Posts tagged autism
Posts tagged autism
The brains of children with autism show more connections than the brains of typically developing children do. What’s more, the brains of individuals with the most severe social symptoms are also the most hyper-connected. The findings reported in two independent studies published in the Cell Press journal Cell Reports (1, 2) on November 7th are challenge the prevailing notion in the field that autistic brains are lacking in neural connections.
The findings could lead to new treatment strategies and new ways to detect autism early, the researchers say. Autism spectrum disorder is a neurodevelopmental condition affecting nearly 1 in 88 children.
"Our study addresses one of the hottest open questions in autism research," said Kaustubh Supekar of Stanford University School of Medicine of his and his colleague Vinod Menon’s study aimed at characterizing whole-brain connectivity in children. "Using one of the largest and most heterogeneous pediatric functional neuroimaging datasets to date, we demonstrate that the brains of children with autism are hyper-connected in ways that are related to the severity of social impairment exhibited by these children."
In the second Cell Reports study, Ralph-Axel Müller and colleagues at San Diego State University focused specifically on neighboring brain regions to find an atypical increase in connections in adolescents with a diagnosis of autism spectrum disorder. That over-connection, which his team observed particularly in the regions of the brain that control vision, was also linked to symptom severity.
"Our findings support the special status of the visual system in children with heavier symptom load," Müller said, noting that all of the participants in his study were considered "high-functioning" with IQs above 70. He says measures of local connectivity in the cortex might be used as an aid to diagnosis, which today is based purely on behavioral criteria.
For Supekar and Menon, these new views of the autistic brain raise the intriguing possibility that epilepsy drugs might be used to treat autism.
"Our findings suggest that the imbalance of excitation and inhibition in the local brain circuits could engender cognitive and behavioral deficits observed in autism," Menon said. That imbalance is a hallmark of epilepsy as well, which might explain why children with autism so often suffer with epilepsy too.
"Drawing from these observations, it might not be too far fetched to speculate that the existing drugs used to treat epilepsy may be potentially useful in treating autism," Supekar said.
Researchers at Marcus Autism Center, Children’s Healthcare of Atlanta and Emory University School of Medicine have identified signs of autism present in the first months of life. The researchers followed babies from birth until 3 years of age, using eye-tracking technology, to measure the way infants look at and respond to social cues. Infants later diagnosed with autism showed declining attention to the eyes of other people, from the age of 2 months onwards. The results are reported in the Nov. 6, 2013 advanced online publication of the journal Nature.
The study followed two groups of infants, one at low and one at high risk for having autism spectrum disorders. High-risk infants had an older sibling already diagnosed with autism, increasing the infant’s risk of also having the condition by 20 fold. In contrast, low-risk infants had no first, second, or third degree relatives with autism.
"By following these babies from birth, and intensively within the first six months, we were able to collect large amounts of data long before overt symptoms are typically seen," said Warren Jones, Ph.D., the lead author on the study. Teams of clinicians assessed the children longitudinally and confirmed their diagnostic outcomes at age 3. Then the researchers analyzed data from the infants’ first months to identify what factors separated those who received an autism diagnosis from those who did not. What they found was surprising.
"We found a steady decline in attention to other people’s eyes, from 2 until 24 months, in infants later diagnosed with autism," said co-investigator Ami Klin, Ph.D., director of Marcus Autism Center. Differences were apparent even within the first 6 months, which has profound implications. "First, these results reveal that there are measurable and identifiable differences present already before 6 months. And second, we observed declining eye fixation over time, rather than an outright absence. Both these factors have the potential to dramatically shift the possibilities for future strategies of early intervention."
Jones is director of research at Marcus Autism Center and assistant professor in the Department of Pediatrics at Emory University School of Medicine. Klin is director of Marcus Autism Center, chief of the Division of Autism & Related Disorders in the Department of Pediatrics at Emory University School of Medicine and a Georgia Research Alliance Eminent Scholar.
The researchers caution that what they observed would not be visible to the naked eye, but requires specialized technology and repeated measurements of a child’s development over the course of months.
"To be sure, parents should not expect that this is something they could see without the aid of technology," said Jones, "and they shouldn’t be concerned if an infant doesn’t happen to look at their eyes at every moment. We used very specialized technology to measure developmental differences, accruing over time, in the way that infants watched very specific scenes of social interaction."
