Autism which part of brain is affected




















Though not every baby who is later diagnosed with autism will have excess brain fluid at 6 months of age, and not every autistic adult has an underdeveloped corpus callosum, learning more about these subtypes can help researchers develop biologically based treatments for individuals with autism. By joining the discussion, you agree to our privacy policy.

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News The latest developments in autism research. See All in News. Listen to this story:. TAGS: amygdala , biomarkers , brain imaging , brain size , corpus callosum , cortex , gender , hippocampus , MRI , spoken version. Join The Discussion By joining the discussion, you agree to our privacy policy. We care about your data, and we'd like to use cookies to give you a smooth browsing experience. These genes, called ubiquitin ligases, function like a work order, telling the rest of the cell how to deal with the tagged proteins: This one should be discarded, that one should be rerouted to another part of the cell, a third needs to have its activity dialed up or down.

Patients with autism may carry a mutation that prevents one of their ubiquitin genes from working properly. But how problems with tagging proteins affect how the brain is hardwired and operates, and why such problems may lead to autism, has remained poorly understood. To understand the role of ubiquitin genes in brain development, Bonni, first author Pamela Valnegri, PhD, and colleagues removed the ubiquitin gene RNF8 in neurons in the cerebellum of young mice.

The cerebellum is one of the key brain regions affected by autism. The researchers found that neurons that lacked the RNF8 protein formed about 50 percent more synapses -- the connections that allow neurons to send signals from one to another -- than those with the gene. And the extra synapses worked. By measuring the electrical signal in the receiving cells, the researchers found that the strength of the signal was doubled in the mice that lacked the protein. The cerebellum is indispensable for movement and learning motor skills such as how to ride a bicycle.

Some of the recognizable symptoms of autism -- such as motor incoordination and a tendency to walk tippy-toed -- involve control of movement. The animals missing the RNF8 gene in the neurons of their cerebellum did not have any obvious problems with movement: They walked normally and appeared coordinated.

When the researchers tested their ability to learn motor skills, however, the mice without RNF8 failed miserably. The study also noted that the caudate, a brain region that is responsible for storing and processing memories using data from past experiences to guide future behavior, which is important in the development and application of language responded in the opposite way for people with autism. The activity in that region was much more predictable in the brains of autistic people.

The more a person had inflexible, repetitive behaviors, the more the caudate activity in their brain conformed to predictable patterns. This is likely because changes in the structure of individual brain regions drive the differences in the randomness of neural activity. The researchers behind the eLife study posited that when small brain regions undergo changes in their activity and structure, these changes are what leads to the development of complex autism symptoms.

It is not yet known whether the differences in the brain activity directly cause the symptoms of autism or whether they simply correlate to autistic symptoms. If there is a direct relationship between brain activity and autism symptoms, the researchers suggested that it might be possible to change brain activity via magnetic stimulation to the scalp to potentially reduce the severity of the symptoms.

Other studies have also suggested transcranial magnetic stimulation TMS to ease the symptoms of autism. Other researchers have offered additional theories on the effects of autism on the brain. This difficulty with change is a common symptom of autism spectrum disorder. The result of this extended period of connectivity is that the brain cannot easily switch between processes. Researchers found a defective gene that influenced how neurons connect to and communicate with each other.

Studies on animals that lacked the gene also showed too many connections existing between those key brain neurons and difficulties with learning and memory. Many genes have been connected to autism, but six genes attach ubiquitin, a molecular tag, to proteins. These genes tell the rest of the cell what to do with the tagged proteins, such as discard them, move them to another part of the cell, or increase or decrease activity. People with autism might have a mutation that stops one of the ubiquitin genes from functioning as it should.

Again, it is not known how problems with tagging proteins affect the circuitry and operation of the brain to the point that it leads to the development of autism. In humans, the cerebellum is one of the key regions of the brain that is affected by autism. It is responsible for voluntary movements like speech, coordination, balance, and motor control, but it also plays a role in higher cognitive functions, like attention and language.

People on the autism spectrum often have delayed language development and hyper-focused interest on single topics, to the point of not paying attention to anyone or anything else around them.

Even as experts answer some questions about what autism does to the brain, there are further questions raised about other effects, how these effects lead to the development of autism symptoms, and even broader questions about the full scope of the functioning of the human brain itself.

But in individuals with autism, sensory areas of the brain showed more random activity than in individuals without autism. The most random activity occurred in those with the most severe autism. This suggests that the brains of people with autism cannot hold onto and process sensory input for as long as those of neurotypical people. By contrast, a brain region called the caudate showed the opposite pattern, being more predictable in individuals with autism.

The most predictable caudate activity occurred in those individuals with the most inflexible, repetitive behaviors. These differences in this neural randomness appear to result from changes in the structure of the individual brain regions.



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