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At least 19 recordsLinked to original sources
PubMed1992

Inverse relationship between age at onset of Huntington disease and paternal age suggests involvement of genetic imprinting.

It is well recognized that age at onset of Huntington disease (HD) is strongly influenced by the sex of the affected parent, and this has lead to suggestions that genetic imprinting or maternal specific factors may play a role in the expression of the disease. This study evaluated maternal and paternal ages, birth order, parental age at onset, and sex of the affected parent and grandparent in 1,764 patients in the National HD Roster by using linear-regression techniques which incorporated a weighted least-squares approach to accommodate the correlation among siblings. It was found that paternal age is negatively associated with age at onset of HD, particularly among subjects who inherit the mutant gene from grandfathers. Apparent associations between age at onset and birth order and between age at onset and maternal age were not significant after adjustment for paternal age. The paternal age effect is strongest among juvenile-onset cases and individuals with anticipation of greater than or equal to 10 years, although it is detectable across the entire age-at-onset distribution. The tendency for older fathers, including those not transmitting the HD gene, to have affected offspring with early-onset disease may be consistent with a gene imprinting mechanism involving DNA methylation. Because paternal age in unaffected fathers is also a significant determinant of age at onset, methylation in this context might involve HD modifier genes or the normal HD allele.

Adolescent↗
PubMed1978

Reexamination of paternal age effect in Down's syndrome.

Paternal age distribution for 1279 cases of Down's syndrome born in 1952--1968 was compared with the corresponding distribution for the general population, corrected for the maternal age as well as for the year of birth of the patients. Although there was no difference in the mean paternal age, the two distributions differed significantly, largely due to the excess of fathers aged 55 years and over and to the deficit of those aged 40--44 years in the patients born to mothers aged 30 years and over. The overall pattern of the relative incidence of Down's syndrome with advancing paternal age, with maternal age controlled, seems consistent with the hypothesis proposed by Stene et al. (1977). It increased from 0.8 for fathers aged 20--24 years slowly up to 1.2 for those aged 45--49 years, though with an intermediate drop to 0.8 at the age of 40--44 years, and then sharply to 2.4 for those aged 55 years and over. This rising pattern of the relative incidence with paternal age was essentially the same for the patients born in 1952--1960 and for those born in 1961--1968, although the slope was less steep in the latter than in the former group.

Adolescent↗
PubMed1978

Down syndrome, paternal age, maternal age and birth order.

Recent cytogenetic evidence has shown that trisomy 21 can arise, perphaps even in substantial proportion, from paternal nondisjunction. The statistical association between Down syndrome incidence and maternal age, paternal age and birth order has been studied in a sample of over 4000 cases. The size of this sample made it possible to control for the effect of maternal age by single years of age during the search for a paternal age effect and vice versa, and the importance of such stringent control is emphasized. The maternal age association was confirmed with an extremely high degree of statistical significance while no independent effect of paternal age was found; indeed, the rates at paternal ages over 45 years appear to be nearly constant. After adjusting for the effects of parental age, a significant inverse association of birth order with incidence was noted. It also appears that the incidence among very young mothers may be high: for maternal ages 15 years and less the rates seem to be equivalent to those found at 30 or 35 years. In order to help answer the question of whether the maternal age association is the result of increasing rates of nondisjunction or of some other mechanism (for example, an age related defect in a spontaneous abortion screening mechanism), the proportion of cases due to maternal and paternal nondisjunction at different parental ages must be determined.

Adolescent↗
PubMed1977

Paternal age effect in Down's syndrome.

Increasing incidence of Down's syndrome with advancing paternal age for given maternal age has been demonstrated. Comparisons are made between an almost complete Down's syndrome sample from the Copenhagen Metropolitan Area and a randomly selected sample of births from the same area and the same time period. Men above 55 years have a significantly increased risk of getting children with Down's syndrome.

Adolescent↗
PubMed1975

Older paternal age and fresh gene mutation: data on additional disorders.

Older paternal age has previously been documented as a factor in sporadic fresh mutational cases of several autosomal dominant disorders. In this collaborative study, an older mean paternal age has been documented in sporadic cases of at least five additional dominantly inheritable disorders; the basal cell nevus syndrome, the Waardenburg syndrome, the Crouzon syndrome, the oculo-dental-digital sysdrome, and the Treacher-Collins syndrome. It was also found to be a factor in acrodysostosis and progeria, suggesting a fresh mutant gene etiology for these two conditions in which virtually all cases have been sporadic and the mode of genetic etiology has been unknown.

Age Factors↗
PubMed1977

Statistical methods for detecting a moderate paternal age effect on incidence of disorder when a maternal one is present.

A statistical method is developed for detecting a moderate effect on the incidence of a disorder caused by advancing age of one parent when it is known that advancing age of the other parent is of great aetiological importance. The method is a conditional test procedure given the parental ages, therefore no assumptions about the parental age distributions have to be made. The method is applied on Danish material on Down's syndrome, for which a paternal age effect is demonstrated. Methods used in some well-known previous investigations have been discussed. Several of them, e.g. the classical one of Penrose (1933), could hardly detect any paternal age effect in Down's syndrome on the available data, because these methods are heavily affected by certain fertility patterns not recognized previously.

Denmark↗
PubMed1992

A study of paternal age and sex ratio in sperm chromosome complements.

