(dailyRx News) While the cause of autism remains a mystery, scientists are zeroing in on the structure of the disease. It's a molecular puzzle. Scientists have discovered that two major brain regions - the cerebral cortex and the temporal lobe - are not distinguishable in people with autism.
A new UCLA study shows that autism makes its mark at the molecular level, resulting in an autistic brain that differs dramatically in structure from a healthy one. This discovery opens new avenues to understanding what causes the disorder.
The collaborative research team, led by Dr. Daniel Geschwind, professor of neurology and psychiatry at the David Geffen School of Medicine at UCLA, compared the brain tissue samples obtained after death from 19 autism patients and 17 healthy volunteers.
Researchers focused on gene expression that directs how information is processed. The first surprise finding was a similar gene expression pattern in most austistic brains.
"Given autism's numerous causes, this was an unexpected and exciting finding," said first author Irina Voineagu, a UCLA postdoctoral fellow in neurology.
Next, they looked for common patterns in two major processing centers in the brain:
- The cerebral cortex's frontal lobe, which plays a role in judgment, creativity, emotions and speech, and
- Temporal lobes that regulate hearing, language and the processing and interpreting of sounds
In healthy brains, scientists saw that more than 500 genes were expressed at different levels in the two regions. In other words, these two regions were very different from one another at the molecular level.
But there were virtually no differences between the two regions in the autistic brains studied.
"In a healthy brain, hundreds of genes behave differently from region to region, and the frontal and temporal lobes are easy to tell apart," Geschwind said. "We didn't see this in the autistic brain. Instead, the frontal lobe closely resembles the temporal lobe. Most of the features that normally distinguish the two regions had disappeared."
What's important about this study, according to Geschwind, is that this discovery suggests "that the common molecular changes in neuron function and communication are a cause, not an effect, of the disease."
The University of Toronto and King's College London collaborated in this study, the findings of which are published in the May, 2011 edition of Nature.