Washington, August 23 (ANI): A new UCLA study has identified unique patterns of gene activity in human brains that could shed light on how we evolved differently than our closest relative, chimps.
These genes' identification could improve understanding of human brain diseases like autism and schizophrenia, as well as learning disorders and addictions.
"Scientists usually describe evolution in terms of the human brain growing bigger and adding new regions. 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," explained principal investigator Dr. Daniel Geschwind, Gordon and Virginia MacDonald Distinguished Professor of Human Genetics and a professor of neurology at the David Geffen School of Medicine at UCLA.
Using post-mortem brain tissue, 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. What they saw surprised them.
"When we looked at gene expression in the frontal lobe, we saw a striking increase in molecular complexity in the human brain," said Geschwind, who is also a professor of psychiatry at the Semel Institute for Neuroscience and Behavior at UCLA.
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," explained first author Genevieve Konopka, a former postdoctoral researcher in Geschwind's lab who is now the Jon Heighten Scholar in Autism Research at University of Texas Southwestern Medical Center.
"We believe that the intricate signaling pathways and enhanced cellular function that arose within the frontal lobe created a bridge to human evolution," Konopka noted.
The researchers took their hypothesis one step further by evaluating how the modified genes linked to changes in function.
"The biggest differences occurred in the expression of human genes involved in plasticity - the ability of the brain to process information and adapt. This supports the premise that the human brain evolved to enable higher rates of learning," said Konopka.
One gene in particular, CLOCK, behaved very differently in the human brain. Considered the master regulator of Circadian rhythm, CLOCK is disrupted in mood disorders like depression and bipolar syndrome.
When comparing the human brain to the non-human primates, the researchers saw more connections among gene networks that featured FOXP1 and FOXP2. Earlier studies have linked these genes to humans' unique ability to produce speech and understand language.
The UCLA team's next step will be to expand their comparative search to 10 or more regions of the human, chimpanzee and maque brains.
The finding was published in the advance online edition of Neuron. (ANI)
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