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Journal articles on the topic 'Ageing Clock'

Author: Grafiati

Published: 23 August 2023

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1

Guevara, Elaine E., Richard R. Lawler, Nicky Staes, Cassandra M. White, Chet C. Sherwood, John J. Ely, William D. Hopkins, and Brenda J. Bradley. "Age-associated epigenetic change in chimpanzees and humans." Philosophical Transactions of the Royal Society B: Biological Sciences 375, no. 1811 (September 21, 2020): 20190616. http://dx.doi.org/10.1098/rstb.2019.0616.

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Methylation levels have been shown to change with age at sites across the human genome. Change at some of these sites is so consistent across individuals that it can be used as an ‘epigenetic clock’ to predict an individual's chronological age to within a few years. Here, we examined how the pattern of epigenetic ageing in chimpanzees compares with humans. We profiled genome-wide blood methylation levels by microarray for 113 samples from 83 chimpanzees aged 1–58 years (26 chimpanzees were sampled at multiple ages during their lifespan). Many sites (greater than 65 000) showed significant change in methylation with age and around one-third (32%) of these overlap with sites showing significant age-related change in humans. At over 80% of sites showing age-related change in both species, chimpanzees displayed a significantly faster rate of age-related change in methylation than humans. We also built a chimpanzee-specific epigenetic clock that predicted age in our test dataset with a median absolute deviation from known age of only 2.4 years. However, our chimpanzee clock showed little overlap with previously constructed human clocks. Methylation at CpGs comprising our chimpanzee clock showed moderate heritability. Although the use of a human microarray for profiling chimpanzees biases our results towards regions with shared genomic sequence between the species, nevertheless, our results indicate that there is considerable conservation in epigenetic ageing between chimpanzees and humans, but also substantial divergence in both rate and genomic distribution of ageing-associated sites. This article is part of the theme issue ‘Evolution of the primate ageing process'.

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O’Brien, Yvonne, and Mary B. Wingfield. "Reproductive ageing—turning back the clock?" Irish Journal of Medical Science (1971 -) 188, no. 1 (March 2, 2018): 161–67. http://dx.doi.org/10.1007/s11845-018-1769-2.

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3

Gibbs, W. Wayt. "Biomarkers and ageing: The clock-watcher." Nature 508, no. 7495 (April 2014): 168–70. http://dx.doi.org/10.1038/508168a.

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AGRELL, BERIT, and OVE DEHLIN. "The clock-drawing test." Age and Ageing 27, no. 3 (1998): 399–403. http://dx.doi.org/10.1093/ageing/27.3.399.

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5

Agrell, B., and O. Dehlin. "The clock-drawing test." Age and Ageing 41, suppl 3 (November 1, 2012): iii41—iii45. http://dx.doi.org/10.1093/ageing/afs149.

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6

Halmos, Tamás, and Ilona Suba. "Physiological and pathophysiological role of the circadian clock system." Orvosi Hetilap 153, no. 35 (September 2012): 1370–79. http://dx.doi.org/10.1556/oh.2012.29436.

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It has been well known for ages that in living organisms the rhythmicity of biological processes is linked to the ~ 24-hour light–dark cycle. However, the exact function of the circadian clock system has been explored only in the past decades. It came to light that the photosensitive primary “master clock” is situated in the suprachiasmatic photosensitive nuclei of the special hypothalamic region, and that it is working according to ~24-hour changes of light and darkness. The master clock sends its messages to the peripheral “slave clocks”. In many organs, like pancreatic β-cells, the slave clocks have autonomic functions as well. Two essential components of the clock system are proteins encoded by the CLOCK and BMAL1 genes. CLOCK genes are in interaction with endonuclear receptors such as peroxisoma-proliferator activated receptors and Rev-erb-α, as well as with the hypothalamic-pituitary-adrenal axis, regulating the adaptation to stressors, energy supply, metabolic processes and cardiovascular system. Melatonin, the product of corpus pineale has a significant role in the functions of the clock system. The detailed discovery of the clock system has changed our previous knowledge about the development of many diseases. The most explored fields are hypertension, cardiovascular diseases, metabolic processes, mental disorders, cancers, sleep apnoe and joint disorders. CLOCK genes influence ageing as well. The recognition of the periodicity of biological processes makes the optimal dosing of certain drugs feasible. The more detailed discovery of the interaction of the clock system might further improve treatment and prevention of many disorders. Orv. Hetil., 2012, 153, 1370–1379.

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El-Houni, Zeyad, Alexander Eckersley, Mike Bell, Eleanor Bradley, Victoria Newton, Michael Sherratt, and Qing Jun Meng. "P12 Tetrapeptide matrikines synchronize circadian rhythms and promote proliferation in human skin cells." British Journal of Dermatology 189, no. 1 (July 2023): e18-e18. http://dx.doi.org/10.1093/bjd/ljad174.033.

