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Variation in the form, pattern and pace of ageing is studied by scientists in multiple disciplines and there is much to be gained from more cross-disciplinary communication. This chapter suggests here that the framework provided by Tinbergen’s ‘Four Questions’ is useful in integrating ageing research. It emphasizes the need to separate biological and chronological age and describe several markers of age-related deterioration that could be used more widely to measure biological age, with a focus on those that can be deployed outside of the standard laboratory setting and be used repeatedly in individuals to enable longitudinal studies. Whole organism frailty measures are currently little used by evolutionary ecologists and this chapter describes how these could be used more extensively. Telomere attrition and mitochondrial function are highly conserved processes and have been studied in an increasingly wide range of taxa in recent years. The chapter also discusses other markers, including those related to immune function, oxidative damage, inflammation and DNA methylation. Great progress is currently being made in the use of epigenetic alterations to provide information on chronological and biological age in a range of (predominantly) vertebrate taxa. The chapter outlines how this integrative approach could be developed further and highlight future directions.
Advances in comparative ageing research strongly depend on data quality and quantity. Across the world, zoos and aquariums gather data on the physiology, morphology, health and demography of the animals under their care to facilitate their management. Many of these data are hosted in a centralized database, the Species360 Zoological Information Management System (ZIMS). As of 2022, ZIMS held records on ~10 million individuals across 22,000 species and over 1200 member institutions, with historical animal records dating back to the mid-1800s. These millions of age-specific data could enable analyses testing hypotheses at individual and species levels and between species with vastly different life history strategies. This chapter summarizes the diversity of questions (ranging from evolutionary theories to mechanistic hypotheses) for ageing research that could be addressed using data from zoo and aquarium populations. In addition, many of these studies could inform the management and conservation of animals, not only in zoos and aquariums, but also in the wild.
Sex differences in lifespan have been labelled as one of the most robust features in biology. In human populations, women live consistently longer than men, a pattern that encompasses most mammalian species. However, when expanding both the taxonomic scope beyond mammals and the range of mortality metrics the female survival advantage over males is no longer the rule. Moreover, current evidence suggests that sex differences in actuarial ageing parameters (i.e. age at the onset of ageing and rate of ageing) are far from consistent across the tree of life. This chapter first reviews current knowledge of sex differences in mortality patterns across animals and appraises how these diverse patterns can be explained by the current evolutionary framework. It then emphasizes the relevance of going beyond the differences in mortality patterns by exploring how natural and sexual selection have shaped age- and sex-specific changes in reproductive performance and body mass across the tree of life, and by identifying some possible biological pathways modulating ageing in a sex-specific way. Finally, it highlights how evolutionary theories can be relevant to understand the widespread differences in causes of death between sexes, offering a complementary approach to gain a comprehensive understanding of the evolution of sex differences in health and ageing, with likely biomedical implications.
Humans age. Domestic animals age. But is that true for all species? Is ageing a necessary consequence of evolution? Yes - for a long time, this was the undisputed answer of classic evolutionary theories of ageing. This chapter tells the story about how this paradigm of inevitable ageing has been challenged and refuted. Thanks to decades of monitoring individual survival and death across species in captivity and in the wild, researchers have been able to study patterns of the ageing process’s ultimate consequence - age trajectories of mortality. Though ageing is a complex, multiscale process, increasing mortality with age is, overall, indicative of a loss of functioning with age - senescence. Constant or declining mortality with adult age is indicative of maintained or improved functioning - negligible or negative senescence. Evidence supports that ageing patterns across the tree of life are diverse. Whether current evidence for negligible or negative senescence truly reflects an absence of senescence or just an absence of evidence is an open challenge. Similarly, why certain types of species show certain types of senescence patterns is an open research question. Future evolutionary theories of ageing will have to include trade-offs justified by structural arguments - genetic structure, physiological structure, social structure, ecological structure - to explain types of ageing patterns across types of species.
