NewsMakers
Autism in males linked to defect in brain immune cells, microglia
Many cases of autism spectrum disorders (ASDs) may result from problems in immune cells that normally work to trim back unneeded brain connections in early life.

Many cases of autism spectrum disorders (ASDs) may result from problems in immune cells that normally work to trim back unneeded brain connections in early life, suggests a new study led by scientists at Scripps Research.
The study, published in Nature Communications, examined the effects of a set of gene mutations that account for a small percentage of autism disorders. These mutations are known to cause a general overproduction of many proteins in brain cells, but how that overproduction leads to autism behaviors has been a mystery.
The scientists found evidence that the most relevant effect of this protein overproduction occurs in brain-based immune cells called microglial cells. These cells normally prune unneeded brain connections, or synapses, as the brain develops in childhood.
Working in mice, the scientists determined that the protein overproduction impairs microglial cells in a way that hampers their synapse-pruning function, but only in males, leading to autism-like social behavior deficits.
The finding dovetails with the long-standing observation that autism disorders are four to five times more prevalent in males than females. It is also consistent with recent evidence that in people with ASDs, the brain commonly has a higher number of synapses than normal.
“Our study suggests that impairments in microglia play a key role in the development of autism behaviors, at least in some cases, and may help explain the higher prevalence of autism disorders in males,” says study senior author Baoji Xu, PhD, professor in the Department of Neuroscience at Scripps Research. “That, in turn, suggests that microglia might be a good target for future drugs that prevent or treat autism spectrum disorders.”
ASDs are found in an estimated 2.4 percent of boys and 0.5 percent of girls. They involve a variety of abnormalities including social skill deficits, repetitive behaviors, and hypersensitivities to sounds and light. Research suggests that these disorders are largely genetic but can be caused by abnormalities in a variety of different genes acting alone or in combination. To date, well over 100 gene mutations and variants have been linked to ASDs.
One set of autism-linked gene abnormalities–which include mutations in the genes PTEN, TSC1, TSC2, and FMR1–accounts for about 3 percent of ASD cases. The common effect of these abnormalities is to disrupt a pathway that normally regulates the level of protein production in cells, allowing protein production to rise.
Xu and his team sought to determine if there is a particular cell type in the brain that explains the connection between elevated protein production and ASD-like behaviors. They engineered mice to make–in just one cell type at a time–abnormally high levels of a protein-production factor called eIF4E. A high level of eIF4E is thought to be one of the common events that links PTEN, TSC1 and other autism mutations that increase protein production.
The team found that when high eIF4E levels occurred in microglial cells, the mice developed ASD-like abnormalities in social behavior, as well as cognitive deficits and repetitive behaviors. Curiously, although protein production rose in the microglial cells of both male and female mice, the ASD-type abnormalities occurred only in male mice.
The same behavioral abnormalities were not seen at all when the high eIF4E levels occurred in neurons or in helper cells called astrocytes, although mice whose neurons had high eIF4E levels showed more anxiety-like behaviors.
The researchers examined affected microglial cells for clues to how elevated protein synthesis in these cells could lead to ASD-like behavioral changes. They found that in young male mice, microglial cells in important brain regions, including the medial prefrontal cortex, the hippocampus and the striatum, were significantly larger and also more numerous, whereas in females these changes were much more subtle and transient.
Microglia during brain development normally prune synapses that are unused or otherwise unwanted. Xu and his colleagues found that in the male ASD-like mice with elevated microglial eIF4E, there were more synapses than normal, suggesting a pruning deficit–a pattern also thought to be widely present in people with autism.
The affected microglia in the mice showed gene activity patterns indicating an enhanced capacity to prune synapses. However, experiments also revealed that the cells lacked the usual motility, or movement ability, that would enable them to carry out their synapse pruning functions. Xu and his colleagues suspect that this reduction in microglial motility may be the most important factor, so that on balance the cells’ synapse-pruning abilities are impaired, leading to ASD-like brain changes.
The researchers now are following up with studies to discover precisely why protein increases affect microglia in males so much more than in females. That discovery could prove to be an important piece of the puzzle of sex differences in autism–and could suggest new targets for autism treatments.
NewsMakers
Surgery in kids with mild sleep-disordered breathing tied to fewer doctor visits, meds
Surgery, called adenotonsillectomy, was tied to a 32% reduction in medical visits and a 48% reduction in prescription use among children with a mild form of the condition.