Before they can crawl or walk, babies explore the world intensively by looking at it, and they look at faces, bodies, and objects, as well as other people’s eyes. This exploration is a natural and necessary part of infant development, and it sets the stage for brain growth.
The critical implications of the study relate to what it reveals about the early development of social disability. Although the results indicate that attention to others’ eyes is already declining by 2 to 6 months in infants later diagnosed with autism, attention to others’ eyes does not appear to be entirely absent. If infants were identified at this early age, interventions could more successfully build on the levels of eye contact that are present. Eye contact plays a key role in social interaction and development, and in the study, those infants whose levels of eye contact diminished most rapidly were also those who were most disabled later in life. This early developmental difference also gives researchers a key insight for future studies.
"The genetics of autism have proven to be quite complex. Many hundreds of genes are likely to be involved, with each one playing a role in just a small fraction of cases, and contributing to risk in different ways in different individuals," said Jones. "The current results reveal one way in which that genetic diversity may be converted into disability very early in life. Our next step will be to expand these studies with more children, and to combine our eye-tracking measures with measures of gene expression and brain growth."
Researchers at Johns Hopkins say they have found that a gene already implicated in human speech disorders and epilepsy is also needed for vocalizations and synapse formation in mice. The finding, they say, adds to scientific understanding of how language develops, as well as the way synapses — the connections among brain cells that enable us to think — are formed. A description of their experiments appears in Science Express on Oct. 31.
A group led by Richard Huganir, Ph.D., director of the Solomon H. Snyder Department of Neuroscience and a Howard Hughes Medical Institute investigator, set out to investigate genes involved in synapse formation. Gek-Ming Sia, Ph.D., a research associate in Huganir’s laboratory, first screened hundreds of human genes for their effects on lab-grown mouse brain cells. When one gene, SRPX2, was turned up higher than normal, it caused the brain cells to erupt with new synapses, Sia found.
When Huganir’s team injected fetal mice with an SRPX2-blocking compound, the mice showed fewer synapses than normal mice even as adults, the researchers found. In addition, when SRPX2-deficient mouse pups were separated from their mothers, they did not emit high-pitched distress calls as other pups do, indicating they lacked the rodent equivalent of early language ability.
Other researchers’ analyses of the human genome have found that mutations in SRPX2 are associated with language disorders and epilepsy, and when Huganir’s team injected the human SRPX2 with the same mutations into the fetal mice, they also had deficits in their vocalization as young pups.
Another research group at Institut de Neurobiologie de la Méditerranée in France had previously shown that SRPX2 interacts with FoxP2, a gene that has gained wide attention for its apparently crucial role in language ability.
Huganir’s team confirmed this, showing that FoxP2 controls how much protein the SRPX2 gene makes and may affect language in this way. “FoxP2 is famous for its role in language, but it’s actually involved in other functions as well,” Huganir comments. “SRPX2 appears to be more specialized to language ability.” Huganir suspects that the gene may also be involved in autism, since autistic patients often have language impairments, and the condition has been linked to defects in synapse formation.
This study is only the beginning of teasing out how SRPX2 acts on the brain, Sia says. “We’d like to find out what other proteins it acts on, and how exactly it regulates synapses and enables language development.”
When you experience something, neurons in the brain send chemical signals called neurotransmitters across synapses to receptors on other neurons. How well that process unfolds determines how you comprehend the experience and what behaviors might follow. In people with Fragile X syndrome, a third of whom are eventually diagnosed with Autism Spectrum Disorder, that process is severely hindered, leading to intellectual impairments and abnormal behaviors.
In a study published in the online journal PLoS One, a team of UNC School of Medicine researchers led by pharmacologist C.J. Malanga, MD, PhD, describes a major reason why current medications only moderately alleviate Fragile X symptoms. Using mouse models, Malanga discovered that three specific drugs affect three different kinds of neurotransmitter receptors that all seem to play roles in Fragile X. As a result, current Fragile X drugs have limited benefit because most of them only affect one receptor.
Nearly one million people in the United States have Fragile X Syndrome, which is the result of a single mutated gene called FMR1. In people without Fragile X, the gene produces a protein that helps maintain the proper strength of synaptic communication between neurons. In people with Fragile X, FMR1 doesn’t produce the protein, the synaptic connection weakens, and there’s a decrease in synaptic input, leading to mild to severe learning disabilities and behavioral issues, such as hyperactivity, anxiety, and sensitivity to sensory stimulation, especially touch and noise.
