Offspring innate immunity varies with parental age in a long-lived seabird.

Recent studies of wild populations provide compelling evidence that survival and reproduction decrease with age because of senescence, a decline in functional capacities at old ages. However, in the wild, little is known about effects of parental senescence on offspring quality. We used data from a 21-year study to examine the role of parental age on offspring probability of recruitment in a long-lived bird, the blue-footed booby (Sula nebouxii). Offspring probability of recruiting into the breeding population varied over the life of parents and effects age were similar in mothers and fathers. Offspring recruitment was high when parents were roughly 6–12 years old and low before and after then. Effects of parental age on offspring recruitment varied with lifespan (parental age at last reproduction) and previous breeding experience. Offspring recruitment from young and old parents with long reproductive lifespans was greater than that of offspring from parents with short lifespans at young and old ages. For parents with little previous breeding experience recruitment of offspring decreased with their hatch date, but experienced parents were no similarly affected. We found evidence of terminal effects on offspring recruitment in young parents but not in older parents, suggesting that senescence is more likely a gradual process of deterioration than a process of terminal illness. Failure to recruit probably reflects mortality during the first years after independence but also during the fledgling transition to full independence. Our results show effects of parental age and quality on offspring viability in a long-lived wild vertebrate and support the idea that wild populations are composed of individuals of different quality, and that this individual heterogeneity can influence the dynamics of age-structured populations.

Effect of post-hatch transportation duration and parental age on broiler chicken quality, welfare, and productivity

Effect of parental age and developmental rate on the production of active form of Callosobruchus maculatus (F.) (Coleoptera: Bruchidae)

Offspring of older parents in many species have decreased longevity, a faster ageing rate and lower fecundity than offspring born to younger parents. Biomarkers of ageing, such as telomeres, that tend to shorten as individuals age, may provide insight into the mechanisms of such parental age effects. Parental age may be associated with offspring telomere length either directly through inheritance of shortened telomeres or indirectly, for example, through changes in parental care in older parents affecting offspring telomere length. Across the literature there is considerable variation in estimates of the heritability of telomere length, and in the direction and extent of parental age effects on telomere length. To address this, we experimentally tested how parental age is associated with the early-life telomere dynamics of chicks at two time points in a captive population of house sparrows Passer domesticus. We experimentally separated parental age from sex effects, and removed effects of age-assortative mating, by allowing the parent birds to only mate with young, or old partners. The effect of parental age was dependent on the sex of the parent and the chicks, and was found in the father-daughter relationship only; older fathers produced daughters with longer telomere lengths post-fledging. Overall we found that chick telomere length increased between the age of 0.5 and 3 months at the population and individual level. This finding is unusual in birds with such increases more commonly associated with non-avian taxa. Our results suggest parental age effects on telomere length are sex-specific either through indirect or direct inheritance. The study of similar patterns in different species and taxa will help us further understand variation in telomere length and its evolution.

with the hypothesis that parents of intermediate ages produce a greater proportion of female offspring than do younger or older parents. Lowe (1969) and Meadows (1969) implied that the differences Kamaljan reported were statistically significant. Further, Lowe (1969) examined data from red deer, Cervus elaphus, for such an effect, found it, and constructed fecundity tables on the assumption that females between 5 and 8 years of age produce more female than male offspring. If this effect is real and general, most current models of mammalian population dynamics will require modification. Before such a large step is taken, it might be as well to re-examine the evidence on which the hypothesis is based. Kamaljan (1962) presented sex ratios of offspring classified by age of both parents. Parents were divided into 'young', 'intermediate' and 'old', the interval of years these classes represent being given for each species in Table 1. Table 2 shows the 2 values of association between sex ratio of the offspring and the age of the parents. Each results from a 2 x 3 contingency test, the three age-classes of parents being those in Table 1. Since each test has two degrees of freedom, a 2 of at least 5-99 is required before an association is acceptable at the 5% level of significance. Of the ten examples, only one comparison (age of male parent against sex ratio of first-born offspring in man) reached the required level. In each of Kamaljan's examples, parents of intermediate ages produced offspring whose sex ratio was biassed further towards females than was the sex ratio of offspring produced by younger or older parents. This provides strong evidence in favour of the hypothesis, regardless of the general lack ofsignificance shown by individual examples. There is, however, an alternative explanation. When sampling variation is high consequent on low numbers, it is possible unconsciously to choose a set of contiguous ages ofparents whose offspring have a sex ratio deviating from the mean, as may have happened here. Table 1 shows inconsistency in Kamaljan's choice of an intermediate-age set. That for male cattle is narrower than for females, in pigs it is broader for males, and in horses the intermediate age interval is the same for both parental sexes. Even so, the subjectivity evident in the choice of age intervals should have little effect if the number of offspring is large. But, in the present case, subjectivity of selection cannot be ignored as a possible influence on the results: the ranks of