Surgical removal of enlarged tonsils and adenoids in children with mild sleep-disordered breathing (SDB) appears to significantly reduce the frequency of medical office visits and prescription medicine use in this group, according to a clinical study supported by the National Institutes of Health (NIH).
The findings, published in JAMA Pediatrics, show that the surgery, called adenotonsillectomy, was tied to a 32% reduction in medical visits and a 48% reduction in prescription use among children with a mild form of the condition.
SDB refers to breathing disturbances during sleep that can range from loud snoring to occasional breathing pauses. About 6 to 17% of children in the United States have it, and for those with moderate to severe cases, adenotonsillectomy is a standard treatment commonly used. It can help reduce breathing problems, minimize behavioral issues, and also lower the risk of high blood pressure, full-blown sleep apnea, and other problems that may occur if the condition is left untreated. A recent NIH-supported clinical trial showed that for children with mild SDB, the surgery helped lower blood pressure and improve sleep and quality of life.
In the new study, researchers sought to determine whether adenotonsillectomy in comparison to watchful waiting (non-intervention) with supportive care is associated with fewer health care encounters and prescriptions. To find out, the researchers analyzed data from a randomized clinical trial that involved 459 children and adolescents with mild SDB who were recruited between 2016 and 2021 and followed for one year. The participants were ages 3 to 12 and were studied at seven academic sleep centers in the U.S.
During the trial, half the participants received an adenotonsillectomy, and the other half received supportive care without surgery, which included standardized education on healthy sleep and lifestyle and referral for untreated allergies or asthma. An analysis after the 12-month study period found 32% fewer health care encounters and 48% fewer prescriptions used among participants who underwent adenotonsillectomy, compared to those who did not undergo the surgery. For every 100 children, this equates to 125 fewer health care encounters and 253 fewer prescriptions — including for pain, skin, and respiratory medications — administered during the first year following surgery.
The reduced health care encounters included fewer office visits and outpatient procedures, particularly for sleep- and respiratory-related problems, but the mechanisms linking SDB treatment to health care outcomes are not clear.
NewsMakers
Maternal depression can lead to children’s emotional overeating, study shows
“In our sample, almost 12% of mothers met the criteria for postpartum depression, and we found that maternal postpartum depression at six weeks negatively influenced children’s executive function with inhibition and emotional control at 24 months and overeating at 48 months.”

Up to 25% of new mothers suffer from postpartum depression, which can significantly impact their parenting behavior and the wellbeing of their children. A new study from the University of Illinois Urbana-Champaign looks at long-term effects of early maternal depression on children, underscoring the need to provide adequate support for mothers who might be struggling.
“We wanted to explore how mother’s early postpartum depression might influence children’s executive function and emotional overeating, focusing on the psychological mechanisms driving the effects,” said lead author Samantha Iwinski, postdoctoral research associate in the Department of Human Development and Family Studies at Illinois.
“Emotional overeating is about using food to cope with stress or emotions rather than using it to satisfy hunger. Instead of thinking about food as a source of nourishment or enjoyment, it becomes a coping strategy for negative emotions. If children aren’t able to talk about their emotions or show how they really feel, they may react to a stressful situation by grabbing something to eat,” Iwinski said.
The study included families participating in the Midwest STRONG Kids2 project, which investigates how individual biology interacts with the family environment to promote healthy eating habits in young children. Mothers filled out questionnaires to assess postpartum depression at six weeks, children’s emotional functioning at 24 months, and children’s eating behavior at 48 months.
The researchers analyzed the data using the biopsychosocial pathways model, which outlines how interactions between biological, psychological, and social factors affect health outcomes, including appetite self-regulation. They focused on postpartum depression as a critical social factor predicting children’s emotional overeating, mediated through emotional and cognitive psychological processes.
“In our sample, almost 12% of mothers met the criteria for postpartum depression, and we found that maternal postpartum depression at six weeks negatively influenced children’s executive function with inhibition and emotional control at 24 months and overeating at 48 months,” Iwinski said.
“Inhibition involves being able to control one’s attention, behaviors, and thoughts. This can include doing what may be appropriate in a given situation, which may involve overriding internal predispositions For example, if a child is doing their homework and the TV is playing, they can direct their attention and focus on their homework rather than the TV. Emotional control is about being able to regulate oneself when certain situations are happening; for example, crying might help in response to distress.”
