Property:Abstract
From Complex Time
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Cognitive ageing research examines the cognitive abilities that are preserved and/or those that decline with advanced age. There is great individual variability in cognitive ageing trajectories. Some older adults show little decline in cognitive ability compared with young adults and are thus termed ‘optimally ageing’. By contrast, others exhibit substantial cognitive decline and may develop dementia. Human neuroimaging research has led to a number of important advances in our understanding of the neural mechanisms underlying these two outcomes. However, interpreting the age-related changes and differences in brain structure, activation and functional connectivity that this research reveals is an ongoing challenge. Ambiguous terminology is a major source of difficulty in this venture. Three terms in particular — compensation, maintenance and reserve — have been used in a number of different ways, and researchers continue to disagree about the kinds of evidence or patterns of results that are required to interpret findings related to these concepts. As such inconsistencies can impede progress in both theoretical and empirical research, here, we aim to clarify and propose consensual definitions of these terms. +
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Consumer–resource interactions are often influenced by other species in the community. At present these ‘trophic interaction modifications’ are rarely included in ecological models despite demonstrations that they can drive system dynamics. Here, we advocate and extend an approach that has the potential to unite and represent this key group of non-trophic interactions by emphasising the change to trophic interactions induced by modifying species. We highlight the opportunities this approach brings in comparison to frameworks that coerce trophic interaction modifications into pairwise relationships. To establish common frames of reference and explore the value of the approach, we set out a range of metrics for the ‘strength’ of an interaction modification which incorporate increasing levels of contextual information about the system. Through demonstrations in three-species model systems, we establish that these metrics capture complimentary aspects of interaction modifications. We show how the approach can be used in a range of empirical contexts; we identify as specific gaps in current understanding experiments with multiple levels of modifier species and the distributions of modifications in networks. The trophic interaction modification approach we propose can motivate and unite empirical and theoretical studies of system dynamics, providing a route to confront ecological complexity. +
Contemporary niche theory is a powerful conceptual framework for understanding how organisms interact with each other and with their shared environment. Here we show that a large segment of niche theory is equivalent to a Minimum Environmental Perturbation Principle (MEPP): ecosystems self-organize into a state that minimizes the impact of organisms on their environment. Different choices of environmental dynamics naturally give rise to distinct dissimilarity measures for quantifying environmental impact. The MEPP allows for the analysis of ecosystems with large numbers of species and environmental factors and provides a new avenue for analyzing ecological invasions. The MEPP also rigorously connects ecological bistability with the existence of multiple minima in a statistical-physics inspired landscapes. We show that the presence of environmental feedbacks where organisms can produce new resources in addition to depleting them violates the global MEPP. However, even in the presence of such feedbacks, a weaker, local version of the MEPP still applies in a limited region of resource space. +
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Defined as the invariance of system structure or function following a nontrivial perturbation to one or more important system components, robustness is a characteristic property of all adaptive systems. This chapter reviews the theory of robustness in biology, the design of experiments used to assay robustness (including the functional behavior or outputs of a system), and the adaptive response of those parts or components which are compromised by a perturbation. Emphasis is given to a rigorous logic of measurements that carefully factors apart the many casual contributions to robust function. Insights from the study of robustness in biology are applied to the social and decision-making domains, and modifications of experimental design and theory are proposed to account for challenges unique to human agents. +
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Delirium occurring in patients with dementia is referred to as delirium superimposed on dementia (DSD). People who are older with dementia and who are institutionalized are at increased risk of developing delirium when hospitalized. In addition, their prior cognitive impairment makes detecting their delirium a challenge. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition and the International Statistical Classification of Diseases and Related Health Problems, 10th Revision are considered the standard reference for the diagnosis of delirium and include criteria of impairments in cognitive processes such as attention, additional cognitive disturbances, or altered level of arousal. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition and the International Statistical Classification of Diseases and Related Health Problems, 10th Revision does not provide guidance regarding specific tests for assessment of the cognitive process impaired in delirium. Importantly, the assessment or inclusion of preexisting cognitive impairment is also not addressed by these standards. The challenge of DSD gets more complex as types of dementia, particularly dementia with Lewy bodies, which has features of both delirium and dementia, are considered. The objective of this article is to critically review key elements for the diagnosis of DSD, including the challenge of neuropsychological assessment in patients with dementia and the influence of particular tests used to diagnose DSD. To address the challenges of DSD diagnosis, we present a framework for guiding the focus of future research efforts to develop a reliable reference standard to diagnose DSD. A key feature of a reliable reference standard will improve the ability to clinically diagnose DSD in facility-based patients and research studies. +
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Dietary restriction (DR) increases life-span in organisms from yeast to mammals, presumably by slowing the accumulation of aging-related damage. Here we show that in Drosophila, DR extends life-span entirely by reducing the short-term risk of death. Two days after the application of DR at any age for the first time, previously fully fed flies are no more likely to die than flies of the same age that have been subjected to long-term DR. DR of mammals may also reduce short-term risk of death, and hence DR instigated at any age could generate a full reversal of mortality. +