Evidence indicates an association between older parents at birth and increased risk for schizophrenia and autism. Patients with schizophrenia and autism and their first-degree relatives have impaired social functioning; hence, impaired social functioning is probably an intermediate phenotype of the illness. This study tested the hypothesis that advanced father's age at birth would be associated with poorer social functioning in the general population. To test this hypothesis, we examined the association between parental age at birth and the social functioning of their adolescent male offspring in a population-based study. Subjects were 403486, 16- to 17-year-old Israeli-born male adolescents assessed by the Israeli Draft Board. The effect of parental age on social functioning was assessed in analyses controlling for cognitive functioning, the other parent's age, parental socioeconomic status, birth order, and year of draft board assessment. Compared with offspring of parents aged 25-29 years, the prevalence of poor social functioning was increased both in offspring of fathers younger than 20 years (odds ratio [OR] = 1.27, 95% confidence interval [CI] = 1.08-1.49) and in offspring of fathers 45 years old (OR = 1.52, 95% CI = 1.43-1.61). Male adolescent children of mothers aged 40 years and above were 1.15 (95% CI = 1.07-1.24) times more likely to have poor social functioning. These modest associations between parental age and poor social functioning in the general population parallel the associations between parental age and risk for schizophrenia and autism and suggest that the risk pathways between advanced parental age and schizophrenia and autism might, at least partially, include mildly deleterious effects on social functioning.

As organisms age, the fitness of the offspring they produce can decline, which is often attributed to parental senescence. However, few studies have tested for effects of parental age on offspring fitness in wild populations or in short-lived vertebrates, and only recently have studies begun to examine such effects in male and female offspring independently. Here, we use five generations of mark-recapture and genetic parentage data from an island population of a short-lived lizard, the brown anole (Anolis sagrei), to test for effects of maternal and paternal age on the survival to adulthood, first-year reproductive success, longevity, and lifetime fitness of their offspring. When comparing parents of different ages within the same offspring cohort, survival to adulthood increased with paternal age in sons, but we found no effects of maternal or paternal age on any component of fitness in daughters and no evidence that parental age effects differed based on the sex of the parent or the offspring. When considering repeated measures of individual parents sampled at multiple ages, we found that first-year reproductive success of sons decreased with paternal age, but longevity of sons increased with maternal age. However, when pooling sons and daughters, we found no overall effects of parental age on any component of offspring fitness, and little evidence that parental age effects differed between sons and daughters. Our study adds to the growing literature suggesting that negative effects of parental age on offspring fitness may not be as prevalent as once thought, particularly in wild populations.

Background: Alzheimer’s disease (AD) is the most common cause of dementia worldwide, accounting for 50–75% of all cases. While older maternal and paternal age at childbirth are established risk factors for Down syndrome which is associated with later AD, it is still not entirely clear whether parental age is a risk factor for AD. Previous studies have suggested contradictory findings. Objectives: We conducted a systematic review and meta-analysis to examine whether parental (maternal and paternal) age at birth was associated with AD and whether individuals born to younger or older parents were at an increased risk for AD. Methods: Two reviewers searched the electronic database of PubMed for relevant studies. Eligibility for the meta-analysis was based on the following criteria: (1) studies involving patients with AD and an adequate control group, (2) case control or cohort studies, (3) studies investigating parental age. All statistical analyses were completed in STATA/IC version 16. Results: Eleven studies involving 4,371 participants were included in the systematic review and meta-analysis. Meta-analysis demonstrated no significant association between maternal (weighted mean difference [WMD] 0.49, 95% CI –0.52 to 1.49, p = 0.34) and paternal age and AD (WMD 1.00, 95% CI –0.55 to 2.56, p = 0.21). Similarly, individuals born to younger (<25 years) or older parents (>35 years) did not demonstrate a differential risk for AD. Conclusions: Overall, this meta-analysis did not demonstrate an association between parental age and the risk of AD in offspring. These findings should be interpreted with caution given the limited power of the overall meta-analysis and the methodological limitations of the underlying studies as in many cases no adjustment for potential confounders was included.