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Abstract Circadian rhythms are intrinsically generated 24 h rhythms that play a vital role in enabling the skin to adapt temporally to various external stimuli. These include ultraviolet radiation, physical trauma and water loss. At the molecular level, circadian clocks consist of various clock genes and proteins, including Per2/Cry1 and Bmal1/Clock, forming autoregulatory feedback loops. Although these rhythms are known to be impaired in ageing skin, there are limited therapeutic options to restore skin cell circadian function. As small peptides with homology to amino acid sequences found in extracellular matrix proteins (matrikines) can beneficially affect clinical and histological markers of skin ageing, in this study we characterized the ability of two novel tetrapeptides to influence the cellular circadian clocks of skin cells. HaCat keratinocytes transduced with a human Per2::luc promoter-driven reporter were used to monitor the effects of two synthetically generated peptides, GPKG and LSVD, on the cells’ intrinsic circadian clock. Following administration of these peptides at various concentrations (4–16 ppm), the oscillatory activity of the cells was amplified up to twofold vs. the vehicle control. LSVD was found to induce Per2::luc promoter activity significantly (P < 0.05). In addition to enhancing circadian rhythmicity, both peptides were assessed for their proliferative effect (by Incucyte imaging and MTT cell proliferation assays). At the higher concentrations tested, both GPKG and LSVD significantly increased proliferation in HaCat keratinocytes (P < 0.05). In conclusion, these peptides have been found to be highly effective in synchronizing the circadian clock in skin cells, leading to changes in their behaviour. This implies that these new peptides may have beneficial effects on skin cells, in part, by improving their circadian function. Given the findings of clock disruption in a number of diseases, as well as with age, identifying compounds that can reset the clock in skin cells is an important approach to developing treatments that can improve the functioning of cutaneous physiological processes that are under circadian control. Funding sources: this study was funded by the No. 7 Beauty Company.

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8

FRIEDMAN, PAUL J. "Clock Drawing in Acute Stroke." Age and Ageing 20, no. 2 (1991): 140–45. http://dx.doi.org/10.1093/ageing/20.2.140.

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9

Liu, Zuyun, and Yimin Zhu. "Epigenetic clock: a promising mirror of ageing." Lancet Healthy Longevity 2, no. 6 (June 2021): e304-e305. http://dx.doi.org/10.1016/s2666-7568(21)00098-2.

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10

Kloeden, P. E., R. Rössler, and O. E. Rössler. "Does a Centralized Clock for Ageing Exist?" Gerontology 36, no. 5-6 (1990): 314–22. http://dx.doi.org/10.1159/000213216.

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11

Raj, Kenneth, and Steve Horvath. "Current perspectives on the cellular and molecular features of epigenetic ageing." Experimental Biology and Medicine 245, no. 17 (April 10, 2020): 1532–42. http://dx.doi.org/10.1177/1535370220918329.

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It has been noted for quite some time that DNA methylation levels decline with age. The significance of this change remained unknown until it became possible to measure methylation status of specific sites on the DNA. It was observed that while the methylation of some sites does indeed decrease with age, that of others increase or remain unchanged. The application of machine learning methods to these quantitative changes in multiple sites, allowed the generation of a highly accurate estimator of age, called the epigenetic clock. The application of this clock on large human epidemiological data sets revealed that discordance between the predicted (epigenetic age) and chronological age is associated with many age-related pathologies, particularly when the former is greater than the latter. The epigenetic clock clearly captures to some degree, biological features that accompany the ageing process. Despite the ever-increasing scope of pathologies that are found to be associated with accelerated epigenetic ageing, the basic principles that underlie the ticking of the clock remain elusive. Here, we describe the known molecular and cellular attributes of the clock and consider their properties, and proffer opinions as to how they may be connected and what might be the underlying mechanism. Emerging from these considerations is the inescapable view that epigenetic ageing begins from very early moments after the embryonic stem cell stage and continues un-interrupted through the entire life-course. This appears to be a consequence of processes that are necessary for the development of the organism from conception and to maintain it thereafter through homeostasis. Hence, while the speed of ageing can, and is affected by external factors, the essence of the ageing process itself is an integral part of, and the consequence of the development of life. Impact statement The field of epigenetic ageing is relatively new, and the speed of its expansion presents a challenge in keeping abreast with new discoveries and their implications. Several reviews have already addressed the great number of pathologies, health conditions, life-style, and external stressors that are associated with changes to the rate of epigenetic ageing. While these associations highlight and affirm the ability of epigenetic clock to capture biologically meaningful changes associated with age, they do not inform us about the underlying mechanisms. In this very early period since the development of the clock, there have been rather limited experimental research that are aimed at uncovering the mechanism. Hence, the perspective that we proffer is derived from available but nevertheless limited lines of evidence that together provide a seemingly coherent narrative that can be tested. This, we believe would be helpful towards uncovering the workings of the epigenetic clock.

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Zaina, Silvio, Manel Esteller, Isabel Gonçalves, and Gertrud Lund. "Dynamic epigenetic age mosaicism in the human atherosclerotic artery." PLOS ONE 17, no. 6 (June 3, 2022): e0269501. http://dx.doi.org/10.1371/journal.pone.0269501.

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Accelerated epigenetic ageing, a promising marker of disease risk, has been detected in peripheral blood cells of atherosclerotic patients, but evidence in the vascular wall is lacking. Understanding the trends of epigenetic ageing in the atheroma may provide insights into mechanisms of atherogenesis or identify targets for molecular therapy. We surveyed DNA methylation age in two human artery samples: a set of donor-matched, paired atherosclerotic and healthy aortic portions, and a set of carotid artery atheromas. The well-characterized pan-tissue Horvath epigenetic clock was used, together with the Weidner whole-blood-specific clock as validation. For the first time, we document dynamic DNA methylation age mosaicism of the vascular wall that is atherosclerosis-related, switches from acceleration to deceleration with chronological ageing, and is consistent in human aorta and carotid atheroma. At CpG level, the Horvath epigenetic clock showed modest differential methylation between atherosclerotic and healthy aortic portions, weak association with atheroma histological grade and no clear evidence for participation in atherosclerosis-related cellular pathways. Our data suggest caution when assigning a unidirectional DNA methylation age change to the atherosclerotic arterial wall. Also, the results support previous conclusions that epigenetic ageing reflects non-disease-specific cellular alterations.