More than two decades ago, researchers discovered that – in people with mental and behavior problems – a receptor called mGluR5 could not properly regulate the effect of the neurotransmitter, glutamate. Since then, pharmaceutical companies have been trying to develop drugs that target glutamate receptors. “It’s been a challenging goal,” Malanga said. “No one so far has made it work very well, and kids with Fragile X have been illustrative of this.”
But there are other receptors that regulate other neurotransmitters in similar ways to mGluR5. And there are drugs already available for human use that act on those receptors. So Malanga’s team checked how those drugs might affect mice in which the Fragile X gene has been knocked out.
By electrically stimulating specific brain circuits, Malanga’s team first learned how the mice perceived reward. The mice learned very quickly that if they press a lever, they get rewarded via a mild electrical stimulation. Then his team provided a drug molecule that acts on the same reward circuitry to see how the drugs affect the response patterns and other behaviors in the mice.
His team studied one drug that blocked dopamine receptors, another drug that blocked mGluR5 receptors, and another drug that blocked mAChR1, or M1, receptors. Three different types of neurotransmitters – dopamine, glutamate, and acetylcholine – act on those receptors. And there were big differences in how sensitive the mice were to each drug.
“Turns out, based on our study and a previous study we did with my UNC colleague Ben Philpot, that Fragile X mice and Angelman Syndrome mice are very different,” Malanga said. “And how the same pharmaceuticals act in these mouse models of Autism Spectrum Disorder is very different.”
Malanga’s finding suggests that not all people with Fragile X share the same biological hurdles. The same is likely true, he said, for people with other autism-related disorders, such as Rett syndrome and Angelman syndrome.
“Fragile X kids likely have very different sensitivities to prescribed drugs than do other kids with different biological causes of autism,” Malanga said.
A novel autism intervention program using theatre to teach reciprocal communication skills is improving social deficits in adolescents with the disorder that now affects an estimated one in 88 children, Vanderbilt University researchers released today in the journal Autism Research.
The newly released study assessed the effectiveness of a two-week theatre camp on children with autism spectrum disorder and found significant improvements were made in social perception, social cognition and home living skills by the end of the camp. There were also positive changes in the participants’ physiological stress and reductions in self-reported parental stress.
Called SENSE Theatre, the Social Emotional Neuroscience & Endocrinology (SENSE) program evaluates the social functioning of children with autism and related neurodevelopmental disorders.
Camp participants ages 8 to 17 years join with typically developing peers who are specially trained to serve as models for social interaction and communication, skills that are difficult for children with autism. The camp uses techniques such as role-play and improvisation and culminates in public performances of a play.
“The findings show that treatment can be delivered in an unconventional setting, and children with autism can learn from unconventional ‘interventionists’ – their typically developing peer,” said lead author Blythe Corbett, Ph.D., associate professor of Psychiatry.
Social perception and interaction skills were measured before and after the camp using neuropsychological measures, play with peers and parental reporting. Significant differences were found in face processing, social awareness and social cognition, and duration of interaction with familiar peers increased significantly over the course of the camp.
Additionally, the stress hormone cortisol was measured through saliva samples taken both at home and throughout the camp to compare the stress level of participants at home, at the beginning of the camp and at the end of the camp. Cortisol levels rose on the first day of camp when compared to home values but declined by the end of treatment and during post-treatment play with peers.
“Our findings show that the SENSE Theatre program contributes to improvement in core social deficits when engaging with peers both on and off the stage,” Corbett said. “This research also shows it’s never too late to make a significant difference in the lives of children and youth with autism spectrum disorder, as [this program] targets children who are much older than kids who are participating in early intervention, yet we are still seeing significant gains in the core deficits of autism, and in a rather brief intervention.”
This research was supported by the Martin McCoy-Jesperson Discovery Grant in Positive Psychology and a grant from the National Institute of Mental Health (Grant No. R01 MH085717).
Corbett will continue using theatre techniques to study areas of social functioning among children with autism through a newly awarded grant from the National Institute of Mental Health (Grant No. R34 MH097793). This forthcoming study will explore treatment length and peer familiarity as factors in optimizing and generalizing gains and will enroll more than 30 youth with autism ages 8 to 16 in a 10-week program model beginning January 2014.
