A new UCLA study pinpoints uniquely human patterns of gene activity in the brain that could shed light on how we evolved differently than chimps.
The identification of these genes could improve understanding of human brain diseases like autism and schizophrenia, as well as learning disorders and addictions.
"Our research suggests that it's not only size, but the rising complexity within brain centers, that led humans to evolve into their own species," principal investigator Dr Daniel Geschwind, professor of neurology at the David Geffen School of Medicine at UCLA.
Geschwind and his colleagues applied next-generation sequencing and other modern methods to study gene activity in humans, chimpanzees and rhesus macaques, a common ancestor for both chimpanzee and humans that allowed the researchers to see where changes emerged between humans and chimpanzees.
They zeroed in on three brain regions - the frontal cortex, hippocampus and striatum.
By tracking gene expression, the process by which genes manufacture the amino acids that make up cellular proteins, the scientists were able to search the genomes for regions where the DNA diverged between the species.
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"When we looked at gene expression in the frontal lobe, we saw a striking increase in molecular complexity in the human brain," said Geschwind.
While the caudate nucleus remained fairly similar across all three species, the frontal lobe changed dramatically in humans.
"Although all three species share a frontal cortex, our analysis shows that how the human brain regulates molecules and switches genes on and off unfolds in a richer, more elaborate fashion," said first author Genevieve Konopka.
"We believe that the intricate signaling pathways and enhanced cellular function that arose within the frontal lobe created a bridge to human evolution," Konopka said.
The finding was published in the advance journal 'Neuron'.