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Colombini, Barbara, Monica Dinu, Emanuele Murgo, Sofia Lotti, Roberto Tarquini, Francesco Sofi, and Gianluigi Mazzoccoli. "Ageing and Low-Level Chronic Inflammation: The Role of the Biological Clock." Antioxidants 11, no. 11 (November 11, 2022): 2228. http://dx.doi.org/10.3390/antiox11112228.

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Ageing is a multifactorial physiological manifestation that occurs inexorably and gradually in all forms of life. This process is linked to the decay of homeostasis due to the progressive decrease in the reparative and regenerative capacity of tissues and organs, with reduced physiological reserve in response to stress. Ageing is closely related to oxidative damage and involves immunosenescence and tissue impairment or metabolic imbalances that trigger inflammation and inflammasome formation. One of the main ageing-related alterations is the dysregulation of the immune response, which results in chronic low-level, systemic inflammation, termed “inflammaging”. Genetic and epigenetic changes, as well as environmental factors, promote and/or modulate the mechanisms of ageing at the molecular, cellular, organ, and system levels. Most of these mechanisms are characterized by time-dependent patterns of variation driven by the biological clock. In this review, we describe the involvement of ageing-related processes with inflammation in relation to the functioning of the biological clock and the mechanisms operating this intricate interaction.

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Adams, D. D., W. O. Lucas, B. G. Williams, B. B. Berkeley, K. W. Turner, and J. C. Schofield. "A mouse genetic locus with death clock and life clock features." Mechanisms of Ageing and Development 122, no. 2 (February 2001): 173–89. http://dx.doi.org/10.1016/s0047-6374(00)00230-x.

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15

Wijaya, Joan C., Ramin Khanabdali, Harry M. Georgiou, and Bill Kalionis. "Ageing in human parturition: impetus of the gestation clock in the decidua†." Biology of Reproduction 103, no. 4 (June 26, 2020): 695–710. http://dx.doi.org/10.1093/biolre/ioaa113.

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Abstract Despite sharing many common features, the relationship between ageing and parturition remains poorly understood. The decidua is a specialized lining of endometrial tissue, which develops in preparation for pregnancy. The structure and location of the decidua support its role as the physical scaffold for the growing embryo and placenta, and thus, it is vital to sustain pregnancy. Approaching term, the physical support properties of the decidua are naturally weakened to permit parturition. In this review, we hypothesize that the natural weakening of decidual tissue at parturition is promoted by the ageing process. Studies of the ageing-related functional and molecular changes in the decidua at parturition are reviewed and classified using hallmarks of ageing as the framework. The potential roles of decidual mesenchymal stem/stromal cell (DMSC) ageing in labor are also discussed because, although stem cell exhaustion is also a hallmark of ageing, its role in labor is not completely understood. In addition, the potential roles of extracellular vesicles secreted by DMSCs in labor, and their parturition-related miRNAs, are reviewed to gain further insight into this research area. In summary, the literature supports the notion that the decidua ages as the pregnancy progresses, and this may facilitate parturition, suggesting that ageing is the probable impetus of the gestational clocks in the decidua. This conceptual framework was developed to provide a better understanding of the natural ageing process of the decidua during parturition as well as to encourage future studies of the importance of healthy ageing for optimal pregnancy outcomes.

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16

Lowe, Donna, Steve Horvath, and Kenneth Raj. "Epigenetic clock analyses of cellular senescence and ageing." Oncotarget 7, no. 8 (February 14, 2016): 8524–31. http://dx.doi.org/10.18632/oncotarget.7383.

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17

van Hout, H. "Inter-rater reliability of the clock-drawing test." Age and Ageing 28, no. 3 (May 1, 1999): 327–28. http://dx.doi.org/10.1093/ageing/28.3.327.

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18

Kondratova, Anna A., and Roman V. Kondratov. "The circadian clock and pathology of the ageing brain." Nature Reviews Neuroscience 13, no. 5 (March 7, 2012): 325–35. http://dx.doi.org/10.1038/nrn3208.

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19

Hoylaerts, Marc F. "Animal Models of Aging Research." Blood 126, no. 23 (December 3, 2015): SCI—4—SCI—4. http://dx.doi.org/10.1182/blood.v126.23.sci-4.sci-4.

