Researchers have recently discovered rare genetic variants transferred between parents without autism and their children. The study finds that such variants are making it substantially more possible for the child to develop autism.
A NEWS10 ABC report said, the cause of autism is not something that has been completely figured out by science. Previous studies have shown various links that play a vital role in children who develop the condition.
A team of researchers working with Simons Foundation in New York said this inherited or genetic connection is particularly prominent among complex families, where other members of that particular family have autism, even if both of their parents don't have it.
According to the study authors led by the University of Washington's Amy Wilfert, Ph.D., new technology and cutting costs on technology and genetic research have enabled them to collect information of thousands of genes from individuals with autism and their families.
Read also: New Study Finding: Autism Is Thrice More Common in Boys, and Vitamin D Has Something To Do With It
'De Novo Mutations'
The study investigators examined almost 11,000 individuals with autism to determine new mutations passed from healthy parents to children on the autism spectrum.
In their study, Recent ultra-rare inherited variants implicate new autism candidate risk genes, published in Nature Genetics; the team noted that most autism genes found to date are coming from research on "de novo mutations."
These are genetic differences that initially develop in an individual who has autism and do not exist in their parents' genes.
Such findings show that genetic variants which lead to autism are possible in a different group of genes from the ones affected by de novo mutations.
Rare Genetic Variants
In a statement, according to a EurekAlert! report, Dr. Wilfert explained that while most mutation studies are focused on de novo mutations, the concentration of this particular research is on rare genetic variants which are frequently understudied in this condition.
The lead author added that the variants are distinctly less damaging than de novo mutations. However, they are possible to contribute nearly as much risk and effect, in similar pathways, through a unique set of genes.
Nevertheless, these variants can only persevere in the general population for a few generations before they get opted out by evolution.
It is commonly known and understood in science that de novo mutations do not have the capability of explaining all of autism's genetic causes.
According to Pamela Feliciano, Ph.D., the SPARK or Simons Powering Autism Research scientific director, autism is an occurrence, sometimes called "missing heritability."
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Do All of These Genes Lead to Autism?
SPARK has contributed over 50 percent of the genetic data scientists used for this particular project. The team analyzed genetic material from 21,000 SPARK participants, including over 6,500 volunteers with an autism spectrum disorder or ASD.
The SPARK has contributed more than 50 percent of the genetic data researchers employed for this research. In total, the team analyzed genetic material from over 21,000 SPARK participants. These volunteers also included more than 6,500 individuals who had autism spectrum disorder (ASD).
Despite knowing about many mutations and genes that reveal a link to autism, the study findings reveal that these new ultra-rare genetic variants do not come from the usual pool of autism genes.
According to Dr. Feliciano, what's more interesting is that most of the variants, comprising 95 percent, do not exist in genes already identified as autism genes, specifying that there are more things to learn about autism genetics.
She added, while today's research is not large enough to confidently determine individual genes that have these rare genetic variants, the consortium's scientific director said they are learning more about such genes.
Related information on Genes and Autism is shown on The Disorder Care's YouTube video below:
Check out more news and information on Autism in Science Times.