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Brain state stability during working memory is explained by network control theory, modulated by dopamine D1/D2 receptor function, and diminished in schizophrenia +
Dynamical brain state transitions are critical for flexible working memory but the network mechanisms are incompletely understood. Here, we show that working memory entails brain-wide switching between activity states. The stability of states relates to dopamine D1 receptor gene expression while state transitions are influenced by D2 receptor expression and pharmacological modulation. Schizophrenia patients show altered network control properties, including a more diverse energy landscape and decreased stability of working memory representations. +
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Ecology letters (2011) 14: 914–921AbstractThe Arrhenius equation has emerged as the favoured model for describing the temperature dependence of consumption in predator–prey models. To examine the relevance of this equation, we undertook a meta-analysis of published relationships between functional response parameters and temperature. We show that, when plotted in lin-log space, temperature dependence of both attack rate and maximal ingestion rate exhibits a hump-shaped relationship and not a linear one as predicted by the Arrhenius equation. The relationship remains significantly downward concave even when data from temperatures above the peak of the hump are discarded. Temperature dependence is stronger for attack rate than for maximal ingestion rate, but the thermal optima are not different. We conclude that the use of the Arrhenius equation to describe consumption in predator–prey models requires the assumption that temperatures above thermal optima are unimportant for population and community dynamics, an assumption that is untenable given the available data. +
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Empirical findings in the Cognitive Sciences on the relationship between feeling states and subjective time have led to the assumption that time perception entails emotional and interoceptive states. The perception of time would thereafter be embodied; the bodily self, the continuous input from the body is the functional anchor of phenomenal experience and the mental self. Subjective time emerges through the existence of the self across time as an enduring and embodied entity. This relation is prominently disclosed in studies on altered states of consciousness such as in meditative states, under the influence of hallucinogens as well as in many psychiatric and neurological conditions. An increased awareness of oneself coincides with an increased awareness of time. Conversely, a decreased awareness of the self is associated with diminished awareness of time. The body of empirical work within different conceptual frameworks on the intricate relationship between self and time is presented and discussed. +
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Stressor interaction networks suggest antibiotic resistance co-opted from stress responses to temperature +
Environmental factors like temperature, pressure, and pH partly shaped the evolution of life. As life progressed, new stressors (e.g., poisons and antibiotics) arose as part of an arms race among organisms. Here we ask if cells co-opted existing mechanisms to respond to new stressors, or whether new responses evolved de novo. We use a network-clustering approach based purely on phenotypic growth measurements and interactions among the effects of stressors on population growth. We apply this method to two types of stressors—temperature and antibiotics—to discover the extent to which their cellular responses overlap in Escherichia coli. Our clustering reveals that responses to low and high temperatures are clearly separated, and each is grouped with responses to antibiotics that have similar effects to cold or heat, respectively. As further support, we use a library of transcriptional fluorescent reporters to confirm heat-shock and cold-shock genes are induced by antibiotics. We also show strains evolved at high temperatures are more sensitive to antibiotics that mimic the effects of cold. Taken together, our results strongly suggest that temperature stress responses have been co-opted to deal with antibiotic stress. +
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Temperature dependence of trophic interactions are driven by asymmetry of species responses and foraging strategy +
Environmental temperature has systematic effects on rates of species interactions, primarily through its influence on organismal physiology. We present a mechanistic model for the thermal response of consumer-resource interactions. We focus on how temperature affects species interactions via key traits - body velocity, detection distance, search rate and handling time - that underlie per capita consumption rate. The model is general because it applies to all foraging strategies: active-capture (both consumer and resource body velocity are important), sit-and-wait (resource velocity dominates) and grazing (consumer velocity dominates). The model predicts that temperature influences consumer-resource interactions primarily through its effects on body velocity (either of the consumer, resource or both), which determines how often consumers and resources encounter each other, and that asymmetries in the thermal responses of interacting species can introduce qualitative, not just quantitative, changes in consumer-resource dynamics. We illustrate this by showing how asymmetries in thermal responses determine equilibrium population densities in interacting consumer-resource pairs. We test for the existence of asymmetries in consumer-resource thermal responses by analysing an extensive database on thermal response curves of ecological traits for 309 species spanning 15 orders of magnitude in body size from terrestrial, marine and freshwater habitats. We find that asymmetries in consumer-resource thermal responses are likely to be a common occurrence. Overall, our study reveals the importance of asymmetric thermal responses in consumer-resource dynamics. In particular, we identify three general types of asymmetries: (i) different levels of performance of the response, (ii) different rates of response (e.g. activation energies) and (iii) different peak or optimal temperatures. Such asymmetries should occur more frequently as the climate changes and species' geographical distributions and phenologies are altered, such that previously noninteracting species come into contact. 6. By using characteristics of trophic interactions that are often well known, such as body size, foraging strategy, thermy and environmental temperature, our framework should allow more accurate predictions about the thermal dependence of consumer-resource interactions. Ultimately, integration of our theory into models of food web and ecosystem dynamics should be useful in understanding how natural systems will respond to current and future temperature change.