In humans, it is well known that the parental reproductive age has a strong influence on mutations transmitted to their progeny. Meiotic nondisjunction is known to increase in older mothers, and base substitutions tend to go up with paternal reproductive age. Hence, it is clear that the germinal mutation rates are a function of both maternal and paternal ages in humans. In contrast, it is unknown whether the parental reproductive age has an effect on somatic mutation rates in the progeny, because these are rare and difficult to detect. To address this question, we took advantage of the plant model system Arabidopsis (Arabidopsis thaliana), where mutation detector lines allow for an easy quantitation of somatic mutations, to test the effect of parental age on somatic mutation rates in the progeny. Although we found no significant effect of parental age on base substitutions, we found that frameshift mutations and transposition events increased in the progeny of older parents, an effect that is stronger through the maternal line. In contrast, intrachromosomal recombination events in the progeny decrease with the age of the parents in a parent-of-origin-dependent manner. Our results clearly show that parental reproductive age affects somatic mutation rates in the progeny and, thus, that some form of age-dependent information, which affects the frequency of double-strand breaks and possibly other processes involved in maintaining genome integrity, is transmitted through the gametes.

Offspring quality decreases with parental age in many taxa, with offspring of older parents exhibiting reduced life span, reproductive capacity, and fitness, compared to offspring of younger parents. These “parental age effects,” whose consequences arise in the next generation, can be considered as manifestations of parental senescence, in addition to the more familiar age‐related declines in parent‐generation survival and reproduction. Parental age effects are important because they may have feedback effects on the evolution of demographic trajectories and longevity. In addition to altering the timing of offspring life‐history milestones, parental age effects can also have a negative impact on offspring size, with offspring of older parents being smaller than offspring of younger parents. Here, we consider the effects of advancing parental age on a different aspect of offspring morphology, body symmetry. In this study, we followed all 403 offspring of 30 parents of a bilaterally symmetrical, clonally reproducing aquatic plant species, Lemna turionifera, to test the hypothesis that successive offspring become less symmetrical as their parent ages, using the “Continuous Symmetry Measure” as an index. Although successive offspring of aging parents older than one week became smaller and smaller, we found scant evidence for any reduction in bilateral symmetry.

In this study, we draw from the literature on sibling configurations and parental age to investigate the effects of these factors on the academic achievement of children. The study investigates the effects of maternal age at first birth, maternal age when the respondent was born, and father's age when the respondent was born on ACT scores, grade point averages over three years, and whether or not the parents are providing financial aid to their students. We examine the effects of sibship size, ordinal position, and gender composition of the sibship on these same variables. The study also investigates the extent to which the relationship between parental age and academic outcomes is linear. The relationship of sibship size, ordinal position, and gender composition on the quality of relationships with parents is investigated. Using a sample of freshmen at a mid-western university, we find consistent positive effects of parental age on high school and early college achievement, as well as consistent negative birth order effects on achievement at the high school level. Students with older parents and fewer older siblings consistently performed better. Sibship size and the proportion of females in the sibship had no effect on academic outcomes. Using self-reported data from children on a childhood measure of parental support and interaction and quality of relationships with parents during late adolescence, we also investigate the impact of parental age at birth, and sibling characteristics on childhood and adolescent family environment. Ordinal position had a significant positive effect on the quality of relationships with parents during adolescence, and sibship size had a significant negative effect. We find a curvilinear effect for paternal age on childhood support and parental involvement, but not for academic achievement or quality of relationships with parents in late adolescence. Parental education had a positive significant impact on childhood support and involvement. Children from larger sibships and who were later born children were less likely to receive financial aid from their parents. The results are discussed as they relate to the literature on parental age and sibling configurations, and in terms of their implications for student retention and success.

