A group of scientists led by Imperial College London researcher Michael Johnson has identified two ‘gene networks’ associated with human cognitive abilities.
Heatmap of gradient of expression of M1 and M3 spanning fetal development to late adulthood and in topographically distinct cortical regions: A1C – auditory cortex; AMY – amygdala; CBC – cerebellar cortex; DFC – dorsolateral prefrontal cortex; HIP – hippocampus; IPC – posterior inferior parietal cortex; ITC – inferior temporal cortex; M1C – primary motor cortex; MD – mediodorsal nucleus of thalamus; MFC – medial prefrontal cortex; OFC – orbital prefrontal cortex; S1C – primary somatosensory cortex; STC – superior temporal cortex; STR – striatum; V1C – primary visual cortex; VFC – ventrolateral prefrontal cortex. Image credit: Michael R. Johnson et al, doi: 10.1038/nn.4205.
The newly identified gene-regulatory networks, named M1 and M3, appear to influence cognitive function, according to Dr Johnson and his colleagues from Europe, Singapore, and Australia.
The M3 network consists of 150 genes, and M1 has more than 1,100 genes. The networks are likely to be under the control of master regulator switches. Dr Johnson’s team is now keen to identify these switches and explore whether it might be feasible to manipulate them.
“We know that genetics plays a major role in intelligence but until now haven’t known which genes are relevant. This research highlights some of genes involved in human intelligence, and how they interact with each other,” said Dr Johnson, a Consultant Neurologist at Imperial College Healthcare and Deputy Head of the Center for Clinical Translation in the Division of Brain Sciences at Imperial College London.
“What’s exciting about this is that the genes we have found are likely to share a common regulation, which means that potentially we can manipulate a whole set of genes whose activity is linked to human intelligence.”
“Our research suggests that it might be possible to work with these genes to modify intelligence, but that is only a theoretical possibility at the moment – we have just taken a first step along that road.”
Dr Johnson and co-authors looked at samples of human brain from patients who had undergone neurosurgery for epilepsy.
The scientists analyzed thousands of genes expressed in the brain, and then combined these results with genetic information from healthy people who had undergone IQ tests and from people with neurological disorders such as autism spectrum disorder and intellectual disability.
They conducted various computational analyses and comparisons in order to identify the gene networks influencing healthy human cognitive abilities, including memory, attention, processing speed, reasoning and executive function.
Remarkably, the team found that some of the same genes that influence human intelligence in healthy people were also the same genes that cause impaired cognitive ability and epilepsy when mutated.
“We identified two cross-species conserved gene coexpression networks (M1 and M3) associated with healthy human cognitive abilities, and we identified one of these (M3) as a convergent gene network for both cognition and neurodevelopmental disease,” the researchers said.
“We used computer analysis to identify the genes in the human brain that work together to influence our cognitive ability to make new memories or sensible decisions when faced with lots of complex information,” Dr Johnson explained.
“We found that some of these genes overlap with those that cause severe childhood onset epilepsy or intellectual disability.”
The findings were published online December 21 in the journal Nature Neuroscience.
“These results illustrate how systems-level analyses can reveal previously unappreciated relationships between neurodevelopmental disease-associated genes in the developed human brain, and provide empirical support for a convergent gene-regulatory network influencing cognition and neurodevelopmental disease,” Dr Johnson and co-authors said.
_____
Michael R. Johnson et al. Systems genetics identifies a convergent gene network for cognition and neurodevelopmental disease. Nature Neuroscience, published online December 21, 2015; doi: 10.1038/nn.4205