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Ageing is associated with increased hypercoagulability, due to a slow rise of several coagulation factors, factor VIII, fibrinogen and thrombin-antithrombin complexes, markers of fibrinolysis and progressively defective Protein C activation, yet compatible with life at very high age. Mice, naturally aged up to 24 months, likewise show a progressive elevation of coagulation factors, triggering enhanced thrombogenicity during acute injury-induced thrombus formation. To overcome the still gradual natural ageing in mice, several mouse models of premature ageing were characterized, in an effort to allow for more rapid ageing-induced manifestations of natural thrombogenicity. Thus, the Klotho gene, encoding a type-I membrane protein, related to beta-glucosidases underlies degenerative processes, including arteriosclerosis and osteoporosis, observed in chronic renal failure. Mutations within this protein are associated with ageing and bone loss. Defective Klotho gene expression in the mouse accelerates degeneration of multiple age-sensitive traits, whereas its overexpression extends murine life span. The multidomain protein kinases Bub1 and BubR1 are central components of the mitotic checkpoint for spindle assembly (SAC) and self-monitor the eukaryotic cell cycle. Despite their amino acid sequence conservation and similar domain organization, BUB1 and BUBR1 perform different functions in the SAC. Various p53 mutant mice with a BubR1 insufficiency display early onset of ageing-associated phenotypes, whereas the BubR1H/H mouse is characterized by simultaneous vascular defects. Progerin mouse models show phenotypes ranging from being largely restricted to the vascular system to models with a broader progeria-like phenotype (severe growth retardation, fragile bones, alopecia, skin defects and reduced viability). The CLOCK transcription factor is a key component of the molecular circadian clock within pacemaker neurons of the hypothalamic suprachiasmatic nucleus, but the most widespread mouse model of premature ageing consists of a circadian clock gene mutant mouse, the brain and muscle arnt like protein-1 (Bmal1). Mice deficient in this circadian transcription factor have impaired circadian behavior and demonstrate loss of rhythmicity in the expression of target genes. Bmal1-/- mice have reduced lifespan (maximum around 50 weeks) and display symptoms of premature ageing, including sarcopenia, cataracts, less subcutaneous fat, organ shrinkage, and others. Their early ageing phenotype correlates with increased levels of reactive oxygen species in some but not all tissues. These findings and data on CLOCK/BMAL1-dependent control of stress responses were evoked to explain the early onset of age-related pathologies in the absence of Bmal1. Their reduced lifespan is still long enough to enable intervention studies on heart function, renal integrity, tissue degeneration and thrombogenicity, including diet feeding and fat composition studies, analysis of the progressive prothrombotic state and anti-oxidant intervention studies for longevity assessment. Combined though, all these studies raise cautiousness, because no single mouse model can phenocopy human ageing perfectly: even when murine alopecia signals premature ageing, p16INK-4A measurements via qPCR do not always rise, as such is the case during natural mouse ageing and some organs deteriorate more slowly than others (e.g. vascular media and smooth muscle cells), coupled to different exposure/sensitivity to oxidative stress or environmental factors. Also, the major advantage of most accelerated ageing models, i.e. their rapid onset of ageing may insufficiently favor several risk factors, i.e. age-related thrombogenicity factors developing chronically, gradullay deteriorating with ageing. The fragile Bmal1-/- mouse model represents a well-studied compromise, its defects in different organs being well-documented, with a life-span, long enough to allow intervention studies. Disclosures No relevant conflicts of interest to declare.

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Pierpaoli, W., and V. Lesnikov. "Theoretical Considerations on the Nature of the Pineal ‘Ageing Clock’." Gerontology 43, no. 1-2 (1997): 20–25. http://dx.doi.org/10.1159/000213833.

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21

Duggal, Niharika A. "Reversing the immune ageing clock: lifestyle modifications and pharmacological interventions." Biogerontology 19, no. 6 (September 29, 2018): 481–96. http://dx.doi.org/10.1007/s10522-018-9771-7.

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22

Froy, O. "Circadian rhythms, nutrition and implications for longevity in urban environments." Proceedings of the Nutrition Society 77, no. 3 (October 25, 2017): 216–22. http://dx.doi.org/10.1017/s0029665117003962.

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Presently, about 12% of the population is 65 years or older and by the year 2030 that figure is expected to reach 21%. In order to promote the well-being of the elderly and to reduce the costs associated with health care demands, increased longevity should be accompanied by ageing attenuation. Energy restriction, which limits the amount of energy consumed to 60–70% of the daily intake, and intermittent fasting, which allows the food to be available ad libitum every other day, extend the life span of mammals and prevent or delay the onset of major age-related diseases, such as cancer, diabetes and cataracts. Recently, we have shown that well-being can be achieved by resetting of the circadian clock and induction of robust catabolic circadian rhythms via timed feeding. In addition, the clock mechanism regulates metabolism and major metabolic proteins are key factors in the core clock mechanism. Therefore, it is necessary to increase our understanding of circadian regulation over metabolism and longevity and to design new therapies based on this regulation. This review will explore the present data in the field of circadian rhythms, ageing and metabolism.

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Dallimore, B., B. Bhowmick, J. Meara, and P. Hobson. "Clock Drawing in Elderly Stroke Patients." Age and Ageing 26, suppl 3 (January 1, 1997): P14. http://dx.doi.org/10.1093/ageing/26.suppl_3.p14-c.

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24

He, Lingxiao. "Epigenetic Clock: A Novel Tool for Nutrition Studies of Healthy Ageing." Journal of nutrition, health & aging 26, no. 4 (April 2022): 316–17. http://dx.doi.org/10.1007/s12603-022-1773-0.

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Horvath, Steve, and Kenneth Raj. "DNA methylation-based biomarkers and the epigenetic clock theory of ageing." Nature Reviews Genetics 19, no. 6 (April 11, 2018): 371–84. http://dx.doi.org/10.1038/s41576-018-0004-3.

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ŁASZKIEWICZ, A., S. CEBRAT, and D. STAUFFER. "SCALING EFFECTS IN THE PENNA AGEING MODEL." Advances in Complex Systems 08, no. 01 (March 2005): 7–14. http://dx.doi.org/10.1142/s0219525905000294.

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We have analyzed the possibility of scaling the sexual Penna ageing model. Assuming that the number of genes expressed before the reproduction age grows linearly with the genome size and that the mutation rate per genome and generation is constant, we have found that the fraction of defective genes expressed before the minimum reproduction age drops with the genome size, while the number of defective genes eliminated by the genetic death grows with genome size. Thus, the evolutionary costs decrease with increasing genome size. After rescaling the time scale according to the mutational clock, age distributions of populations do not depend on the genome size. Nevertheless, enlarging the genome increases the reproduction potential of populations.

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Sharma-Oates, A., N. Rivera, N. Duggal, K. Raza, L. Padyukov, A. Pratt, E. Niemantsverdriet, A. van der Helm-van Mil, S. Jones, and J. Lord. "AB0091 INCREASED BIOLOGICAL AGE IN MALE PARTICIPANTS OF SWEDISH AND UK RHEUMATOID ARTHRITIS COHORTS IS NOT LINKED TO DISEASE." Annals of the Rheumatic Diseases 81, Suppl 1 (May 23, 2022): 1177.1–1177. http://dx.doi.org/10.1136/annrheumdis-2022-eular.4502.