Joint research from the University of Alabama at Birmingham Department of Psychology and Auburn University indicates that brain scans show signs of autism that could eventually support behavior-based diagnosis of autism and effective early intervention therapies. The findings appear online today in Frontiers in Human Neuroscience as part of a special issue on brain connectivity in autism.
“This research suggests brain connectivity as a neural signature of autism and may eventually support clinical testing for autism,” said Rajesh Kana, Ph.D., associate professor of psychology and the project’s senior researcher. “We found the information transfer between brain areas, causal influence of one brain area on another, to be weaker in autism.”
The investigators found that brain connectivity data from 19 paths in brain scans predicted whether the participants had autism, with an accuracy rate of 95.9 percent.
Kana, working with a team including Gopikrishna Deshpande, Ph.D., from Auburn University’s MRI Research Center, studied 15 high-functioning adolescents and adults with autism, as well as 15 typically developing control participants ages 16-34 years. Kana’s team collected all data in his autism lab at UAB that was then analyzed using a novel connectivity method at Auburn.
The current study showed that adults with autism spectrum disorders processed social cues differently than typical controls. It also revealed the disrupted brain connectivity that explains their difficulty in understanding social processes.
“We can see that there are consistently weaker brain regions due to the disrupted brain connectivity,” Kana said. “There’s a very clear difference.”
Participants in this study were asked to choose the most logical of three possible endings as they watched a series of comic strip vignettes while a functional MRI scanner measured brain activity.
The scenes included a glass about to fall off a table and a man enjoying the music of a street violinist and giving him a cash tip. Most participants in the autism group had difficulty in finding a logical end to the violinist scenario, which required an understanding of emotional and mental states. The current study showed that adults with autism spectrum disorders struggle to process subtle social cues, and altered brain connectivity may underlie their difficulty in understanding social processes.
“We can see that the weaker connectivity hinders the cross-talk among brain regions in autism,” Kana said.
Kana plans to continue his research on autism.
“Over the next five to 10 years, our research is going in the direction of finding objective ways to supplement the diagnosis of autism with medical testing and testing the effectiveness of intervention in improving brain connectivity,” Kana said.
Autism is currently diagnosed through interviews and behavioral observation. Although autism can be diagnosed by 18 months, in reality, earliest diagnoses occur around ages 4-6 as children face challenges in school or social settings.
“Parents usually have a longer road before getting a firm diagnosis for their child now,” Kana said. “You lose a lot of intervention time, which is so critical. Brain imaging may not be able to replace the current diagnostic measures; but if it can supplement them at an earlier age, that’s going to be really helpful.”
Video-based teaching helps teens with autism learn important social skills, and the method eventually could be used widely by schools with limited resources, a Michigan State University researcher says.
The diagnosis rate for Autism Spectrum Disorder for 14- to 17-year-olds has more than doubled in the past five years, according to the Centers for Disease Control and Prevention. Yet previous research has found very few strategies for helping adolescents with autism develop skills needed to be successful, especially in group settings.
“Teaching social skills to adolescents with ASD has to be effective and practical,” said Joshua Plavnick, assistant professor of special education at MSU. “Using video-based group instruction regularly could promote far-reaching gains for students with ASD across many social behaviors.”
Plavnick developed group video teaching techniques with colleagues while a postdoctoral fellow at the University of North Carolina’s Frank Porter Graham Child Development Institute. Their findings are published in the research journal Exceptional Children.
Previous studies have shown many people with autism are more likely to pay attention when an innovative technology delivers information. Before Plavnick’s work, however, there were no investigations of video modeling as an option for teaching social skills to more than one adolescent with ASD at the same time.
The team recruited 13- to 17-year-old students with ASD and used laptops or iPads to offer group video instruction on social behaviors, such as inviting a peer to join an activity. One facilitator showed four students video footage of people helping one another clean up a mess, for example, and then gave them opportunities to practice the same skills in the classroom.
According to the researchers, the students demonstrated a rapid increase in the level of complex social behaviors each time video-based group instruction was used. Students sustained those social behaviors at high levels, even when the videos were used less often.
The students’ parents also completed anonymous surveys and indicated high levels of satisfaction. One reported their child started asking family members to play games together, a skill the teen had never before displayed at home.
Most schools do not have appropriate staff resources to provide one-on-one help for students with autism. The video can be used with a small group all at once and has been shown to be effective.