There is conflicting evidence as to whether the secondary sex ratio in humans decreases with paternal age. Such an age effect could be caused by an altered frequency in the production of X-chromosome and Y-chromosome-bearing sperm as a man ages. To study this possibility we analysed 9,225 sperm karyotypes from 143 men aged 21-55 years. Human pronuclear sperm chromosome complements were obtained after fusion with golden hamster oocytes. The percentage of X- and Y-chromosome complements was not significantly related to donor age.

Adult↗
PubMed1979

Anencephaly in Japan: paternal age, maternal age and birth order.

The statistical association between incidence of anencephaly and paternal age, maternal age and birth order was analysed in 1815 cases of foetal deaths with anencephaly reported during 1975--6. The birth order association was confirmed with an extremely high degree of statistical significance.

Adolescent↗
PubMed1979

Paternal age and Down syndrome.

The frequency of Down syndrome (DS) in infants of older fathers has been examined in two sets of data. The effect of maternal age was controlled by single years of age. Lack of tight control has been an important weakness of other studies on this subject. Data obtained in metropolitan Atlanta by an intensive case-ascertainment program showed no overall excess of DS infants born to older fathers. Nor was there evidence of such an effect in recent birth certificate data made available by the National Center for Health Statistics. The Atlanta data suggest an increased number of DS infants born to older fathers who had children by women less than or equal to 34 years. However, there was a small deficiency of DS infants born to older fathers by women greater than or equal to 35 years. The possibility of a paternal-age effect remains open, but the available data suggest that, if it exists, it is quite small.

Adult↗
PubMed1976

Paternal age, stillbirths and mutation.

Previous suggestions that accumulation of mutations in the germ line of ageing fathers causes an increased stillbirth rate were based on analyses of data which were heterogeneous for social variables whose effects were confounded with possible paternal age effects. This study was confined to the analysis of stillbirth rates of groups of women selected to be homogeneous for education, previous pregnancy outcomes, age, race and marital status. It is concluded that stillbirth rates do not increase with father's age independently of maternal variables. Neither accumulation of mutations in the paternal germ line nor other biological change associated with father's age can be inferred to cause an increase in risk of stillbirth with increasing paternal age.

Birth Order↗
PubMed1992

Reduced recombination and paternal age effect in Klinefelter syndrome.

The parental origin of the additional sex chromosome was studied in 47 cases with an XXY sex chromosome constitution. In 23 cases (49%), the error occurred during the first paternal meiotic division. Maternal origin of the additional chromosome was found in the remaining 24 cases (51%). Centromeric homo- versus heterozygosity could be determined in 18 out of the 24 maternally derived cases. According to the centromeric status and recombination rate, the nondisjunction was attributable in 9 cases (50%) to an error at the first maternal meiotic division, in 7 cases (39%) to an error at the second maternal meiotic division and in 2 cases (11%) to a nullo-chiasmata nondisjunction at meiosis II or to postzygotic mitotic error. No recombination, and in particular none in the pericentromeric region, was found in any of the 9 cases due to nondisjunction at the first maternal meiotic division. Significantly increased paternal age was found in the paternally derived cases. Maternal age was significantly higher in the maternally derived cases due to a meiotic I error compared with those due to a meiotic II error. There were no significant clinical differences between patients with respect to the origin of the additional X chromosome.

Adult↗
PubMed1979

Paternal age effect in fibrodysplasia ossificans progressiva.

Analysis by the method of Smith (1972) of birth order and parental age data collected from 38 of 42 patients with fibrodysplasia ossificans progressive shows a significant paternal age effect. This finding among the sporadically occurring cases would support the proposition that this condition usually arises as a new dominant mutation.

Adult↗
PubMed1979

The secondary sex ratio, paternal age, maternal age and birth order in Japan.

The simultaneous effects of several variables on the secondary sex ratio have been examined using data from over 3.7 million births which occurred in Japan during 1975--6. A weak and negative association between sex ratio and birth order was observed but it was not significant in the statistical sense. A negative effect of paternal age--birth order interaction was obtained when maternal age was controlled. The quadratic model is much more powerful than the linear model in explaining the sex ratio variability.

Adolescent↗
PubMed1992

Genetics of neurofibromatosis 1 in Japan: mutation rate and paternal age effect.

We have performed formal genetic studies on 26 patients (14 males, 12 females) with neurofibromatosis 1 (von Recklinghausen's disease, NF1) in Japan. Family studies of 74 members of 18 kindreds revealed that 50% of the cases were caused by a new mutation; the mutation rate was assumed to be 7.3-10.5 x 10(-5). A tendency of paternal age effect, which was not accounted for by the maternal age effect, was observed, but live-birth order had no significant effect. Genetic linkage of neurofibromatosis 1 to the NF1 gene or the genetic marker in the pericentric region of chromosome 17 was established in 3 informative families.

Age Factors↗
PubMed1991

Factors associated with failure to receive antenatal care.

A community-based case-control study was conducted to characterize pregnant women who did not receive antenatal care. 1,274 deliveries over a 1-year period were documented by weekly visits to 120 study villages. Eighty five women (6.7%) received no antenatal care. By univariate analysis, factors found to be associated with failure to receive antenatal care included maternal age, paternal age, paternal education, home ownership, availability of toilet, annual income, housing condition, gravidity, parity, history of infant death and birth intervals. After logistic regression analysis, only paternal age, paternal education, parity and lack of toilet in the household were found to be associated with failure to receive antenatal care.

Adolescent↗