961 research outputs found
The new biology of ageing
Human life expectancy in developed countries has increased steadily for over 150 years, through improvements in public health and lifestyle. More people are hence living long enough to suffer age-related loss of function and disease, and there is a need to improve the health of older people. Ageing is a complex process of damage accumulation, and has been viewed as experimentally and medically intractable. This view has been reinforced by the realization that ageing is a disadvantageous trait that evolves as a side effect of mutation accumulation or a benefit to the young, because of the decline in the force of natural selection at later ages. However, important recent discoveries are that mutations in single genes can extend lifespan of laboratory model organisms and that the mechanisms involved are conserved across large evolutionary distances, including to mammals. These mutations keep the animals functional and pathology-free to later ages, and they can protect against specific ageing-related diseases, including neurodegenerative disease and cancer. Preliminary indications suggest that these new findings from the laboratory may well also apply to humans. Translating these discoveries into medical treatments poses new challenges, including changing clinical thinking towards broad-spectrum, preventative medicine and finding novel routes to drug development
Anxiety: An Evolutionary Approach
Anxiety disorders are among the most common mental illnesses, with huge attendant suffering. Current treatments are not universally effective, suggesting that a deeper understanding of the causes of anxiety is needed. To understand anxiety disorders better, it is first necessary to understand the normal anxiety response. This entails considering its evolutionary function as well as the mechanisms underlying it. We argue that the function of the human anxiety response, and homologues in other species, is to prepare the individual to detect and deal with threats. We use a signal detection framework to show that the threshold for expressing the anxiety response ought to vary with the probability of threats occurring, and the individual's vulnerability to them if they do occur. These predictions are consistent with major patterns in the epidemiology of anxiety. Implications for research and treatment are discussed
Individual variation in ageâdependent reproduction: Fast explorers live fast but senesce young?
Adaptive integration of life history and behaviour is expected to result in variation in the paceâofâlife. Previous work focused on whether âriskyâ phenotypes live fast but die young, but reported conflicting support. We posit that individuals exhibiting risky phenotypes may alternatively invest heavily in earlyâlife reproduction but consequently suffer greater reproductive senescence.
We used a 7âyear longitudinal dataset with >1,200 breeding records of >800 female great tits assayed annually for exploratory behaviour to test whether withinâindividual age dependency of reproduction varied with exploratory behaviour. We controlled for biasing effects of selective (dis)appearance and withinâindividual behavioural plasticity.
Slower and faster explorers produced moderateâsized clutches when young; faster explorers subsequently showed an increase in clutch size that diminished with age (with moderate support for declines when old), whereas slower explorers produced moderateâsized clutches throughout their lives. There was some evidence that the same pattern characterized annual fledgling success, if so, unpredictable environmental effects diluted personalityârelated differences in this downstream reproductive trait.
Support for ageârelated selective appearance was apparent, but only when failing to appreciate withinâindividual plasticity in reproduction and behaviour.
Our study identifies withinâindividual ageâdependent reproduction, and reproductive senescence, as key components of lifeâhistory strategies that vary between individuals differing in risky behaviour. Future research should thus incorporate ageâdependent reproduction in paceâofâlife studies
Dietary and serum tyrosine, white matter microstructure and inter-individual variability in executive functions in overweight adults: Relation to sex/gender and age
Tyrosine (tyr), the precursor of the neurotransmitter dopamine, is known to modulate cognitive functions including executive attention. Tyr supplementation is suggested to influence dopamine-modulated cognitive performance. However, results are inconclusive regarding the presence or strength and also the direction of the association between tyr and cognitive function. This pre-registered cross-sectional analysis investigates whether diet-associated serum tyr relates to executive attention performance, and whether this relationship is moderated by differences in white matter microstructure. 59 healthy, overweight, young to middle-aged adults (20 female, 28.3 ± 6.6 years, BMI: 27.3 ± 1.5 kg/m2) drawn from a longitudinal study reported dietary habits, donated blood and completed diffusion-weighted brain magnetic resonance imaging and the attention network test. Main analyses were performed using linear regressions and non-parametric voxel-wise inference testing. Confirmatory analyses did neither support an association between dietary and serum tyr nor a relationship between relative serum tyr/large neutral amino acids (LNAA) levels or white matter microstructure and executive attention performance. However, exploratory analyses revealed higher tyr intake, higher serum tyr and better executive attention performance in the male sex/gender group. In addition, older age was associated with higher dietary tyr intake and lower fractional anisotropy in a widespread cluster across the brain. Finally, a positive association between relative serum tyr/LNAA and executive attention performance was found in the male sex/gender group when accounting for age effects. Our analysis advances the field of dopamine-modulated cognitive functions by revealing sex/gender and age differences which might be diet-related. Longitudinal or intervention studies and larger sample sizes are needed to provide more reliable evidence for links between tyr and executive attention
Analytical solution of a generalized Penna model
In 1995 T.J.Penna introduced a simple model of biological aging. A modified
Penna model has been demonstrated to exhibit behaviour of real-life systems
including catastrophic senescence in salmon and a mortality plateau at advanced
ages. We present a general steady-state, analytic solution to the Penna model,
able to deal with arbitrary birth and survivability functions. This solution is
employed to solve standard variant Penna models studied by simulation.
