 5, no. 2 (March 1, 2005): 197–203. http://dx.doi.org/10.2174/1566524053586545.

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39

Melo, Laércio Almeida de, Lidiane Maria de Brito Macedo Ferreira, Marquiony Marques dos Santos, and Kenio Costa de Lima. "Socioeconomic, regional and demographic factors related to population ageing." Revista Brasileira de Geriatria e Gerontologia 20, no. 4 (August 2017): 493–501. http://dx.doi.org/10.1590/1981-22562017020.170004.

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Abstract Objective: the present study aims to investigate the association between population ageing in municipal regions in the state of Rio Grande do Norte, and socioeconomic, demographic and regional factors. Method: an ecological study that used municipal regions of the state of Rio Grande do Norte as a unit of analysis was carried out. Data collection was conducted through databases from the Brazilian Institute of Geography and Statistics, the Institute of Applied Economic Research and the Atlas of Human Development. The factor of Increased Age was created based on factor analysis, which was related to socioeconomic, demographic and regional variables. The chi-squared test with a significance level of 5% was used in addition to the Hosmer and Lemeshow technique for logistic regression. Result: it was found that municipal regions in the Central mesoregion have an older/ageing population, while those with intermediate populations have the oldest individuals. Furthermore, it was found that municipal regions with unequal income distribution and higher levels of education have an older population. Conclusion: it can be concluded that municipal regions classified as older/more aged were associated with the mesoregion to which the municipal region belongs; and those with intermediate population size were associated with favorable educational levels and unequal income distribution.
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40

I. S. Rattan, Suresh. "Biological Basis of Ageing, Age-related Diseases and Interventions." Current Pharmacogenomics and Personalized Medicine 13, no. 2 (May 12, 2016): 90–92. http://dx.doi.org/10.2174/1875692114999160502130603.

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41

Brissaud, Florent, Cyrille Folleau, and Benoit de Cournuaud. "Reliability and availability models for ageing safety-related systems." Journal of Loss Prevention in the Process Industries 75 (February 2022): 104712. http://dx.doi.org/10.1016/j.jlp.2021.104712.

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42

Tiwari, Mamta, Anurag Pandey, Poonam Chaudhari, Pawankumar Godatwar, and Arvind Kumar Gupta. "AYURVEDIC APPROACH FOR MANAGEMENT OF AGEING AND RELATED DISORDER." International Journal of Research in Ayurveda and Pharmacy 4, no. 1 (February 27, 2013): 27–30. http://dx.doi.org/10.7897/2277-4343.04117.

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43

Pijacka, Wioletta, Jaap A. Joles, Chantal Tilburgs, Bethan Clifford, Simon Langley-Evans, and Sarah McMullen. "1076 SEX-SPECIFIC MECHANISMS OF AGEING-RELATED RENAL INJURY." Journal of Hypertension 30 (September 2012): e313. http://dx.doi.org/10.1097/01.hjh.0000420533.59788.53.

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44

Tuohy, Dympna. "176Older Women’s Experiences of Ageing and Health Related Issues." Age and Ageing 46, Suppl_3 (September 2017): iii1—iii12. http://dx.doi.org/10.1093/ageing/afx145.33.

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45

Vasto, Sonya, Giuseppina Candore, Carmela Rita Balistreri, Marco Caruso, Giuseppina Colonna-Romano, Maria Paola Grimaldi, Florinda Listi, Domenico Nuzzo, Domenico Lio, and Calogero Caruso. "Inflammatory networks in ageing, age-related diseases and longevity." Mechanisms of Ageing and Development 128, no. 1 (January 2007): 83–91. http://dx.doi.org/10.1016/j.mad.2006.11.015.

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Wilson, David M., Vilhelm A. Bohr, and Peter J. McKinnon. "DNA damage, DNA repair, ageing and age-related disease." Mechanisms of Ageing and Development 129, no. 7-8 (July 2008): 349–52. http://dx.doi.org/10.1016/j.mad.2008.02.013.

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Ferri, Cleusa P. "Population Ageing in Latin America: Dementia and Related Disorders." Revista Brasileira de Psiquiatria 34, no. 4 (December 2012): 371–74. http://dx.doi.org/10.1016/j.rbp.2012.08.005.

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Timmons, James A. "Molecular Diagnostics of Ageing and Tackling Age-related Disease." Trends in Pharmacological Sciences 38, no. 1 (January 2017): 67–80. http://dx.doi.org/10.1016/j.tips.2016.11.005.

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Šaršounová, Zuzana. "The Inconveniences Related to Accelerated Thermal Ageing of Cables." Transportation Research Procedia 40 (2019): 90–95. http://dx.doi.org/10.1016/j.trpro.2019.07.015.

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Wei, Jie, Guokun Zhang, Xiao Zhang, Dexin Xu, Jun Gao, and Jungang Fan. "Anthocyanins Delay Ageing-Related Degenerative Changes in the Liver." Plant Foods for Human Nutrition 72, no. 4 (October 26, 2017): 425–31. http://dx.doi.org/10.1007/s11130-017-0644-z.

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