In addition to the indirect effects on eating behavior through executive functioning, there was also a direct correlation between maternal depression and children’s overeating.
Mothers who suffer from postpartum depression may be less responsive to their children’s cognitive and emotional needs, which can affect healthy development and capacity for self-regulation. Women with postpartum depression symptoms may also engage in appetite fluctuation, modeling this behavior for their children.
The researchers say their findings underscore the need for early intervention and support for women who suffer from depression.
“By supporting the mother’s mental health, we’re really supporting the families, because of the long-term effects on children. It’s important to have early identification of what might be happening in order to help families teach their children healthy strategies for coping with emotions, such as play, mindfulness, or even just talking about our feelings,” Iwinski stated.
“Teachers and other supportive adults can also participate in supporting children and families. For example, they can be looking at eating patterns, noticing how children might be reacting in certain situations, and if food might be a coping mechanism for them. They can then use that information to talk about other ways to deal with emotions and bring the family more into the conversation.”
The paper, “Maternal postpartum depression and children’s emotional overeating: The mediating role of executive function,” is published in Eating Behaviors. Authors include Samantha Iwinski, Sehyun Ju, Qiujie Gong, and Kelly Bost.
NewsMakers
Poor sleep health linked to increased Type 2 diabetes risk in high-risk women with history of gestational diabetes
By prioritising better sleep, women with a history of GDM can take proactive steps toward reducing their long-term risk of developing T2D and improving overall metabolic health.

Underscoring the critical role of sleep in diabetes prevention, investigators from the Global Centre for Asian Women’s Health (GloW) and the Department of Obstetrics and Gynaecology, based at the NUS Yong Loo Lin School of Medicine (NUS Medicine), in collaboration with Harvard T.H. Chan School of Public Health, Brigham and Women’s Hospital and Harvard Medical School, has identified a significant link between sleep health and the risk of developing Type 2 diabetes (T2D) among women with a history of gestational diabetes (GDM).
GDM is one of the most common pregnancy complications, affecting up to 30% of pregnancies globally. Women with a history of GDM are nearly 10 times more likely to develop T2D later in life compared to those without GDM. More strikingly, in Singapore, more than 40 per cent of women may develop T2D within 5 years following pregnancies complicated by GDM. While lifestyle factors such as diet and exercise are well-known preventive measures, this study sheds light on the often-overlooked role of sleep health in mitigating diabetes risk.
By prioritising better sleep, women with a history of GDM can take proactive steps toward reducing their long-term risk of developing T2D and improving overall metabolic health. Led by Professor Zhang Cuilin, Director of GloW, and Dr Yin Xin, Research Fellow at GloW, their team analysed data of nearly 3,000 women with a history of GDM over 17 years from the Nurses’ Health Study II and found that those who slept six hours or fewer per night had a 32 per cent higher risk of developing T2D compared to those who met the recommended seven to eight hours of sleep.
Additionally, regular snoring—defined as snoring most nights per week or every night—was associated with a 61% increased risk of T2D. Women who experienced both short sleep duration and regular snoring faced more than double the risk compared to those with healthy sleep patterns. Beyond increasing diabetes risk, regular snoring was also associated with unfavourable glucose metabolism biomarkers, including elevated levels of HbA1c, insulin, and C-peptide, all of which signal potential metabolic dysfunction.
“Our research highlights that improving sleep habits—such as increasing sleep duration and addressing snoring—can be a powerful, actionable step in preventing Type 2 diabetes among women with a high-risk of diabetes,” said Prof Zhang. She further emphasised, “Given the rising prevalence of GDM and diabetes, particularly in Asia, it is crucial to expand prevention strategies to include the improvement of sleep health, especially for women with a history of GDM. Dr Yin also pointed out that, “Women with GDM may have had sub-optimal glucose metabolism even before pregnancy.”
Having opened new avenues for diabetes prevention, the study’s researchers are now looking to develop tailored interventions for Asian women that include improving sleep quality, diet, and other lifestyles, and to better understand underlying molecular mechanisms.
The study titled ‘Sleep Characteristics and Long-Term Risk of Type 2 Diabetes Among Women With Gestational Diabetes’ was published in JAMA Network Open.
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