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BackgroundImmunesenescence in the adaptive immune system, subsequent to thymic involution, results in compromised immunity and increased susceptibility to autoimmune disease and chronic inflammation. There are reports in the literature that immunesenescence, including thymic atrophy and telomere shortening, is accelerated in patients with rheumatoid arthritis (RA)1. What is unclear is whether RA includes accelerated biological ageing overall in addition to immune ageing which may help to explain the increased risk of age-related diseases in RA2. Recent studies have identified a set of DNA methylated sites across the genome that are highly correlated with chronological age and mortality, termed epigenetic clocks3,4 or DNAm age (DNAma), and can be used to determine an individual’s biological age.ObjectivesThe aim of our study is to determine if the biological epigenetic clocks of RA patients are accelerated.MethodsWe evaluated the Horvath3 and Hannum4 epigenetic clocks of control and RA patients using published DNAm data sets, accessions GSE42861 (EIRA, Swedish cohort of 342 RA patients and 328 non-RA controls) and E-MTAB-6988 (77 RA discordant monozygotic twins).ResultsWe did not detect significant differences between DNAma of RA and non-RA twins. Similarly, there were no significant differences between the DNAma of RA patients and controls from the Swedish EIRA cohort. However, we detected a significant acceleration in DNAma of male discordant twins, both RA and non-RA, by 5.4 years (p=3.29e-5) and 2.8 years (p=0.04) using the Hannum and Horvath clocks, respectively. Male participants, both control and RA patients, from the EIRA cohort also exhibited an accelerated DNAma, by 1.5 years (p=7.55e-5) using the Hannum clock but using the Horvath clock a significant DNAma acceleration, by 1.4 years (p=0.002) was detected in male RA patients from the EIRA cohort.ConclusionOverall, we detected a significant biological age acceleration in male participants from both RA and control groups and only found a significant difference between DNAma of Non-RA controls and RA patients for one of the epigenetic clocks. Further analysis using additional cohort data and biological clock algorithms is needed to confirm our findings.References[1]Goronzy, J.J. and Weyand CM (2001). Thymic function and peripheral T-cell homeostasis in rheumatoid arthritis. Trends Immunol. 22(5):251-5.[2]Meune C, et al. (2009) Trends in cardiovascular mortality in patients with rheumatoid arthritis over 50 years: a systematic review and meta-analysis of cohort studies. Rheumatol 48:1309-1313.[3]Horvath S (2013) DNA methylation age of human tissues and cell types. Genome Biol 14:R115.[4]Hannum G, et al (2013) Genome-wide Methylation Profiles Reveal Quantitative Views of Human Aging Rates. Mol Cell 49:359-367.AcknowledgementsThe study was funded by FOREUMDisclosure of InterestsNone declared

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Vitale, Jacopo, Matteo Bonato, Antonio La Torre, and Giuseppe Banfi. "The Role of the Molecular Clock in Promoting Skeletal Muscle Growth and Protecting against Sarcopenia." International Journal of Molecular Sciences 20, no. 17 (September 3, 2019): 4318. http://dx.doi.org/10.3390/ijms20174318.

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The circadian clock has a critical role in many physiological functions of skeletal muscle and is essential to fully understand the precise underlying mechanisms involved in these complex interactions. The importance of circadian expression for structure, function and metabolism of skeletal muscle is clear when observing the muscle phenotype in models of molecular clock disruption. Presently, the maintenance of circadian rhythms is emerging as an important new factor in human health, with disruptions linked to ageing, as well as to the development of many chronic diseases, including sarcopenia. Therefore, the aim of this review is to present the latest findings demonstrating how circadian rhythms in skeletal muscle are important for maintenance of the cellular physiology, metabolism and function of skeletal muscle. Moreover, we will present the current knowledge about the tissue-specific functions of the molecular clock in skeletal muscle.

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Dudek, Michal, Nan Yang, Jayalath PD Ruckshanthi, Jack Williams, Elzbieta Borysiewicz, Ping Wang, Antony Adamson, et al. "The intervertebral disc contains intrinsic circadian clocks that are regulated by age and cytokines and linked to degeneration." Annals of the Rheumatic Diseases 76, no. 3 (August 3, 2016): 576–84. http://dx.doi.org/10.1136/annrheumdis-2016-209428.

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ObjectivesThe circadian clocks are internal timing mechanisms that drive ∼24-hour rhythms in a tissue-specific manner. Many aspects of the physiology of the intervertebral disc (IVD) show clear diurnal rhythms. However, it is unknown whether IVD tissue contains functional circadian clocks and if so, how their dysregulation is implicated in IVD degeneration.MethodsClock gene dynamics in ex vivo IVD explants (from PER2:: luciferase (LUC) reporter mice) and human disc cells (transduced with lentivirus containing Per2::luc reporters) were monitored in real time by bioluminescence photon counting and imaging. Temporal gene expression changes were studied by RNAseq and quantitative reverse transcription (qRT)-PCR. IVD pathology was evaluated by histology in a mouse model with tissue-specific deletion of the core clock gene Bmal1.ResultsHere we show the existence of the circadian rhythm in mouse IVD tissue and human disc cells. This rhythm is dampened with ageing in mice and can be abolished by treatment with interleukin-1β but not tumour necrosis factor α. Time-series RNAseq revealed 607 genes with 24-hour patterns of expression representing several essential pathways in IVD physiology. Mice with conditional knockout of Bmal1 in their disc cells demonstrated age-related degeneration of IVDs.ConclusionsWe have established autonomous circadian clocks in mouse and human IVD cells which respond to age and cytokines, and control key pathways involved in the homeostasis of IVDs. Genetic disruption to the mouse IVD molecular clock predisposes to IVD degeneration. These results support the concept that disruptions to circadian rhythms may be a risk factor for degenerative IVD disease and low back pain.

