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Significance The exact causes of aging are still not understood, and it is unclear why some species live less than 1 d, while others can live more than 400 y. Research suggests that telomeres are related to the aging process, but a clear relationship between the life span of a species and initial telomere length has not been observed. Here, we measure the telomere lengths of a variety of different species. We find that, in fact, there is no strong correlation between the life span of a species and initial telomere length. However, we find a strong correlation between the telomere shortening rate and the life span of a species., Telomere shortening to a critical length can trigger aging and shorter life spans in mice and humans by a mechanism that involves induction of a persistent DNA damage response at chromosome ends and loss of cellular viability. However, whether telomere length is a universal determinant of species longevity is not known. To determine whether telomere shortening can be a single parameter to predict species longevities, here we measured in parallel the telomere length of a wide variety of species (birds and mammals) with very different life spans and body sizes, including mouse (Mus musculus), goat (Capra hircus), Audouin’s gull (Larus audouinii), reindeer (Rangifer tarandus), griffon vulture (Gyps fulvus), bottlenose dolphin (Tursiops truncatus), American flamingo (Phoenicopterus ruber), and Sumatran elephant (Elephas maximus sumatranus). We found that the telomere shortening rate, but not the initial telomere length alone, is a powerful predictor of species life span. These results support the notion that critical telomere shortening and the consequent onset of telomeric DNA damage and cellular senescence are a general determinant of species life span.

Background: This article reviews findings about the rise of life expectancy, current levels of life expectancy in countries with high life expectancies, and possible future trends in life expectancy. Maximum lifespans and the equality of lifespans are also considered. Methods: Demographic data on age-specific mortality are used to estimate life expectancy. Validated data on exceptional lifespans are used to study the maximum length of life. Findings of the most significant publications are critically summarized.Results: In the countries doing best, life expectancy started to increase around 1840 at a pace of almost 2.5 years per decade. This trend has continued until the present. Contrary to classical evolutionary theories of senescence and contrary to the predictions of many experts, the frontier of survival is advancing to higher ages. Furthermore, lifespans are becoming more equal, with octogenarians and nonagenarians accounting for most deaths in countries with high life expectancy. Extrapolation of the trend indicates that most children born this millennium will celebrate their 100th birthdays. Considerable uncertainty, however, clouds forecasts of life expectancy and maximum lifespans: life expectancy and maximum lifespan might increase very little if at all or longevity might rise much faster than in the past. Conclusions: Substantial progress has been made over the past three decades in deepening understanding of how long humans have lived and have long they might live. The social, economic, health, cultural and political consequences of further increases in longevity are so significant that the development of more powerful methods of forecasting is a priority.

Brain plasticity is dynamically regulated across the life span, peaking during windows of early life. Typically assessed in the physiological range of milliseconds (real time), these trajectories are also influenced on the longer timescales of developmental time (nurture) and evolutionary time (nature), which shape neural architectures that support plasticity. Properly sequenced critical periods of circuit refinement build up complex cognitive functions, such as language, from more primary modalities. Here, we consider recent progress in the biological basis of critical periods as a unifying rubric for understanding plasticity across multiple timescales. Notably, the maturation of parvalbumin-positive (PV) inhibitory neurons is pivotal. These fast-spiking cells generate gamma oscillations associated with critical period plasticity, are sensitive to circadian gene manipulation, emerge at different rates across brain regions, acquire perineuronal nets with age, and may be influenced by epigenetic factors over generations. These features provide further novel insight into the impact of early adversity and neurodevelopmental risk factors for mental disorders.

Whittemore et al. (1) find significant correlations between maximum life span (MLS) and telomere shortening rate (TSR) in mammalian and avian species. This interesting study comes to the conclusion that “critical telomere shortening and the consequent onset of telomeric DNA damage and cellular senescence are a general determinant of species life span.” An important issue, however, has not been dealt with by the authors. The use of linear regressions (those used by the authors) assumes that samples are independent, but this is not the case in interspecies studies. In fact, the samples (i.e., the values for each species) have different grades of dependency, which derive from their phylogenetic relationship (2). This is why all tests should be performed using phylogenetic corrections, like phylogenetic-independent contrast (3 … [↵][1]1Email: ion.udroiu{at}uniroma3.it. [1]: #xref-corresp-1-1

Significance There is increasing evidence that socioeconomic conditions early in life have an impact on cognitive functioning in later life. Based on the large longitudinal sample from SHARE we find a clear pattern in cognitive functioning in old age, related to childhood socioeconomic conditions: Those from more affluent households show higher levels of fluid intelligence in old age and experience stronger decline over time in executive functions. The latter phenomenon is not often documented. Although modifications in cognitive functioning with aging are inevitable, life course socioeconomic circumstances impact the timing of this process. We conclude that the etiology of cognitive aging is the result of multiple social processes, defined by the socioeconomic conditions in childhood and all along the life course., Cognitive aging is characterized by large heterogeneity, which may be due to variations in childhood socioeconomic conditions (CSC). Although there is substantial evidence for an effect of CSC on levels of cognitive functioning at older age, results on associations with cognitive decline are mixed. We examined by means of an accelerated longitudinal design the association between CSC and cognitive trajectories from 50 to 96 years. Cognition included two functions generally found to decline with aging: delayed recall and verbal fluency. Data are from six waves of the Survey of Health, Aging, and Retirement in Europe (SHARE), conducted between 2004 and 2015 (n = 24,066 at baseline; 56% female, age 50+). We found a consistent CSC pattern in levels of cognitive functioning in later life. Older people with disadvantaged CSC had lower levels of cognitive functioning than those with more advantaged CSC. We also find that decline is almost 1.6 times faster in the most advantaged group compared with the most disadvantaged group. The faster decline for people with more advantaged CSC becomes less pronounced when we additionally control for adulthood socioeconomic conditions and current levels of physical activity, depressive symptoms, and partner status. Our findings are in line with the latency, pathway, and cumulative model and lend support to theories of cognitive reserve, stating that neuronal loss can no longer be repaired in people with more cognitive reserve once the underlying pathology is substantial and speed of decline is accelerated.