“Video-based group instruction is important, given the often limited resources in schools that also face increasing numbers of students being diagnosed with ASD,” said Plavnick, who also has begun implementing the strategy as part of a daily high school-based program.
A study led by Xiaoching Li, PhD, at the LSU Health Sciences Center New Orleans Neuroscience Center of Excellence, has shown for the first time how two tiny molecules regulate a gene implicated in speech and language impairments as well as autism disorders, and that social context of vocal behavior governs their function. The findings are published in the October 16, 2013 issue of The Journal of Neuroscience.
Speech and language impairments affect the lives of millions of people, but the underlying neural mechanisms are largely unknown and difficult to study in humans. Zebra finches learn to sing and use songs for social communications. Because the vocal learning process in birds has many similarities with speech and language development in humans, the zebra finch provides a useful model to study the neural mechanisms underlying speech and language in humans.
Mutations in the FOXP2 gene have been linked to speech and language deficits and in autism disorders. A current theory is that a precise amount of FOXP2 is required for the proper development of the neural circuits processing speech and language, so it is important to understand how the FOXP2 gene is regulated. In this study, the research team identified two microRNAs, or miRNAs, – miR-9 and miR-140-5p – that regulate the levels of FOXP2. (MicroRNAs are a new class of small RNA molecules that play an important regulatory role in cell biology. They prevent the production of a particular protein by binding to and destroying the messenger RNA that would have produced the protein.) The researchers showed that in the zebra finch brain, these miRNAs are expressed in a basal ganglia nucleus that is required for vocal learning, and their function is regulated during vocal learning. More intriguingly, the expression of these two miRNAs is also regulated by the social context of song behavior – in males singing undirected songs.
"Because the FOXP2 gene and these two miRNAs are evolutionarily conserved, the insights we obtained from studying birds are highly relevant to speech and language in humans and related neural developmental disorders such as autism," notes Xiaoching Li, PhD,
LSUHSC Assistant Professor of Cell Biology and Anatomy as well as Neuroscience. “Understanding how miRNAs regulate FOXP2 may open many possibilities to influence speech and language development through genetic variations in miRNA genes, as well as behavioral and environmental factors.”
Language ability is usually located in the left side of the brain. Researchers studying brain development in young children who were acquiring language expected to see increasing levels of myelin, a nerve fiber insulator, on the left side. They didn’t: The larger myelin structure was already there. Their study underscores the importance of environment in language development.
Researchers from Brown University and King’s College London have gained surprising new insights into how brain anatomy influences language acquisition in young children.
Their study, published in the Journal of Neuroscience, found that the explosion of language acquisition that typically occurs in children between 2 and 4 years old is not reflected in substantial changes in brain asymmetry. Structures that support language ability tend to be localized on the left side of the brain. For that reason, the researchers expected to see more myelin — the fatty material that insulates nerve fibers and helps electrical signals zip around the brain — developing on the left side in children entering the critical period of language acquisition. But that is not what the research showed.
“What we actually saw was that the asymmetry of myelin was there right from the beginning, even in the youngest children in the study, around the age of 1,” said the study’s lead author, Jonathan O’Muircheartaigh, the Sir Henry Wellcome Postdoctoral Fellow at King’s College London. “Rather than increasing, those asymmetries remained pretty constant over time.”
That finding, the researchers say, underscores the importance of environment during this critical period for language.
O’Muircheartaigh is currently working in Brown University’s Advanced Baby Imaging Lab. The lab uses a specialized MRI technique to look at the formation of myelin in babies and toddlers. Babies are born with little myelin, but its growth accelerates rapidly in the first few years of life.
The researchers imaged the brains of 108 children between ages 1 and 6, looking for myelin growth in and around areas of the brain known to support language.
While asymmetry in myelin remained constant over time, the relationship between specific asymmetries and language ability did change, the study found. To investigate that relationship, the researchers compared the brain scans to a battery of language tests given to each child in the study. The comparison showed that asymmetries in different parts of the brain appear to predict language ability at different ages.
“Regions of the brain that weren’t important to successful language in toddlers became more important in older children, about the time they start school,” O’Muircheartaigh said. “As language becomes more complex and children become more proficient, it seems as if they use different regions of the brain to support it.”
Interestingly, the association between asymmetry and language was generally weakest during the critical language period.