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Wang, Yali, Dongjun Lv, Wenwen Liu, Siyue Li, Jing Chen, Yun Shen, Fen Wang, Li-Fang Hu, and Chun-Feng Liu. "Disruption of the Circadian Clock Alters Antioxidative Defense via the SIRT1-BMAL1 Pathway in 6-OHDA-Induced Models of Parkinson’s Disease." Oxidative Medicine and Cellular Longevity 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/4854732.

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Parkinson’s disease (PD) is the second most common neurodegenerative disease and is known to involve circadian dysfunction and oxidative stress. Although antioxidative defense is regulated by the molecular circadian clock, few studies have examined their function in PD and their regulation by silent information regulator 1 (SIRT1). We hypothesize that reduced antioxidative activity in models of PD results from dysfunction of the molecular circadian clock via the SIRT1 pathway. We treated rats and SH-SY5Y cells with 6-hydroxydopamine (6-OHDA) and measured the expression of core circadian clock and associated nuclear receptor genes using real-time quantitative PCR as well as levels of SIRT1, brain and muscle Arnt-like protein 1 (BMAL1), and acetylated BMAL1 using Western blotting. We found that 6-OHDA treatment altered the expression patterns of clock and antioxidative molecules in vivo and in vitro. We also detected an increased ratio of acetylated BMAL1:BMAL1 and a decreased level of SIRT1. Furthermore, resveratrol, an activator of SIRT1, decreased the acetylation of BMAL1 and inhibited its binding with CRY1, thereby reversing the impaired antioxidative activity induced by 6-OHDA. These results suggest that a dysfunctional circadian clock contributes to an abnormal antioxidative response in PD via a SIRT1-dependent BMAL1 pathway.

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Harley, Calvin B. "Telomere loss: mitotic clock or genetic time bomb?" Mutation Research/DNAging 256, no. 2-6 (March 1991): 271–82. http://dx.doi.org/10.1016/0921-8734(91)90018-7.

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32

Declerck, Ken, and Wim Vanden Berghe. "Back to the future: Epigenetic clock plasticity towards healthy aging." Mechanisms of Ageing and Development 174 (September 2018): 18–29. http://dx.doi.org/10.1016/j.mad.2018.01.002.

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33

Pierpaoli, Walter. "The pineal gland: A circadian or seasonal aging clock?" Aging Clinical and Experimental Research 3, no. 2 (June 1991): 99–101. http://dx.doi.org/10.1007/bf03323985.

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34

Kippert, F. "An ultradian clock controls locomotor behaviour and cell division in isolated cells of Paramecium tetraurelia." Journal of Cell Science 109, no. 4 (April 1, 1996): 867–73. http://dx.doi.org/10.1242/jcs.109.4.867.

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An ultradian clock operates in fast growing cells of the large ciliate, Paramecium tetraurelia. The period of around 70 minutes is well temperature-compensated over the temperature range tested, i.e. between 18 degrees C and 33 degrees C. The Q10 between 18 degrees C and 27 degrees C is 1.08; above 27 degrees C there is a slight overcompensation. The investigation of individual cells has revealed that two different cellular functions are under temporal control by this ultradian clock. First, locomotor behaviour, which is an alternation between a phase of fast swimming with only infrequent turning, and a phase of slow swimming with frequent spontaneous changes of direction. In addition, the ultradian clock is involved in the timing of cell division. Generation times are not randomly distributed, but occur in well separated clusters. At all of the six temperatures tested, the clusters are separated by around 70 minutes which corresponds well to the period of the locomotor behaviour rhythm at the respective temperatures. Whereas the interdivision times were gradually lengthened both above and below the optimum growth temperature, the underlying periodicity remained unaffected. Also cells of different clonal age had identical periods, suggesting that neither the differences in DNA content, not other changes associated with ageing in Paramecium have an effect on the clock. A constant phase relationship was observed between the rhythm in locomotor behaviour and the time window for cell division; this strongly suggests that the same ultradian clock exerts temporal control over both processes.

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35

Shireby, Gemma, Eilis Hannon, Paul Francis, Katie Lunnon, Emma Dempster, Emma Walker, and Jonathan Mill. "S51RECALIBRATING THE EPIGENETIC CLOCK: APPLICATIONS FOR ASSESSING BIOLOGICAL AGEING IN THE HUMAN BRAIN." European Neuropsychopharmacology 29 (October 2019): S140. http://dx.doi.org/10.1016/j.euroneuro.2019.08.052.

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36

Jacome Burbano, Maria Sol, and Eric Gilson. "Long-lived post-mitotic cell aging: is a telomere clock at play?" Mechanisms of Ageing and Development 189 (July 2020): 111256. http://dx.doi.org/10.1016/j.mad.2020.111256.

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37

Rogers, Eve H., John A. Hunt, and Vanja Pekovic-Vaughan. "Adult stem cell maintenance and tissue regeneration around the clock: do impaired stem cell clocks drive age-associated tissue degeneration?" Biogerontology 19, no. 6 (October 29, 2018): 497–517. http://dx.doi.org/10.1007/s10522-018-9772-6.

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38

Vetter, Valentin Max, Dominik Spira, Verena Laura Banszerus, and Ilja Demuth. "Epigenetic Clock and Leukocyte Telomere Length Are Associated with Vitamin D Status but not with Functional Assessments and Frailty in the Berlin Aging Study II." Journals of Gerontology: Series A 75, no. 11 (April 23, 2020): 2056–63. http://dx.doi.org/10.1093/gerona/glaa101.