Why and how we age are deep and enduring questions. The quest for a theoretical framework explaining the evolutionary origins and proximate mechanisms of ageing has led to the elaboration of hundreds of theories of very diverse kinds. The aim of this chapter is twofold. First, it will provide an historical perspective of the numerous theories of ageing. Second, it will emphasize the need for a unified framework merging both evolutionary and mechanistic theories by demonstrating that such theoretical frameworks are required to promote innovative research projects involving the joint effort of multiple research disciplines.
This opening chapter provides an overview of the future societal and subsequenl scientific challenges associated with population ageing. More specifically, it emphasizes how the field of biodemography constitutes a relevant framework for future research programmes aiming to address questions of paramount importance regarding both the causes (e.g. evolutionary, mechanistics) and consequences (demographic, medical) of the ageing process. Finally, this chapter details the book contents.
A life-course approach to enhance tolerance to and prevent dementia and senescence is increasingly embraced by scientists, clinicians and policy makers to promote healthy ageing. Tolerance enhancement and prevention remain the most sensible courses of action given the lack of effective dementia treatment. We discuss the modifiable risk factors of dementia, and address social isolation and loneliness in view of their importance from a psychological and societal perspective. The effectiveness of prevention strategies and non-pharmacological intervention is increasingly supported by scientific evidence. They support an actionable model of dementia and senescence prevention that is cost effective and converges with established public health programmes (diet, exercise, mental health). They also relate to central societal issues (social inequality, pollution, healthcare), and translate to multidisciplinary professional interventions that are tailored to the individual. Changing lifestyle might be an effective way to address the challenges of dementia and senescence in our ageing populations, but also represents one of the most formidable psychosocial and societal challenges.
It is well accepted that the impact of diseases is generally more detrimental in elderly individuals than in younger ones. Changes in the immune system due to ageing can directly affect the ability to respond effectively to infections and may contribute to the higher morbidities and mortalities in the elderly population. Leishmaniasis is a complex of clinically unique diseases caused by obligate intracellular protozoa belonging to genus Leishmania, wherein visceral leishmaniasis (VL) is the most severe form and is fatal if left untreated. In this study, aged mice (72 weeks old) presented increased susceptibility to L. infantum infection compared to younger mice (4–6-week-old), with notable parasitism in both the spleen and liver, as well as exhibiting hepatosplenomegaly. A pronounced inflammatory profile was observed in the aged-infected mice, with excessive production of TNF-α and nitrite, along with diminished IFN-γ production and reduced proliferative capacity of T cells (assessed by expression of the Ki67 marker). Additionally, both CD4+ and CD8+ T cells from the aged-infected mice presented increased expression of the inhibitory receptors PD-1 and KLRG1 that strongly correlated with the parasitism found in the liver and spleen of this group. Overall, the data reported in this study suggests for the first time that ageing may negatively impact the VL outcome and provides a perspective for new therapeutic strategies involving manipulation of immunosenescence features against Leishmania infection.
Head and neck squamous cell carcinoma (HNSCC) is a common malignancy that develops in or around the throat, larynx, nose, sinuses and mouth, and is mostly treated with a combination of chemo- and radiotherapy (RT). The main goal of RT is to kill enough of the cancer cell population, whilst preserving the surrounding normal and healthy tissue. The mechanisms by which conventional photon RT achieves this have been extensively studied over several decades, but little is known about the cell death pathways that are activated in response to RT of increasing linear energy transfer (LET), including proton beam therapy and heavy ions. Here, we provide an up-to-date review on the observed radiobiological effects of low- versus high-LET RT in HNSCC cell models, particularly in the context of specific cell death mechanisms, including apoptosis, necrosis, autophagy, senescence and mitotic death. We also detail some of the current therapeutic strategies targeting cell death pathways that have been investigated to enhance the radiosensitivity of HNSCC cells in response to RT, including those that may present with clinical opportunities for eventual patient benefit.