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Evolution drives, and is driven by, demography. A genotype moulds its phenotype’s age patterns of mortality and fertility in an environment; these two patterns in turn determine the genotype’s fitness in that environment. Hence, to understand the evolution of ageing, age patterns of mortality and reproduction need to be compared for species across the tree of life. However, few studies have done so and only for a limited range of taxa. Here we contrast standardized patterns over age for 11 mammals, 12 other vertebrates, 10 invertebrates, 12 vascular plants and a green alga. Although it has been predicted that evolution should inevitably lead to increasing mortality and declining fertility with age after maturity, there is great variation among these species, including increasing, constant, decreasing, humped and bowed trajectories for both long- and short-lived species. This diversity challenges theoreticians to develop broader perspectives on the evolution of ageing and empiricists to study the demography of more species. +
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Explaining the strong variation in lifespan among organisms remains a major challenge in evolutionary biology. Whereas previous work has concentrated mainly on differences in selection regimes and selection pressures, we hypothesize that differences in genetic drift may explain some of this variation. We develop a model to formalize this idea and show that the strong positive relationship between lifespan and genetic diversity predicted by this model indeed exists among populations of Daphnia magna, and that ageing is accelerated in small populations. Additional results suggest that this is due to increased drift in small populations rather than adaptation to environments favoring faster life histories. First, the correlation between genetic diversity and lifespan remains significant after statistical correction for potential environmental covariates. Second, no trade-offs are observed; rather, all investigated traits show clear signs of increased genetic load in the small populations. Third, hybrid vigor with respect to lifespan is observed in crosses between small but not between large populations. Together, these results suggest that the evolution of lifespan and ageing can be strongly affected by genetic drift, especially in small populations, and that variation in lifespan and ageing may often be nonadaptive, due to a strong contribution from mutation accumulation. +
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Fisher's geometrical model and the mutational patterns of antibiotic resistance across dose gradients +
Fisher's geometrical model (FGM) has been widely used to depict the fitness effects of mutations. It is a general model with few underlying assumptions that gives a large and comprehensive view of adaptive processes. It is thus attractive in several situations, for example adaptation to antibiotics, but comes with limitations, so that more mechanistic approaches are often preferred to interpret experimental data. It might be possible however to extend FGM assumptions to better account for mutational data. This is theoretically challenging in the context of antibiotic resistance because resistance mutations are assumed to be rare. In this article, we show with Escherichia coli how the fitness effects of resistance mutations screened at different doses of nalidixic acid vary across a dose-gradient. We found experimental patterns qualitatively consistent with the basic FGM (rate of resistance across doses, gamma distributed costs) but also unexpected patterns such as a decreasing mean cost of resistance with increasing screen dose. We show how different extensions involving mutational modules and variations in trait covariance across environments, can be discriminated based on these data. Overall, simple extensions of the FGM accounted well for complex mutational effects of resistance mutations across antibiotic doses. +
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Food webs have markedly non-random network structure. Ecologists maintain that this non-random structure is key for stability, since large random ecological networks would invariably be unstable and thus should not be observed empirically. Here we show that a simple yet overlooked feature of natural food webs, the correlation between the effects of consumers on resources and those of resources on consumers, substantially accounts for their stability. Remarkably, random food webs built by preserving just the distribution and correlation of interaction strengths have stability properties similar to those of the corresponding empirical systems. Surprisingly, we find that the effect of topological network structure on stability, which has been the focus of countless studies, is small compared to that of correlation. Hence, any study of the effects of network structure on stability must first take into account the distribution and correlation of interaction strengths. +
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In Vivo Amelioration of Age-Associated Hallmarks by Partial Reprogramming Cellular reprogramming by transient expression of Yamanaka factors ameliorates age-associated symptoms, prolongs lifespan in progeroid mice, and improves tissue homeostasis in older +
Graphical Abstract Highlights d Partial reprogramming erases cellular markers of aging in mouse and human cells d Induction of OSKM in progeria mice ameliorates signs of aging and extends lifespan d In vivo reprogramming improves regeneration in 12-month-old wild-type mice +