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Abstract DNA methylation (DNAm) age acceleration, a parameter derived via the epigenetic clock, has recently been suggested as a biomarker of aging. We hypothesized that accelerated biological aging, measured by both this new and the established biomarker of aging, relative leukocyte telomere length (rLTL), are associated with vitamin D deficiency. Moreover, we tested for an association between rLTL/DNAm age acceleration and different clinical assessments for functional capacity, including the Fried frailty score. Cross-sectional data of 1,649 participants of the Berlin Aging Study II was available (~50% female, age: 22–37 and 60–84 years). A seven cytosine-phosphate-guanine clock was estimated to calculate the DNAm age acceleration. rLTL was measured by quantitative real-time polymerase chain reaction (PCR). 25-hydroxyvitamin D (25(OH)D) serum levels <25 nmol/L was defined as vitamin D deficiency and <50 nmol/L as vitamin D insufficiency. Vitamin D-sufficient individuals had a 1.4 years lower mean DNAm age acceleration (p < .05, analysis of variance [ANOVA]) and a 0.11 longer rLTL (p < .001, ANOVA) than vitamin D-deficient participants. Likewise, vitamin D-sufficient participants had lower DNAm age acceleration (β = 1.060, p = .001) and longer rLTL (β = −0.070; p < .001) than vitamin D nonsufficient subjects in covariate-adjusted analysis. Neither DNAm age acceleration nor rLTL were significantly associated with the Fried frailty score or the functional assessments. Only the clock drawing test was associated with DNAm age acceleration (subgroup of older men: β = 1.898, p = .002). Whether the analyzed biomarkers of aging can be used to predict an individual’s functional capacity or will be associated with frailty in the advanced course of aging, will be clarified by future longitudinal analyses.

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Cornelissen, Germaine, and Kuniaki Otsuka. "Chronobiology of Aging: A Mini-Review." Gerontology 63, no. 2 (October 22, 2016): 118–28. http://dx.doi.org/10.1159/000450945.

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Aging is generally associated with weakening of the circadian system. The circadian amplitude is reduced and the circadian acrophase becomes more labile, tending to occur earlier with advancing age. As originally noted by Franz Halberg, similar features are observed in the experimental laboratory after bilateral lesioning of the suprachiasmatic nuclei, suggesting the involvement of clock genes in the aging process as they are in various disease conditions. Recent work has been shedding light on underlying pathways involved in the aging process, with the promise of interventions to extend healthy life spans. Caloric restriction, which is consistently and reproducibly associated with prolonging life in different animal models, is associated with an increased circadian amplitude. These results indicate the critical importance of chronobiology in dealing with problems of aging, from the circadian clock machinery orchestrating metabolism to the development of geroprotectors. The quantitative estimation of circadian rhythm characteristics interpreted in the light of time-specified reference values helps (1) to distinguish effects of natural healthy aging from those associated with disease and predisease; (2) to detect alterations in rhythm characteristics as markers of increased risk before there is overt disease; and (3) to individually optimize by timing prophylactic and/or therapeutic interventions aimed at restoring a disturbed circadian system and/or enhancing a healthy life span. Mapping changes in amplitude and/or acrophase that may overshadow any change in average value also avoids drawing spurious conclusions resulting from data collected at a fixed clock hour. Timely risk detection combined with treatment optimization by timing (chronotherapy) is the goal of several ongoing comprehensive community-based studies focusing on the well-being of the elderly, so that longevity is not achieved at the cost of a reduced quality of life.

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Terzibasi-Tozzini, Eva, Antonio Martinez-Nicolas, and Alejandro Lucas-Sánchez. "The clock is ticking. Ageing of the circadian system: From physiology to cell cycle." Seminars in Cell & Developmental Biology 70 (October 2017): 164–76. http://dx.doi.org/10.1016/j.semcdb.2017.06.011.

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Rowland, Joshua, Artur Akbarov, Akhlaq Maan, James Eales, John Dormer, and Maciej Tomaszewski. "Tick-Tock Chimes the Kidney Clock – from Biology of Renal Ageing to Clinical Applications." Kidney and Blood Pressure Research 43, no. 1 (2018): 55–67. http://dx.doi.org/10.1159/000486907.

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Borson, S., M. Brush, E. Gil, J. Scanlan, P. Vitaliano, J. Chen, J. Cashman, M. M. Sta Maria, R. Barnhart, and J. Roques. "The Clock Drawing Test: Utility for Dementia Detection in Multiethnic Elders." Journals of Gerontology Series A: Biological Sciences and Medical Sciences 54, no. 11 (November 1, 1999): M534—M540. http://dx.doi.org/10.1093/gerona/54.11.m534.

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43

Huang, Zhihao, Aoxiao He, Jiakun Wang, Hongcheng Lu, Rongguiyi Zhang, Linquan Wu, and Qian Feng. "The circadian clock is associated with prognosis and immune infiltration in stomach adenocarcinoma." Aging 13, no. 12 (June 23, 2021): 16637–55. http://dx.doi.org/10.18632/aging.203184.

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44

Pinho, Gabriela M., Julien G. A. Martin, Colin Farrell, Amin Haghani, Joseph A. Zoller, Joshua Zhang, Sagi Snir, et al. "Hibernation slows epigenetic ageing in yellow-bellied marmots." Nature Ecology & Evolution 6, no. 4 (March 7, 2022): 418–26. http://dx.doi.org/10.1038/s41559-022-01679-1.