Two properties – robustness and plasticity – characterize development as the bridge between genotype and phenotype. Developmental robustness is the capacity of a developmental system to produce the same phenotype irrespective of changes in external conditions (and, to some extent, of genetic change). Developmental plasticity is the production of different phenotypes by individuals with the same genotype, as a response to exposure to different external conditions. This outcome is called polyphenism if there is a clear discontinuity between the produced phenotypes, e.g. male vs. female in the alligator, in response to different temperatures in a critical phase of embryonic development. Phenotypic differences are not restricted to morphology, but extend to the temporal dimension, e.g. in the annual, biennial or perennial habit of plants, or in their flowering calendar. Periodization of development is to some extent arbitrary even in organisms where the individual’s life is punctuated by events such as moults in arthropods. The determination of age is also to some extent arbitrary. Senescence is conspicuous (often dramatic) in many organisms, but apparently non-existent in others.
Apicomplexan parasites are well-known to modulate their host cells at diverse functional levels. As such, apicomplexan-induced alteration of host cellular cell cycle was described and appeared dependent on both, parasite species and host cell type. As a striking evidence of species-specific reactions, we here show that Eimeria bovis drives primary bovine umbilical vein endothelial cells (BUVECs) into a senescence-like phenotype during merogony I. In line with senescence characteristics, E. bovis induces a phenotypic change in host cell nuclei being characterized by nucleolar fusion and heterochromatin-enriched peripheries. By fibrillarin staining we confirm nucleoli sizes to be increased and their number per nucleus to be reduced in E. bovis-infected BUVECs. Additionally, nuclei of E. bovis-infected BUVECs showed enhanced signals for HH3K9me2 as heterochromatin marker thereby indicating an infection-induced change in heterochromatin transition. Furthermore, E. bovis-infected BUVECs show an enhanced β-galactosidase activity, which is a well-known marker of senescence. Referring to cell cycle progression, protein abundance profiles in E. bovis-infected endothelial cells revealed an up-regulation of cyclin E1 thereby indicating a cell cycle arrest at G1/S transition, signifying a senescence key feature. Similarly, abundance of G2 phase-specific cyclin B1 was found to be downregulated at the late phase of macromeront formation. Overall, these data indicate that the slow proliferative intracellular parasite E. bovis drives its host endothelial cells in a senescence-like status. So far, it remains to be elucidated whether this phenomenon indeed reflects an intentionally induced mechanism to profit from host cell-derived energy and metabolites present in a non-dividing cellular status.
Since the mid-1980s, swarms of the rhizostome Rhopilema nomadica have been an annual phenomenon in Israeli Mediterranean coastal waters during the summer months. Despite its annual prominence and the potential impact on food webs and ecosystem services, studies concerning its feeding ecology and its interactions with other biota in the marine food web have not been conducted. During summer 2015 gut contents of 41 R. nomadica were analysed as well as ambient plankton assemblages. More than 60% of the medusae diet was found to consist of microzooplankton <150 μm. Size correlations revealed that larger R. nomadica consumed faster swimming prey while smaller medusae relied more on the slower swimming taxa. The medusan diet reflected most of the ambient plankton taxa, but no statistically significant correlations between the relative abundance in diet and ambient plankton were found. As summer progressed, there was a gradual decrease in both mean medusa bell diameter (from 42.2–16 cm) and integrity of feeding structures. These findings suggest that R. nomadica, at least at the time of its appearance in Israeli coastal waters, may exert less predatory pressure on the plankton than we might otherwise expect.
The chapter “Aging Theory” makes three related points about the intersection of narrative, time, and aging. First, it draws on the idea of surface reading to argue for renewed attention to the effects of aging. By drawing aging to the surface of the body and its representation in the novel, this approach resists the modern tendency of repressing the duration of aging. The second section draws together the diachronic analyses of narrative theory with the metaphysics of Henri Bergson and Gilles Deleuze, contending that the reader’s temporal encounter with the materiality of a text’s discourse serves as a tacit reminder of the reader’s own aging. By doing so, narrative temporality reflects to the reader the very duration that falls out of his or her experience of aging. The final section suggests that the novel’s realism naturalizes a crisis model of character development by positing life-changing events as a part of “everyday” reality. As realism relies upon a model of change where duration surprisingly disappears, it diminishes the role of aging in the development of subjectivity over time.
