Researchers at the NYU Langone Medical Center and the Nathan S. Kline Institute for Psychiatric Research (NKI) found that slow-wave sleep — a deep period of sleep during which the brain consolidates each day’s memories — was disrupted in adult mice that had been exposed to high levels of alcohol during brain development. This study may explain some of the long-term effects of fetal alcohol spectrum disorder in humans and could open the door to new forms of treatment.
The results of this study were published in the prestigious scientific journal Neuroscience.
What is fetal alcohol spectrum disorder?
Fetal alcohol spectrum disorder, sometimes shortened to FASD, is a collection of disorders caused by alcohol exposure in the womb, the most serious of which is fetal alcohol syndrome. FASDs can result in difficulties with memory, emotional regulation, problem-solving, socialization, communication and other daily life skills such as feeding and bathing. People with FASDs might also have lower than average body weight, hyperactive behavior, poor coordination and abnormal facial features among other symptoms.
FASD is not curable, but some of its symptoms can be managed with medication and/or behavioral therapy.
The research team was led by Donald Wilson, Ph.D., a professor in NYU Langone’s Departments of Child and Adolescent Psychiatry and Neuroscience and Physiology. The researchers found that mice that were exposed to alcohol seven days postbirth — the equivalent of the third trimester brain development in a human fetus — demonstrated significant sleep fragmentation as adults. They also experienced significantly less time in slow-wave sleep than their peers.
Not only did these mice have difficulties with sleep, but they were also hyperactive, a common symptom of FASD, when compared to normal mice. Most importantly, however, they experienced memory deficits, the severity of which was directly correlated with the extent of sleep fragmentation.
“We have known for a long time that sleep fragmentation is associated with impaired cognitive function, attention and emotional regulation,” Wilson explained in a press release. “Our study shows for the first time that binge alcohol exposure early in life results in long-lasting slow-wave sleep fragmentation, which, in turn, is associated with learning problems.”
What does this mean?
Since clinicians now know that slow-wave sleep is significantly disrupted in mice with early-life alcohol exposure — and that the severity of that disruption is tied with memory deficits — it may mean that it’s possible to craft new therapeutic interventions at the human level.
“Targeting therapeutic interventions toward sleep may help to relieve aspects of the diverse disorders linked to fetal alcohol exposure, and may open new avenues for treatment of this far too common condition,” Wilson said.
Of course, mice are far from miniature humans, and more testing will be required before we know for certain if FASD symptoms can be ameliorated with sleep interventions. In the meantime, these encouraging results bring us one step closer to understanding the long-term biological consequences of alcohol exposure in the womb.
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About the author
Courtney Lopresti, M.S., is a senior staff writer for the Sovereign Health Group where she uses her scientific background to write online blogs and articles for a general audience. At the University of Pittsburgh, where she earned her Master’s in neuroscience, she used functional neuroimaging to study how the human cerebellum contributes to language processing. In her spare time, she writes fiction, reads Oliver Sacks and spends time with her two cats and bird. Courtney is currently located in Minneapolis. For more information and other inquiries about this article, contact the author at email@example.com.
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