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AbstractSpecies that hibernate generally live longer than would be expected based solely on their body size. Hibernation is characterized by long periods of metabolic suppression (torpor) interspersed by short periods of increased metabolism (arousal). The torpor–arousal cycles occur multiple times during hibernation, and it has been suggested that processes controlling the transition between torpor and arousal states cause ageing suppression. Metabolic rate is also a known correlate of longevity; we thus proposed the ‘hibernation–ageing hypothesis’ whereby ageing is suspended during hibernation. We tested this hypothesis in a well-studied population of yellow-bellied marmots (Marmota flaviventer), which spend 7–8 months per year hibernating. We used two approaches to estimate epigenetic age: the epigenetic clock and the epigenetic pacemaker. Variation in epigenetic age of 149 samples collected throughout the life of 73 females was modelled using generalized additive mixed models (GAMM), where season (cyclic cubic spline) and chronological age (cubic spline) were fixed effects. As expected, the GAMM using epigenetic ages calculated from the epigenetic pacemaker was better able to detect nonlinear patterns in epigenetic ageing over time. We observed a logarithmic curve of epigenetic age with time, where the epigenetic age increased at a higher rate until females reached sexual maturity (two years old). With respect to circannual patterns, the epigenetic age increased during the active season and essentially stalled during the hibernation period. Taken together, our results are consistent with the hibernation–ageing hypothesis and may explain the enhanced longevity in hibernators.

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45

Paparazzo, Ersilia, Silvana Geracitano, Vincenzo Lagani, Denise Bartolomeo, Mirella Aurora Aceto, Patrizia D’Aquila, Luigi Citrigno, Dina Bellizzi, Giuseppe Passarino, and Alberto Montesanto. "A Blood-Based Molecular Clock for Biological Age Estimation." Cells 12, no. 1 (December 21, 2022): 32. http://dx.doi.org/10.3390/cells12010032.

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In the last decade, extensive efforts have been made to identify biomarkers of biological age. DNA methylation levels of ELOVL fatty acid elongase 2 (ELOVL2) and the signal joint T-cell receptor rearrangement excision circles (sjTRECs) represent the most promising candidates. Although these two non-redundant biomarkers echo important biological aspects of the ageing process in humans, a well-validated molecular clock exploiting these powerful candidates has not yet been formulated. The present study aimed to develop a more accurate molecular clock in a sample of 194 Italian individuals by re-analyzing the previously obtained EVOLV2 methylation data together with the amount of sjTRECs in the same blood samples. The proposed model showed a high prediction accuracy both in younger individuals with an error of about 2.5 years and in older subjects where a relatively low error was observed if compared with those reported in previously published studies. In conclusion, an easy, cost-effective and reliable model to measure the individual rate and the quality of aging in human population has been proposed. Further studies are required to validate the model and to extend its use in an applicative context.

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Frigato, Elena, Mascia Benedusi, Anna Guiotto, Cristiano Bertolucci, and Giuseppe Valacchi. "Circadian Clock and OxInflammation: Functional Crosstalk in Cutaneous Homeostasis." Oxidative Medicine and Cellular Longevity 2020 (April 23, 2020): 1–9. http://dx.doi.org/10.1155/2020/2309437.

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Circadian rhythms are biological oscillations that occur with an approximately 24 h period and optimize cellular homeostasis and responses to environmental stimuli. A growing collection of data suggests that chronic circadian disruption caused by novel lifestyle risk factors such as shift work, travel across time zones, or irregular sleep-wake cycles has long-term consequences for human health. Among the multiplicity of physiological systems hypothesized to have a role in the onset of pathologies in case of circadian disruption, there are redox-sensitive defensive pathways and inflammatory machinery. Due to its location and barrier physiological role, the skin is a prototypical tissue to study the influence of environmental insults induced OxInflammation disturbance and circadian system alteration. To better investigate the link among outdoor stressors, OxInflammation, and circadian system, we tested the differential responses of keratinocytes clock synchronized or desynchronized, in an in vitro inflammatory model exposed to O3. Being both NRF2 and NF-κB two key redox-sensitive transcription factors involved in cellular redox homeostasis and inflammation, we analyzed their activation and expression in challenged keratinocytes by O3. Our results suggest that a synchronized circadian clock not only facilitates the protective role of NRF2 in terms of a faster and more efficient defensive response against environmental insults but also moderates the cellular damage resulting from a condition of chronic inflammation. Our results bring new insights on the role of circadian clock in regulating the redox-inflammatory crosstalk influenced by O3 and possibly can be extrapolated to other pollutants able to affect the oxinflammatory cellular processes.

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47

Biello, Stephany M. "Circadian clock resetting in the mouse changes with age." AGE 31, no. 4 (June 26, 2009): 293–303. http://dx.doi.org/10.1007/s11357-009-9102-7.

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48

Maxwell, Fraser, Liane McGlynn, Campbell S. Roxburgh, Donald C. McMillan, Paul G. Horgan, and Paul Shiels. "S1957 Potential Role of Biological Ageing in Colorectal Cancer: How Many Miles on the Clock?" Gastroenterology 138, no. 5 (May 2010): S—289. http://dx.doi.org/10.1016/s0016-5085(10)61328-5.

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49

Tellez, James O., Michal Mączewski, Joseph Yanni, Pavel Sutyagin, Urszula Mackiewicz, Andrew Atkinson, Shin Inada, et al. "Ageing-dependent remodelling of ion channel and Ca2+clock genes underlying sino-atrial node pacemaking." Experimental Physiology 96, no. 11 (October 26, 2011): 1163–78. http://dx.doi.org/10.1113/expphysiol.2011.057752.

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50

Bovier, Anton, and Véronique Gayrard. "Convergence of clock processes in random environments and ageing in the $p$-spin SK model." Annals of Probability 41, no. 2 (March 2013): 817–47. http://dx.doi.org/10.1214/11-aop705.

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