Our brains are continuously changing and these changes alter brain functions. With maturation, there is growth and unfortunately, even with healthy aging, decline. Aging-related decrements affect neurons and their connectivity, neurotransmitter systems, and even support systems such as glia. Aging affects some brain regions (frontal lobes and hippocampi) more than others. This book reviews and discusses aging-related changes and their influence on the major neurobehavioral domains, beginning with reviews of aging-related changes in anatomy and physiology. Subsequent chapters review cross-sectional and longitudinal studies of aging-related changes in sensory perception (vision, hearing, touch, smell, taste) and cognitive functions (memory, language, motor planning, attention, executive functions, emotions, creativity). In each chapter, mechanisms that may account for these changes are discussed. Declines related to aging per se are distinguished from declines related to aging-associated diseases. Final chapters discuss what can potentially be done to slow or reverse aging-related decline of cognitive functions, including exercise, cognitive rehabilitation, and pharmacological agents. It is hoped this book will help clinicians differentiate between normal aging processes and brain diseases, reduce the adverse effects of brain aging, and stimulate further research on how adverse effects of brain aging can be reversed, stopped, modified, or best managed.
Chapter 1 introduces some fundamental concepts, starting with a tentative definition of reproduction that will be revised and enriched in the following chapters and with the traditional distinction between sexual and asexual reproduction. We address the delicate issues relating to the notions of biological individual, generation and life cycle (but we refrain from discussing these topics from a philosophical perspective). We also deal with the not always clearly defined relationship between reproductive and developmental processes, in particular those related to regeneration.
In the USA, western Washington (WWA) and the Alaska (AK) Interior are two regions where maritime and continental climates, high latitude and cropping systems necessitate early maturing spring wheat (Triticum aestivum L.). Both regions aim to increase the production of hard spring bread wheat for human consumption to support regional agriculture and food systems. The Nordic region of Europe has a history of breeding for early maturing spring wheat and also experiences long daylengths with mixed maritime and continental climates. Nordic wheat also carries wildtype (wt) NAM-B1, an allele associated with accelerated senescence and increased grain protein and micronutrient content, at a higher frequency than global germplasm. Time to senescence, yield, protein and mineral content were evaluated on 42 accessions of Nordic hard red spring wheat containing wt NAM-B1 over 2 years on experimental stations in WWA and the AK Interior. Significant variation was found by location and accession for time to senescence, suggesting potential parental lines for breeding programmes targeting early maturity. Additionally, multiple regression analysis showed that decreased time to senescence correlated negatively with grain yield and positively with grain protein, iron and zinc content. Breeding for early maturity in these regions will need to account for this potential trade-off in yield. Nordic wt NAM-B1 accessions with early senescence yet with yields similar to regional checks are reported. Collaboration among alternative wheat regions can aid in germplasm exchange and varietal development as shown here for the early maturing trait.
To quantitatively test the hypothesis that older patients have increased thyroarytenoid muscle atrophy by comparing thyroarytenoid muscle volumes across different age groups.
Methods
A retrospective chart review was conducted. The study included 111 patients with no history of laryngeal pathology. Two investigators reviewed magnetic resonance imaging studies of these patients and manually traced the thyroarytenoid muscles on multiple slices bilaterally. Thyroarytenoid muscle volumes were then computed using imaging analysis software. Patients were stratified into three age groups (18–50 years, 51–64 years, and 65 years or older) for comparison.
Results
Intra- and inter-rater reliabilities were excellent for all measurements (intraclass correlation co-efficient > 0.90). There was no statistically significant difference in the mean volumes of left and right thyroarytenoid muscles in all age and gender groups.
Conclusion
Given the lack of statistically significant difference in thyroarytenoid muscle volume between age groups on magnetic resonance imaging, the prevailing assumption that age-related thyroarytenoid muscle atrophy contributes to presbyphonia should be re-examined.
