At the beginning of the year, I read an interesting book by Dr. Temple Grandin, a professor of animal science who happens to have Asperger’s Syndrom (a form of autism), called Thinking in Pictures. This interesting and enlightening book describes Grandin’s experience with autism and how it helps her relate to animals.
In this book, she touches on the fact that many people who have autism have trouble interpreting the unsaid innuendos, social cues, and sarcastic remarks often used in everyday conversation. This can cause a feeling of confusion and isolation which often times results in the person pulling away from people around them
In a new study published in the journal Social Neuroscience, a team of researchers from Carnegie Mellon University tries to pin point the underlying mechanism of this experience. Here, they show evidence suggesting that this trouble is a result of faulty social network connections and inefficient neuronal pathways. In other words, messages important for understanding non-verbal social cues in an autistic brain are slow or have lower levels of transmission than in a normal brain.
This research highlights an important study published in Science earlier in the month in which the researches searched the genome of families with shared ancestry to find inherited factors for autism. During the course of their research, they noticed that all of the genes in common within a family had high levels of expression in the brain. They go on to show that many of these genes may mediate neuronal synaptic development and plasticity. Here is an excerpt from their conclusions:
Early brain development is driven largely by intrinsic patterns of gene expression that do not depend on experience-driven synaptic activity. Mutations in the genes active in early development can lead to brain malformations or severe mental retardation. In contrast, postnatal brain development requires input from the environment that triggers the release of neurotransmitter and promotes critical aspects of synaptic maturation. During this process, neural activity alters the expression of hundreds of genes, each with a defined temporal course that may be particularly vulnerable to gene dosage changes. The connection between experience-dependent neural activity and gene expression in the postnatal period forms the basis of learning and memory, and autism symptoms typically emerge during these later stages of development. Our finding that deletions of genes regulated by neuronal activity or regions potentially involved in regulation of gene expression in autism suggests that defects in activity-dependent gene expression may be a cause of cognitive deficits in patients with autism. Therefore, disruption of activity-regulated synaptic development may be one mechanism common to at least a subset of seemingly heterogeneous autism-associated mutations.
Every time you learn something new, a new connection forms in your brain. As you are reading this, you are making new connections! So, according to the authors, before you are born your brain develops according to a set plan but during childhood certain genes need to be working to make these new connections.
The findings from this research suggests that in children with autism there may be a defect in early learning due to genetic mutations which makes it more difficult to form new connections and, therefore, to process and learn new things. Although this makes things more difficult, it is not impossible to make these connections but it will take longer and require more repetition, which is why it is so important for this disease to be diagnosed as early as possible and start teaching these children in a way that benefits them the most.