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Healthy aging has been associated with decreased specialization in brain function. This characterization has focused largely on describing age-accompanied differences in specialization at the level of neurons and brain areas. We expand this work to describe systems-level differences in specialization in a healthy adult lifespan sample (n = 210; 20-89 y). A graph-theoretic framework is used to guide analysis of functional MRI resting-state data and describe systems-level differences in connectivity of individual brain networks. Young adults' brain systems exhibit a balance of within- and between-system correlations that is characteristic of segregated and specialized organization. Increasing age is accompanied by decreasing segregation of brain systems. Compared with systems involved in the processing of sensory input and motor output, systems mediating "associative" operations exhibit a distinct pattern of reductions in segregation across the adult lifespan. Of particular importance, the magnitude of association system segregation is predictive of long-term memory function, independent of an individual's age. +
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Inheritance of immune responsiveness, life span, and disease incidence in interline crosses of mice selected for high or low multispecific antibody production. +
High (H) and low (L) antibody responder lines of mice separated by selective breeding present a maximal interline difference in antibody (Ab) response to Ag of different specificities (general genetic regulation). The analysis of SRBC agglutinin response in H line, L line, F1 hybrids, F2, and backcross segregants demonstrates that Ab responsiveness is a polygenic trait regulated by the additive interaction of 5 to 7 independent loci, with an incomplete dominance (44% +/- 7%) of the high response character, and a 30% +/- 10% impact of the environmental factors. The life span of H, L, F1, F2, and backcross populations is correlated positively with 2-ME-resistant agglutinin response (r = 0.97, p less than 0.001) and negatively with 2-ME-sensitive agglutinin response (r = 0.95, p = 0.01) (interpopulation correlation). Similar correlations are also observed in individuals of the various populations, especially in F1 x L backcross, in which the largest phenotypic variance is found. The positive correlation between Ab responsiveness and life span was confirmed by ELISA titration for distinct IgG isotypes (intrapopulation correlation). Malignant lymphomas and chronic nephritis were the two most common diseases observed. The age-adjusted incidence of such diseases, which is largely affected by environmental factors, accounts for the longer life span of H, as compared with L, mouse populations. The longevity of the 30% or less survivors, chiefly determined by the rate of physiologic aging, is a polygenic character regulated by the cumulative interaction of 3 to 7 independent loci, with a complete dominance of the long life trait and an impact of the environmental factors of about 60%. Thus we have grounds for regarding general Ab responsiveness and life span as polygenic traits regulated by a small number of identical or closely linked gene loci, and immune responsiveness as a defense mechanism against neoplastic and inflammatory diseases. +
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How do children and adults differ in their search for rewards? We consider three different hypotheses that attribute developmental differences to either children’s increased random sampling, more directed exploration towards uncertain options, or narrower generalization. Using a search task in which noisy rewards are spatially correlated on a grid, we compare 55 younger children (age 7-8), 55 older children (age 9-11), and 50 adults (age 19-55) in their ability to successfully generalize about unobserved outcomes and balance the exploration-exploitation dilemma. Our results show that children explore more eagerly than adults, but obtain lower rewards. Building a predictive model of search to disentangle the unique contributions of the three hypotheses of developmental differences, we find robust and recoverable parameter estimates indicating that children generalize less and rely on directed exploration more than adults. We do not, however, find reliable differences in terms of random sampling. +
How producers of public goods persist inmicrobial communities is amajor question in 8 evolutionary biology. Cooperation is evolutionarily unstable, since cheating strains can reproduce 9 quicker and take over. Spatial structure has been shown to be a robustmechanism for the 0 1 evolution of cooperation. Here we study how spatial assortmentmight emerge from native 1 1 dynamics and show that fluid flow shear promotes cooperative behavior. Social structures arise 2 1 naturally from our advection-diffusion-reactionmodel as self-reproducing Turing patterns. We 13 computationally study the effects of fluid advection on these patterns as amechanism to enable or 4 1 enhance social behavior. Our central finding is that flow shear enables and promotes social 5 1 behavior inmicrobes by increasing the group fragmentation rate and thereby limiting the spread of 6 1 cheating strains. Regions of the flow domain with higher shear admit high cooperativity and large 7 1 population density, whereas low shear regions are devoid of life due to opportunisticmutations. +
