Intellectual Disability Tied to Father Being Older at Conception
Published: 2011-10-13 - Updated: 2022-06-20
Author: British Medical Journal (BMJ) | Contact: bmj.com
Peer-Reviewed Publication: N/A
Additional References: Cognitive Disabilities Publications
Synopsis: Chromosomal abnormalities linked to intellectual disability can be traced back to an older father when the child is conceived. Copy number variations or CNVs cause chromosomal abnormalities. These structural variations result in missing, repeated, inverted, or misplaced DNA sequences in cells. A significant increase in the father's age was found in the group of CNVs in non-repetitive DNA sequences - which accounted for most CNVs - providing crucial insight into how and why disease-causing CNVs are formed.
- Chromosomes are thread-like structures located inside the nucleus of animal and plant cells. Each chromosome is made of protein and a single molecule of deoxyribonucleic acid (DNA). Passed from parents to offspring, DNA contains the specific instructions that make each type of living creature unique. Humans have 23 pairs of chromosomes, for a total of 46 chromosomes. Females have two X chromosomes in their cells, while males have one X and one Y chromosome.
Faulty intellectual disability genes linked to older dads at conception. Chromosomal abnormalities linked to intellectual disability can be traced back to the father, particularly those who are older when the child is conceived, finds research published online in the Journal of Medical Genetics.
Chromosomal abnormalities are caused by copy number variations or CNVs. These structural variations result in missing, repeated, inverted, or misplaced DNA sequences in cells. Copy number variations can be inherited or arise anew and are a common cause of disease. However, little is known about how CNVs are formed, for example, if they occur more frequently on the DNA sequence passed on by the mother or the father or if parental age is important.
The research team systematically analyzed the prevalence of rare CNVs in almost 3500 people with intellectual disabilities between 2006 and 2010. They found CNVs that had arisen anew, as opposed to being inherited, in 227 people, meaning the prevalence was around twice as common in this group as among people with autism and three times as common as among those with asthma.
Further analysis to determine the parental origin of the CNVs in the 118 people for whom data were available showed that 90 had come from the father and that three-quarters represented missing DNA sequences.
The researchers compared the father's age at the time of birth in the group with CNVs with people with no intellectual disability, matching for ethnicity and era of birth to minimize the impact of any cultural or social factors. But they found no differences in paternal age between the two groups.
The researchers then divided people with CNVs into two groups:
- Those with CNVs occurring in regions of the genome with highly repetitive DNA sequences.
- Those with CNVs occurring in non - repetitive DNA sequences.
They also compared paternal ages in both groups with those of the people without any intellectual disability.
A significant increase in the father's age was found in the group of CNVs in non-repetitive DNA sequences - which accounted for most CNVs - providing crucial insight into understanding how and why disease-causing CNVs are formed, say the authors.
The findings also indicate that newly arising CNVs not only originate more often from the father's DNA but that the father's age has a role, the authors add.
"In conclusion, our data provide for the first time convincing evidence that CNVs in intellectual disability are largely paternal in origin," they write.
They suggest that ongoing cell divisions of self can explain both the gender and age bias - renewing sperm cells during the fetal development of boys - with the potential for mistakes - as well as impaired DNA genesis and repair as a consequence of the aging process.
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