Higher parental age at childbearing has generated much attention as a potential risk factor for birth disorders; however, previous research findings are mixed. Existing studies have exploited variation in parental age across families, which is problematic because families differ not only in parental age but also in genetic and environmental factors. To isolate the effects of parental age, holding many genetic and environmental factors constant, we exploit the variation in parental age within families and compare outcomes for full siblings. The study data were retrieved from the Medical Birth Registry of Norway, which covers the entire population of births in Norway over an extended period (totaling 1.2 million births). Using variation in parental age when siblings were born, we find large and convex effects of increased parental age on the increased risk of birth disorders. To facilitate comparison with the existing literature, we also estimate the effects of parental age using variation in parental age across families and find that the effects are substantially weaker. We conclude that the existing literature may have underestimated the negative effects of parental aging on adverse offspring outcomes.

Higher parental age at childbearing has generated much attention as a potential risk factor for birth disorders; however, previous research findings are mixed. Existing studies have exploited variation in parental age across families, which is problematic because families differ not only in parental age but also in genetic and environmental factors. To isolate the effects of parental age, holding many genetic and environmental factors constant, we exploit the variation in parental age within families and compare outcomes for full siblings. The study data were retrieved from the Medical Birth Registry of Norway, which covers the entire population of births in Norway over an extended period (totaling 1.2 million births). Using variation in parental age when siblings were born, we find large and convex effects of increased parental age on the increased risk of birth disorders. To facilitate comparison with the existing literature, we also estimate the effects of parental age using variation in parental age across families and find that the effects are substantially weaker. We conclude that the existing literature may have underestimated the negative effects of parental aging on adverse offspring outcomes.

Eggs were collected at intervals of 2 weeks throughout the egg-laying period from beetles maintained at 30°, 25° and 20°C Eggs and larvae were maintained at the same temperature as was used for the parent beetles. Parental age had no effect on the duration of the egg stage or on the weights of the eggs or newly hatched larvae. At each temperature the percentage of eggs which hatched decreased with an increase in parental age, from approximately 90 for those laid during the first 2 months to about 50 for those laid 4 months after emergence. At each temperature, larvae from young parents grew at a slower rate than those from the same parents after they had aged 9 weeks. At 30° there were no other effects of parental age, but at 25° and 20° larvae from young parents required a significantly longer time to complete development and had more molts than those from the same parents after they had aged 1 month or longer. At these temperatures, an increase in parental age resulted in a decrease in the duration of adult life. This effect was not evident until the parents had aged 9 weeks in Series A (water was added to the food after 6 weeks of larval life) and 6 weeks in Series B at 25°C. (water was added to the food throughout the larval period). In every case larvae from Series B grew at a faster rate and required less time for development than those of Series A.

Mutations in proteins involved in telomere maintenance lead to a range of human diseases, including dyskeratosis congenita, idiopathic pulmonary fibrosis and cancer. Telomerase functions to add telomeric repeats back onto the ends of chromosomes, however non-canonical roles of components of telomerase have recently been suggested. Here we use a zebrafish telomerase mutant which harbours a nonsense mutation in tert to investigate the adult phenotypes of fish derived from heterozygous parents of different ages. Furthermore we use whole genome sequencing data to estimate average telomere lengths. We show that homozygous offspring from older heterozygotes exhibit signs of body wasting at a younger age than those of younger parents, and that offspring of older heterozygous parents weigh less irrespective of genotype. We also demonstrate that tert homozygous mutant fish have a male sex bias, and that clutches from older parents also have a male sex bias in the heterozygous and wild-type populations. Telomere length analysis reveals that the telomeres of younger heterozygous parents are shorter than those of older heterozygous parents. These data indicate that the phenotypes observed in offspring from older parents cannot be explained by telomere length. Instead we propose that Tert functions outside of telomere length maintenance in an age-dependent manner to influence the adult phenotypes of the next generation.