“We found that between the ages of 2 and 4, myelin asymmetry doesn’t predict language very well,” O’Muircheartaigh said. “So if it’s not a child’s brain anatomy predicting their language skills, it suggests their environment might be more influential.”
The researchers hope this study will provide a helpful baseline for future research aimed at pinpointing brain structures that might predict developmental disorders.
“Disorders like autism, dyslexia, and ADHD all have specific deficits in language ability,” O’Muircheartaigh said. “Before we do studies looking at abnormalities we need to know how typical children develop. That’s what this study is about.”
“This work is important, as it is the first to investigate the relationship between brain structure and language across early childhood and demonstrate how this relationship changes with age,” said Sean Deoni, assistant professor of engineering, who oversees the Advanced Baby Imaging Lab. “The study highlights the advantage of collaborative work, combining expertise in pediatric imaging at Brown and neuropsychology from the King’s College London Institute of Psychiatry, making this work possible.”
In animal study, inflammation stops cells from accessing iron needed for brain development
Researchers exploring the link between newborn infections and later behavior and movement problems have found that inflammation in the brain keeps cells from accessing iron that they need to perform a critical role in brain development.
Specific cells in the brain need iron to produce the white matter that ensures efficient communication among cells in the central nervous system. White matter refers to white-colored bundles of myelin, a protective coating on the axons that project from the main body of a brain cell.
The scientists induced a mild E. coli infection in 3-day-old mice. This caused a transient inflammatory response in their brains that was resolved within 72 hours. This brain inflammation, though fleeting, interfered with storage and release of iron, temporarily resulting in reduced iron availability in the brain. When the iron was needed most, it was unavailable, researchers say.
“What’s important is that the timing of the inflammation during brain development switches the brain’s gears from development to trying to deal with inflammation,” said Jonathan Godbout, associate professor of neuroscience at The Ohio State University and senior author of the study. “The consequence of that is this abnormal iron storage by neurons that limits access of iron to the rest of the brain.”
The research is published in the Oct. 9, 2013, issue of The Journal of Neuroscience.
The cells that need iron during this critical period of development are called oligodendrocytes, which produce myelin and wrap it around axons. In the current study, neonatal infection caused neurons to increase their storage of iron, which deprived iron from oligodendrocytes.
In other mice, the scientists confirmed that neonatal E. coli infection was associated with motor coordination problems and hyperactivity two months later – the equivalent to young adulthood in humans. The brains of these same mice contained lower levels of myelin and fewer oligodendrocytes, suggesting that brief reductions in brain-iron availability during early development have long-lasting effects on brain myelination.
The timing of infection in newborn mice generally coincides with the late stages of the third trimester of pregnancy in humans. The myelination process begins during fetal development and continues after birth.
Though other researchers have observed links between newborn infections and effects on myelin and behavior, scientists had not figured out why those associations exist. Godbout’s group focuses on understanding how immune system activation can trigger unexpected interactions between the central nervous system and other parts of the body.
“We’re not the first to show early inflammatory events can change the brain and behavior, but we’re the first to propose a detailed mechanism connecting neonatal inflammation to physiological changes in the central nervous system,” said Daniel McKim, a lead author on the paper and a student in Ohio State’s Neuroscience Graduate Studies Program.
The neonatal infection caused several changes in brain physiology. For example, infected mice had increased inflammatory markers, altered neuronal iron storage, and reduced oligodendrocytes and myelin in their brains. Importantly, the impairments in brain myelination corresponded with behavioral and motor impairments two months after infection.
Though it’s unknown if these movement problems would last a lifetime, McKim noted that “since these impairments lasted into what would be young adulthood in humans, it seems likely to be relatively permanent.”
The reduced myelination linked to movement and behavior issues in this study has also been associated with schizophrenia and autism spectrum disorders in previous work by other scientists, said Godbout, also an investigator in Ohio State’s Institute for Behavioral Medicine Research (IBMR).
“More research in this area could confirm that human behavioral complications can arise from inflammation changing the myelin pattern. Schizophrenia and autism disorders are part of that,” he said.
This current study did not identify potential interventions to prevent these effects of early-life infection. Godbout and colleagues theorize that maternal nutrition – a diet high in antioxidants, for example – might help lower the inflammation in the brain that follows a neonatal infection.
“The prenatal and neonatal period is such an active time of development,” Godbout said. “That’s really the key – these inflammatory challenges during critical points in development seem to have profound effects. We might just want to think more about that clinically.”