Individual barnyardgrass plants were grown in the absence of competition in a common garden environment. Cohorts were initiated in mid-March, late April, early June, mid-July, mid-August, and mid-September. Plants within a cohort varied from prostrate to upright. Early and late cohorts required slightly longer to achieve flowering and seed shatter than those initiated in late spring and early summer. The onset and development of senescence varied by as much as 5 wk between individuals within a cohort, and senescence progressed more rapidly for plants in later cohorts. Longest tiller length per plant averaged 150 cm and did not differ by cohort, but within cohort variation was approximately 33%. The number of tillers per plant declined with increasing delay in cohort initiation; within cohort variation exceeded 40%. Leaf numbers decreased from more than 10,000 per plant to less than 400 per plant with increasing delay in cohort initiation date. Individuals within a cohort had more than two-fold variation in leaf numbers. The number of inflorescences decreased from more than 4500 per plant to less than 100 with increasing delay in cohort initiation. Mean inflorescence length and frequency of different inflorescence lengths per plant varied between plants within a cohort. Vegetative biomass exceeded 3000 g for many plants in the early cohorts, and decreased to less than 25 g per plant for some individuals in the September cohort. More than two-fold variation in biomass occurred between plants within a cohort. Plasticity in morphology and phenology may contribute to the success of barnyardgrass as a weed.
The effects of haloxyfop on elongation, mitotic index, and morphology of sorghum and unicorn-plant primary roots were examined. Elongation of sorghum roots was completely inhibited by haloxyfop concentrations of 10–6 M or greater 24 h after treatment, whereas unicorn-plant root elongation was unaffected by the same concentrations 72 h after treatment. Mitotic indices of sorghum roots were reduced by both 10–6 and 10–8 M haloxyfop, with the higher concentration reducing the index to near zero by 24 h of exposure. The mitotic indices of unicorn-plant roots were unaffected by the same levels of the herbicide after both 24- and 48-h treatment. Histological analyses showed that after 24 h exposure to 10–6 M haloxyfop, large vacuoles were present in cells at the root apex that normally did not exhibit these organelles. After 48 h of exposure many cells in the apical region appeared to lack visible cytoplasm and/or nuclei, and by 72 h only cell walls remained visibly evident, and many cells had collapsed. These changes are similar to those that occur in tissues undergoing senescence. Treatment of sorghum roots with 10–8 M haloxyfop did not cause discernible changes after 72 h. Unicorn-plant roots treated with 10–6 M haloxyfop appeared unaffected after 72 h.
The risk of developing cardiovascular diseases is known to begin before birth and the impact of the intrauterine environment on subsequent adult health is currently being investigated from many quarters. Following our studies demonstrating the impact of hypoxia in utero and consequent intrauterine growth restriction (IUGR) on the rat cardiovascular system, we hypothesized that changes extend throughout the vasculature and alter function of the renal artery. In addition, we hypothesized that hypoxia induces renal senescence as a potential mediator of altered vascular function. We demonstrated that IUGR females had decreased responses to the adrenergic agonist phenylephrine (PE; pEC50 6.50 ± 0.05 control v. 6.17 ± 0.09 IUGR, P < 0.05) and the endothelium-dependent vasodilator methylcholine (MCh; Emax 89.8 ± 7.0% control v. 41.0 ± 6.5% IUGR, P < 0.001). In IUGR females, this was characterised by increased basal nitric oxide (NO) modulation of vasoconstriction (PE pEC50 6.17 ± 0.09 IUGR v. 6.42 ± 0.08 in the presence of the NO synthase inhibitor N-nitro-l-arginine methyl ester hydrochloride (l-NAME; P < 0.01) but decreased activated NO modulation (no change in MCh responses in the presence of l-NAME), respectively. In contrast, IUGR males had no changes in PE or MCh responses but demonstrated increased basal NO (PE pEC50 6.29 ± 0.06 IUGR v. 6.42 ± 0.12 plus l-NAME, P < 0.01) and activated NO (Emax 37.8 ± 9.4% control v. −0.8 ± 13.0% plus l-NAME, P < 0.05) modulation. No significant changes were found in gross kidney morphology, proteinuria or markers of cellular senescence in either sex. In summary, renal vascular function was altered by hypoxia in utero in a sex-dependent manner but was unlikely to be mediated by premature renal senescence.