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Abnormal Placenta May Reveal Autism Risk
A relatively high number of abnormal folds and cell growths in the placenta could be a strong indicator of an infant’s risk for developing autism, according to new research at the Yale School of Medicine.
The research team examined 117 placentas from infants of at-risk families — those with one or more previous children with autism. These families were participating in a study called Markers of Autism Risk in Babies – Learning Early Signs. Then the researchers compared these at-risk placentas to 100 control placentas.
The at-risk placentas had as many as 15 trophoblast inclusions, while none of the control placentas had more than two trophoblast inclusions.
According to the researchers, a placenta with four or more trophoblast inclusions conservatively predicted a 96.7 percent probability of the infant being at risk for autism.
Currently, one out of 50 children are diagnosed with an autism spectrum disorder in the United States each year, according to the Centers for Disease Control and Prevention (CDC).
However, this diagnosis is typically made when these children are 3 to 4 years of age or older. By then the best opportunities for intervention have been lost because the brain is most responsive to treatment in the first year of life.
These findings will allow for earlier diagnosis and treatment for the developmental disorder. So far, the best early marker of autism risk has been family history. Parents who have a child with autism are nine times more likely to have another child with autism.
“Regrettably, couples without known genetic susceptibility must rely on identification of early signs or indicators that may not overtly manifest until the child’s second or third year of life,” said senior author Dr. Harvey Kliman, research scientist in the Department of Obstetrics, Gynecology & Reproductive Sciences at the Yale School of Medicine.
“I hope that diagnosing the risk of developing autism by examining the placenta at birth will become routine, and that the children who are shown to have increased numbers of trophoblast inclusions will have early interventions and an improved quality of life as a result of this test,” Kliman added.
The findings are reported online in the journal Biological Psychiatry.
Source: Biological Psychiatry
Fetus in the placenta photo by shutterstock.
Mouse Study Shows Why Sleep Deprivation Temporarily Relieves Depression
Many people have experienced relief from depression after going without a good night’s sleep — but the mood boost typically only lasts until the person falls asleep again.
Although sleep deprivation is an impractical long term treatment, researchers have been interested in the workings behind this phenomenon. Now a research team at Tufts University has pinpointed glia as the key players.
Previously, the researchers found that astrocytes — a star-shaped type of glial cell — regulate the brain chemicals involved in sleepiness.
While we’re awake, astrocytes continuously release the neurotransmitter adenosine, which builds up in the brain and causes “sleep pressure,” the feeling of sleepiness and its related memory and attention deficits.
Adenosine creates this pressure by binding to receptors on the outside of neurons like a key fitting into a lock. As more adenosine builds up, more receptors are triggered, and the urge to sleep gets stronger.
In the new study, the researchers investigated whether this process is responsible for the antidepressant feelings during sleep deprivation. Mice with depressive-like symptoms were given three doses of a compound that triggers adenosine receptors — mimicking sleep deprivation.
Although the mice continued to sleep normally, after 12 hours they showed a significant improvement in mood and behavior, which lasted for 48 hours.
The findings verify that the buildup of adenosine is responsible for the antidepressant effects of a lack of sleep. These results lead to a promising target for new drug development because it suggests that mimicking sleep deprivation chemically may offer the antidepressant benefits without the unwanted side effects of actually losing sleep.
This type of treatment could give immediate relief from depression, especially compared to traditional antidepressants, which often take six to eight weeks to work.
According to Dustin Hines, lead author and a postdoctoral fellow at Tufts, this study may also have implications beyond depression and sleep regulation.
“For many years neuroscientists focused almost exclusively on neurons, whereas the role of glia was neglected,” Hines said.
“We now know that glia play an important role in the control of brain function and have the potential to aid in the development of new treatments for many illnesses, including depression and sleep disorders.”
Source: Translational Psychiatry
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