New research in the journal Nature Genetics identifies individual types of brain cell and brain areas that are involved in insomnia, offering new treatment targets for this condition.
New research helps explain why some people struggle to sleep.
Insomnia affects about a third of people living in the United States and approximately 770 million people worldwide.
As many people with insomnia will know, there is a tendency to think that falling asleep is a matter of willpower.
However, more and more studies are showing that it actually has a strong neurobiological component.
For instance, in 2016, scientists found abnormalities in the white matter tracts of people living with insomnia, as well as in parts of their limbic system. More recent studies have uncovered specific genetic variants linked with insomnia risk.
Now, an international team of researchers has gone further, analyzing genetic data from over 1.3 million people in an attempt to tease out the individual genes, brain cell types, brain areas, and neurobiological processes that underlie insomnia.
Danielle Posthuma, a professor of statistical genetics at the Vrije Universiteit Amsterdam in the Netherlands, led the new research with Eus Van Someren, a neurophysiology professor at the Netherlands Institute for Neuroscience in Amsterdam.
Study yields ‘spectacular results’
Using data from the UK Biobank and DNA testing company 23andMe, the researchers assembled genetic and sleep information on 1,331,010 people, making this the largest genetic dataset that scientists have ever used to study insomnia.
They found 202 genetic loci and 956 risk genes for insomnia. Also, further analyses revealed that some of these genes were key to the functioning of axons, or extensions of nerve cells that facilitate electrical communication with other neurons.
Also, the researchers found a significant number of insomnia risk genes that were switched on in certain cells in the cortical and subcortical tissues of the brain.
Specifically, the types of cell implicated in insomnia included “striatal, hypothalamic, and claustrum neurons.” The results “provide new treatment targets,” explain the study authors.
Prof. Posthuma comments on the findings, saying, “Our study shows that insomnia, like so many other neuropsychiatric disorders, is influenced by [hundreds] of genes, each of small effect.”
“These genes by themselves are not that interesting to look at,” she adds. “What counts is their combined effect on the risk of insomnia.”
Another key finding was that insomnia had more risk genes in common with psychiatric conditions such as depression and anxiety than it did with other sleep characteristics, such as being a “night owl” or a “morning lark.”
This is “[a] very important finding,” notes Prof. Van Someren, “because we have always searched for causes of insomnia in the brain circuits that regulate sleep.”
“We have to shift our attention to the circuits that regulate emotion, stress, and tension. Our first results in that direction are already spectacular.”
Prof. Eus Van Someren
Study co-author Guus Smit, a neurobiologist at Vrije Universiteit Amsterdam, says, “These findings are a breakthrough, since we can now for the first time start searching for underlying mechanisms in individual brain cells in the laboratory.”