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How Does Autism Affect Communication

5 min read

How Does Autism Affect Communication – As alarm grew about the prevalence of autism at the beginning of this century, public discussion of the “epidemic” grew. This language has softened and it is now clear that there were many people with autism all along who were not aware of the condition until recently.

But what causes it? The question that arises today is that there is no single cause – rather, many factors, both genetic and environmental, operate in a complex manner. Because of this complexity and the hundreds of different genes that have been implicated, improving human intelligence can take many paths to a place on the autism spectrum.

How Does Autism Affect Communication

And it may help explain something true about autism: It varies greatly from person to person.

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According to doctors, autism includes deficits in speech and behavior, repetitive behavior that creates obstacles in the beginning of normal relationships. The fine lines of this definition – where does communication difficulty turn into lack of communication? – to encourage the blurring of boundaries between people diagnosed with autism and those who approach, but do not cross the line into the realm of diagnosis.

Those with conditions that show a pattern rather than a continuum of strength. Their use of language varies from not speaking at all to speaking. They may show a special interest in elaborate blinds or a more but more socially acceptable interest in dinosaurs. As with most human characteristics, each trait exists on a spectrum, and they combine in a person to create what clinicians call autism.

By pinpointing risk genes and unraveling their functions, studying the roots of autism also provides new insights into the development of the entire human brain, autistic or not. Here’s a taster of what we currently know and don’t know about the causes of autism—and what research is teaching us about human neurology.

Despite the many and varied threads that can intertwine to cause autism, the disorder is well known. According to James McPartland, a psychologist at the Yale Children’s Center, clinicians often report when they see autism that they see a familiar, if well-defined, constellation of behaviors. “So, of course, there is something true about autism, and everyone who is diagnosed with autism exhibits these characteristics.”

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The number of autism diagnoses in the US has increased over the years, as shown in the graph. Statistical means among 8-year-old children from multiple CDC Autism and Developmental Disabilities Monitoring Network reporting sites. Not all sites reported in each year are shown, and the range can be wide (for example, in 2000, the average was 6.7 per 1,000 children, but the number of different sites reported ranged from 4.5 to 9.9) . Part of the increase is due to increased awareness and changing assessment models.

[Image: Bar chart showing the growth of autism from 2000 to 2014, based on data from the Centers for Disease Control (CDC).]

At the same time, subtle differences in the manifestations of each person with autistic behavior make him unique, says Pauline Chest, child psychiatrist Inserm U 894, Center of Psychiatry and Neuroscience in Paris. “We’re describing a certain quality that’s there – this social instability and complexity. You can have more or less, but it’s there.”

The prevalence or severity of autism can be traced in part to the types of different genes that contribute to it in a given person. Some of these variants have major consequences on their own, while others make minor contributions, and any autistic person may have their own unique combination of both. One thing seems clear: while there may be some truth to autism, as McPartland says, the existence of “one true autism gene” or one gene for every autism is unlikely.

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Instead, the combination of genes and the effects they produce will be measured, says epidemiologist Elise Robinson of Harvard University’s T.H. Chan School of Public Health and Associate Member of the Broad Institute. People with autism and intellectual disability, for example, tend to have more genetic mutations than people with autism alone.

The search for these genetic variants is not just scientific curiosity or the search for potential drug targets. Because many of these genes control the structure of the human brain and how nerve cells interact with each other, studying how they contribute to the development of autism may also reveal more about how the human brain works.

For example, a key characteristic of autism is atypical social behavior, such as sometimes ignoring “social” facial expressions like the eyes. Although the habit of looking someone in the eye seems like something we can learn from other people, autism research has shown that genes are behind this attitude.

In a 2017 study, the authors showed for the first time that identical twins are similar in how they view videos with social content, such as faces. When watching the same video, identical pairs simultaneously shifted their gaze and focused on the same objects more than did non-identical pairs or unrelated children. The fact that almost every pair of twins shares this trait suggests a strong genetic basis for the trait.

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After identifying the strong genetic potential of this disorder, researchers from Emory University and the Marcus Autism Center in Georgia and Washington University in St. Lucie. in autistic children. They concluded that although the idea of ​​looking at other parts of the face is not only genetic, most of it is.

Such studies are a powerful tool for elucidating the number of genes that determine personality, and such studies show that the genetic contribution to autism is substantial. Autism also causes clustering in non-twin family members, with one in five children who have an older sibling with autism also developing autism.

Overall, genetics accounts for 70 to 80 percent of the cause of autism, says neuroscientist Daniel Geschwind, director of the Center for Autism Research and Treatment at the University of California, Los Angeles. In comparison, illnesses such as depression account for less than 50 percent, he says. Alessandro Gozzi, a neuropathologist and group leader at the Istituto Italiano di Tecnologia, measures the genetic power even further, establishing a rate of exchange between twins of up to 95%, depending on the strictness of the diagnostic boundaries. But regardless of the actual significance, he says the “overwhelming consensus” among autism researchers is that genetics is the most powerful determinant of autism.

Moving to the next step, finding specific genes, is a huge task. It’s also something that contributes to understanding how the brain works best.

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There are so many candidate genes today, but few stand out for their ability to have a big impact. Chest cites fragile X syndrome and Rett syndrome as examples, both genetic disorders (called syndromes because they are defined by a group of traits) associated with variants in a single gene or region of a chromosome and closely related to autism.

The gene associated with fragile X syndrome is located on the X chromosome. Its name, FMR1, is easily forgotten, but its diversity results are not. Research into the cause of fragile X shows that the protein that this gene encodes, FMRP, acts as a mobile phone for RNA molecules that are important for communication between nerve cells and plasticity in the brain. In people with weak X, the cells do not make the protein or make very little of it. Fragile X FMR1 variants are the most common cause of intellectual disability and are involved in 1-6 percent of autism cases.

Like FMR1, the genetic mutations associated with Rett syndrome affect brain development. A gene called methyl CpG-binding protein 2, or MECP2, is responsible for turning many brain-related genes on and off. Because of this important role of MECP2, mutations that affect its function can have serious consequences. Some of the causes are so similar to autism that Rett syndrome was classified as an autism spectrum disorder until 2013.

Some genetic syndromes also include autism as a factor. Some are caused by variations in a gene called SHANK3, which, like many genes linked to autism, is involved in brain development and function. It is a protein that helps code for the formation and repair of nerve cells so that a nerve cell can communicate with others. The SHANK3 protein also provides a physical scaffold for attachment of these cells to the surface. Most people who have mutations that prevent the production of the SHANK3 protein, or who are missing part of the gene on chromosome 22, have autism or Phelan-McDermid syndrome, which often includes autism.

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However, another disease results from the loss or duplication of a part of chromosome 16. Researchers have linked this chromosomal change to autism in studies comparing the DNA of people with and without the disorder, picking out a sequence change found only in autistic participants.

Despite their apparent association with autism, these syndromes are rare. “They are together

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