An international team of researchers has identified, for the first time, biological processes in the brain that can lead to a genetic risk of insomnia.
The finding made possible by assessing DNA and sleep features in 1.3 million people. The findings are a major step towards getting grip on the biological mechanisms that cause insomnia.
Insomnia is one of the most common disorders. Many people occasionally have a bad night of sleep. One out of ten people chronically experience poor sleep and suffer severely from the daytime consequences. Worldwide, 770 million people have chronic insomnia.
While treatment alleviates symptoms, most sufferers feel that they remain vulnerable to experiencing poor nights of sleep. The vulnerability to insomnia runs in families and seems hard-wired in the brain. So far, only few genes involved in the vulnerability had been identified. It had also remained enigmatic where in the brain insomnia risk genes exerted their disturbing role. This knowledge is crucial to develop better treatments.
Amsterdam Statistical Genetics professor Danielle Posthuma and Neurophysiology professor Eus Van Someren at the Netherlands Institute for Neuroscience assembled a large group of scientists to find out where in the brain insomnia risk genes exert their effect. Together, they were the first to assemble DNA and sleep data provided by no less than 1.3 million people – the largest genetic dataset ever
The researchers identified 956 genes in which variants contributed to the risk of insomnia. They then extensively investigated which biological processes, cell types and brain areas utilize these genes. They found that part of these genes had an important role in the functionality of axons, which are the long protrusions of brain cells that allow them to communicate with each other. Another significant part of the insomnia risk genes was active in specific cell types of parts of the frontal cortex and the subcortical nuclei of the brain. These brain areas had also recently been marked as suspect in brain imaging studies of people suffering from insomnia. The findings thus seem consistent.
“Our study shows that insomnia, like so many other neuropsychiatric disorders, is influenced by 100’s of genes, each of small effect,” said Posthuma. “These genes by themselves are not that interesting to look at. What counts is their combined effect on the risk of insomnia.”
The researchers compared risk genes of insomnia with those of other traits and disorders. Surprisingly, they found little overlap with genes involved in individual differences in other sleep traits, like being a morning- or evening-type. Instead there was a strong genetic similarity with depression and anxiety.
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