Different Verhulst factors regulating both the birth rate and external death
rate are considered.Comment: 6 figure
Time evolution of the Partridge-Barton Model
The time evolution of the Partridge-Barton model in the presence of the
pleiotropic constraint and deleterious somatic mutations is exactly solved for
arbitrary fecundity in the context of a matricial formalism. Analytical
expressions for the time dependence of the mean survival probabilities are
derived. Using the fact that the asymptotic behavior for large time is
controlled by the largest matrix eigenvalue, we obtain the steady state values
for the mean survival probabilities and the Malthusian growth exponent. The
mean age of the population exhibits a power law decayment. Some Monte
Carlo simulations were also performed and they corroborated our theoretical
results.Comment: 10 pages, Latex, 1 postscript figure, published in Phys. Rev. E 61,
5664 (2000
Change and Aging Senescence as an adaptation
Understanding why we age is a long-lived open problem in evolutionary
biology. Aging is prejudicial to the individual and evolutionary forces should
prevent it, but many species show signs of senescence as individuals age. Here,
I will propose a model for aging based on assumptions that are compatible with
evolutionary theory: i) competition is between individuals; ii) there is some
degree of locality, so quite often competition will between parents and their
progeny; iii) optimal conditions are not stationary, mutation helps each
species to keep competitive. When conditions change, a senescent species can
drive immortal competitors to extinction. This counter-intuitive result arises
from the pruning caused by the death of elder individuals. When there is change
and mutation, each generation is slightly better adapted to the new conditions,
but some older individuals survive by random chance. Senescence can eliminate
those from the genetic pool. Even though individual selection forces always win
over group selection ones, it is not exactly the individual that is selected,
but its lineage. While senescence damages the individuals and has an
evolutionary cost, it has a benefit of its own. It allows each lineage to adapt
faster to changing conditions. We age because the world changes.Comment: 19 pages, 4 figure
The coâevolution of longevity and social life
Living in social groups could influence the evolution of senescence and longevity by affecting key lifeâhistory parameters such as extrinsic mortality and the cost of reproduction. For example, a decrease in extrinsic mortality as a result of social life is predicted to lead to the evolution of increased longevity.
We argue that benefits of social life in terms of increased survival are common only in species in which life in large groups is already the norm, most likely because these species have adapted to depend on social groups. By contrast, species with smaller social groups tend to show no clear association between survival and social group size.
This lack of a consistent benefit of social life on survival casts doubt on the idea that extended longevity should follow the evolution of sociality. In line with this, most rigorous crossâtaxonomic studies failed to find an association between sociality and longevity, suggesting that a social mode of life does not systematically lead to the evolution of extended longevity.
The only effect of sociality on longevity that has been convincingly demonstrated is increased longevity in highâranking individuals from cooperatively breeding vertebrates and social insects, who benefit from the protection and support of their nonâbreeding helpers. In contrast, helpers in these species usually do not show evidence of increased longevity, with the exception of naked mole rats where both breeders and helpers live much longer than related solitary species.
Where longâlived phenotypes exist in highly social species, such as social insect queens and naked mole rats, the scale of longevity increase is often striking. The means by which increased longevity is achieved are still poorly understood, but both social and physiological mechanisms are involved in reducing the burden of disease, including cancer, thus increasing the chances of surviving to old age
Pregnancy and infection [letter]
Pregnant women have an increased severity of infections with some organisms, including influenza virus, hepatitis E virus, herpes simplex virus, and malaria parasites. This review includes an update on immunologic alterations during pregnancy
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