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The brains of individuals with autism express lower levels of proteins that direct neuronal growth compared with those of controls, according to a study published 22 August in Molecular Autism1.
Neurons receive signals at their cell body and then transmit an electrical current down a long projection called an axon. This signal cues the release of a chemical messenger, or neurotransmitter, to other neurons across a junction called the synapse.
Several studies have implicated malfunction at the synapse in autism. Structural imaging studies also show abnormalities in white matter, which contains axons, in the brains of individuals with autism.
The new study suggests that these structural alterations could be the result of abnormalities in proteins that direct axons to their correct place in the brain.
In particular, the study found fewer RNA messages that code for three axon-guidance proteins — PLSNA4, ROBO2 and EFNB3 — in 8 postmortem brains from individuals with autism compared with 13 controls. However, the protein levels of only PLSNA4 and ROBO2, and not of EFNB3, are about 50 percent lower in autism brains than in control brains. This discrepancy could result from various factors that regulate gene expression, such as microRNAs.
The differences in protein levels are only found in the anterior cingulate cortex, a brain region involved in decision-making and reward, the study found. There is no difference in the levels of these proteins in the primary motor cortex, a brain region that regulates motor function.
1: Suda S. et al. Mol. Autism 2, 14 (2011) PubMed