A recent study finds that a new compound reverses many of the major symptoms associated with Fragile X syndrome (FXS), the most common form of inherited intellectual disability and a leading cause of autism. The paper describes the exciting observation that the FXS correction can occur in adult mice, after the symptoms of the condition have already been established.

Fragile X patients suffer from a complex set of neuropsychiatric symptoms of varying severity which include anxiety, hyperactivity, learning and memory deficits, low IQ, social and communication deficits, and seizures. Previous research has suggested that inhibition of mGlu5, a subtype of receptor for the excitatory neurotransmitter glutamate, may be useful for ameliorating many of the major symptoms of the disease.

The new study, a collaboration between a group at F. Hoffmann-La Roche Ltd. in Switzerland, led by Dr. Lothar Lindemann, and a group at the Picower Institute for Learning at the Massachusetts Institute of Technology, led by Dr. Mark Bear, used a newly developed mGlu5 inhibitor called CTEP to examine whether pharmacologic inhibition of mGlu5 could reverse FXS symptoms.
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A major study of the relationships between maternal metabolic conditions and the risk that a child will be born with a neurodevelopmental disorder has found strong links between maternal diabetes and obesity and the likelihood of having a child with autism or another developmental disability.

Conducted by researchers affiliated with the UC Davis MIND Institute, the study found that mothers who were obese were 1-2/3 times more likely to have a child with autism as normal-weight mothers without diabetes or hypertension, and were more than twice as likely to have a child with another developmental disorder.

Mothers with diabetes were found to have nearly 2-1/3 times the chance of having a child with developmental delays as healthy mothers. However, the proportion of mothers with diabetes who had a child with autism was higher than in healthy mothers but did not reach statistical significance.
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Research focuses on the social dysfunction of both disorders and how the causes are different

A UT Dallas professor is studying the differences between the social impairments found in autism and schizophrenia to help develop better treatments for people with both disorders.

Autism spectrum disorder (ASD) and schizophrenia are distinct disorders with unique characteristics, but they share similarities in social dysfunction. For many years, this similarity resulted in confusion in diagnosis. Many young people with ASD were thought to have a childhood version of schizophrenia, said Dr. Noah Sasson, assistant professor in the UT Dallas School of Behavioral and Brain Sciences.

Sasson points out that clear differences exist between people diagnosed with schizophrenia and ASD. Symptoms of ASD can be seen from very early in life, while the onset of schizophrenia typically occurs in young adulthood. And individuals who have schizophrenia often experience hallucinations and delusional thoughts, which are far less common in individuals with ASD.
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Impaired social function is a cardinal symptom of autism spectrum disorders (ASDs). One of the brain circuits that enable us to relate to other people is the "mirror neuron" system. This brain circuit is activated when we watch other people, and allows our brains to represent the actions of others, influencing our ability to learn new tasks and to understand the intentions and experiences of other people.

This mirror neuron system is impaired in individuals with ASD and better understanding the neurobiology of this system could help in the development of new treatments.

In their new study, Dr. Peter Enticott at Monash University and his colleagues used transcranial magnetic stimulation to stimulate the brains of individuals with ASD and healthy individuals while they observed different hand gestures. This allowed the researchers to measure the activity of each individual's mirror neuron system with millisecond precision in response to each observed action.
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