Malaria transmission has been substantially reduced across Africa through the distribution of long-lasting insecticidal nets (LLINs). However, the emergence of insecticide resistance within mosquito vectors risks jeopardizing the future efficacy of this control strategy. The severity of this threat is uncertain because the consequences of resistance for mosquito fitness are poorly understood: while resistant mosquitoes are no longer immediately killed upon contact with LLINs, their transmission potential may be curtailed because of longer-term fitness costs that persist beyond the first 24 h after exposure. Here, we used a Bayesian state-space model to quantify the immediate (within 24 h of exposure) and delayed (>24 h after exposure) impact of insecticides on daily survival and malaria transmission potential of moderately and highly resistant laboratory populations of the major African malaria vector Anopheles gambiae. Contact with LLINs reduced the immediate survival of moderately and highly resistant An. gambiae strains by 60–100% and 3–61%, respectively, and delayed mortality impacts occurring beyond the first 24 h after exposure further reduced their overall life spans by nearly one-half. In total, insecticide exposure was predicted to reduce the lifetime malaria transmission potential of insecticide-resistant vectors by two-thirds, with delayed effects accounting for at least one-half of this reduction. The existence of substantial, previously unreported, delayed mortality effects within highly resistant malaria vectors following exposure to insecticides does not diminish the threat of growing resistance, but posits an explanation for the apparent paradox of continued LLIN effectiveness in the presence of high insecticide resistance.

The Plio-Pleistocene hominin sample from Dmanisi (Georgia), dated to 1.77 million years ago, is unique in offering detailed insights into patterns of morphological variation within a paleodeme of early Homo. Cranial and dentoalveolar morphologies exhibit a high degree of diversity, but the causes of variation are still relatively unexplored. Here we show that wear-related dentoalveolar remodeling is one of the principal mechanisms causing mandibular shape variation in fossil Homo and in modern human hunter–gatherer populations. We identify a consistent pattern of mandibular morphological alteration, suggesting that dental wear and compensatory remodeling mechanisms remained fairly constant throughout the evolution of the genus Homo. With increasing occlusal and interproximal tooth wear, the teeth continue to erupt, the posterior dentition tends to drift in a mesial direction, and the front teeth become more upright. The resulting changes in dentognathic size and shape are substantial and need to be taken into account in comparative taxonomic analyses of isolated hominin mandibles. Our data further show that excessive tooth wear eventually leads to a breakdown of the normal remodeling mechanisms, resulting in dentognathic pathologies, tooth loss, and loss of masticatory function. Complete breakdown of dentognathic homeostasis, however, is unlikely to have limited the life span of early Homo because this effect was likely mediated by the preparation of soft foods.

It has long been known that human cognitive function improves through young adulthood and then declines across the later life span. Here we examined how decision-making function changes across the life span by measuring risk and ambiguity attitudes in the gain and loss domains, as well as choice consistency, in an urban cohort ranging in age from 12 to 90 y. We identified several important age-related patterns in decision making under uncertainty: First, we found that healthy elders between the ages of 65 and 90 were strikingly inconsistent in their choices compared with younger subjects. Just as elders show profound declines in cognitive function, they also show profound declines in choice rationality compared with their younger peers. Second, we found that the widely documented phenomenon of ambiguity aversion is specific to the gain domain and does not occur in the loss domain, except for a slight effect in older adults. Finally, extending an earlier report by our group, we found that risk attitudes across the life span show an inverted U-shaped function; both elders and adolescents are more risk-averse than their midlife counterparts. Taken together, these characterizations of decision-making function across the life span in this urban cohort strengthen the conclusions of previous reports suggesting a profound impact of aging on cognitive function in this domain.

In mice, recent thymic emigrants (RTEs) make up a large part of the naïve T cell pool and have been suggested to be a distinct short-lived pool. In humans, however, the life span and number of RTEs are unknown. Although2H2O labeling in young mice showed high thymic-dependent daily naïve T cell production, long term up- and down-labeling with2H2O in human adults revealed a low daily production of naïve T cells. Using mathematical modeling, we estimated human naïve CD4 and CD8 T cell half-lives of 4.2 and 6.5 years, respectively, whereas memory CD4 and CD8 T cells had half-lives of 0.4 and 0.7 year. The estimated half-life of recently produced naïve T cells was much longer than these average half-lives. Thus, our data are incompatible with a substantial short-lived RTE population in human adults and suggest that the few naïve T cells that are newly produced are preferentially incorporated in the peripheral pool.

During recent years there has developed an increased interest in the question of the dependence of life span on various factors, such as weight, sex, country versus city dwelling, lipoprotein concentration in blood plasma, cigarette smoking, and exposure to high-energy radiation, and much statistical information about it has been gathered.(1) Some effort has also been made, in the case of factors, such as radiation exposure, that can assume a series of values, to express by an equation the relation between the average life span of populations differing with respect to this factor and the parameter representing the factor. Usually a linear equation has been used, often a single term, corresponding to proportionality between the decrease in expected life span and the parameter.