Publisher Health

About one-third of autistic people are unable to communicate using speech, and most are never provided an effective alternative. However, a new study from scientists at the University of Virginia suggests that many of these individuals are literate, raising the possibility that they could learn to express themselves through writing.
The study published in the journal Autism, reports that five times more nonspeaking autistic teenagers and adults demonstrated knowledge of written language conventions than would be expected from previous estimates of their abilities. The finding has important implications for the millions of autistic people around the world who have little or no speech and who are often assumed to be incapable of acquiring literacy.
“If we assume that someone who can’t speak doesn’t understand, it limits the doors we open for them — we may not even try to figure out what they understand,” said Vikram Jaswal, Professor of Psychology at the University of Virginia and the lead author of the study. “Our study shows that nonspeaking autistic people’s capacity for language, for learning, and for literacy has been seriously underestimated.”
The investigators addressed a fundamental question about literacy: whether or not nonspeaking autistic people react to letters, words and sentences in the same way as literate, non-autistic individuals. Jaswal’s team developed a method similar to the arcade game Whac-a-Mole which required participants to tap letters displayed on a tablet as soon as those letters lit up. In some instances, the letters lit up in sequences that spelled out sentences that participants had earlier heard spoken aloud, and in other instances the letters lit up in meaningless sequences. The research team, which included Ph.D. candidate Kayden Stockwell and recent graduate Andrew Lampi made the assumption that a literate individual — who knows how to spell and can convert speech into its written form — can predict the next letter in a sentence they have heard spoken aloud even before seeing that letter light up. Consequently, they could be expected to respond faster to the sentences than to meaningless sequences. Jaswal’s team found that over half of the sample group of 31 nonspeaking autistic participants responded in the same way a literate individual would.
According to Jaswal, the results are striking because they show that even though most participants in the study had not received formal instruction in literacy, many had developed an understanding of how written language works.
“Society has traditionally assumed that people who can’t speak are unable to understand language or to learn to read or write,” Jaswal said. “But our findings suggest that many nonspeaking autistic people have foundational literacy skills. With appropriate instruction and support, it might be possible to harness these skills to provide access to written forms of communication as an alternative to speech. Learning to express themselves through writing would open up educational, employment and social opportunities that nonspeaking autistic people have historically not been given access to.”
“This is cutting-edge research with enormous potential for impact,” said Christa Acampora, dean of the College and Graduate School of Arts & Sciences. “We are truly fortunate to have professor Jaswal and outstanding graduate students like Kayden Stockwell and Andrew Lampi in the College’s research community. Together, they’re asking important questions, and their discovery will have life-changing consequences for many.”

In a potentially game-changing development, scientists with the Fralin Biomedical Research Institute at VTC have revealed a new understanding of sometimes fatal viral infections that affect the heart.
Traditionally, the focus has been on heart inflammation known as myocarditis, which is often triggered by the body’s immune response to a viral infection.
However, a new study led by James Smyth, associate professor at the Fralin Biomedical Research Institute, sheds new light on this notion, revealing that the virus itself creates potentially dangerous conditions in the heart before inflammation sets in.
The discovery, now online and set to appear in the March 29 issue of Circulation Research, suggests completely new directions to diagnose and treat viral infections affecting the heart.
Given the high incidence of viral-related myocarditis leading to sudden cardiac death, the insight is crucial. Up to 42 percent of sudden cardiac deaths in young adults are attributed to myocarditis, and of these cases viral infection is the leading cause.
“From a clinical perspective, our understanding of viral infection of the heart has focused on inflammation, causing problems with the rate or rhythm of the heartbeat,” Smyth said. “But we have found an acute stage when the virus first infects the heart and before the body’s immune response causes inflammation. So even before the tissue is inflamed, the heart is being set up for arrhythmia.”
To make this discovery, researchers focused on adenovirus, a common culprit in cardiac infection and myocarditis, using Mouse Adenovirus Type-3 to replicate the human infection process.

They found that early in the infection, the virus disrupts critical components of the heart’s communication and electrical systems.
As a result, even before symptoms appear, the adenoviral infection creates conditions that disrupt the heart’s gap junctions and ion channels, according to virologist Rachel Padget, the study’s first author who worked in the Smyth lab while completing a doctoral degree from the Virginia Tech Translational Biology, Medicine, and Health graduate program.
Gap junctions are like tiny tunnels between heart cells that allow them to communicate, and ion channels are like gates in the cell membranes that help maintain the right balance of ions needed for the heart to generate normal patterns of electrical activity that allow it to beat properly.
When adenoviral infection disturbs these communication bridges and gatekeepers, it creates a situation where the heart might develop irregular patterns of electrical activity called arrhythmias affecting its mechanical beating and blood pumping capacity, and that can lead to sudden cardiac problems, especially in people with active infections.
Now, by targeting specific heart changes induced by viral infections at the molecular level, researchers aim to reduce the risk of cardiac issues in people grappling with viral illnesses.
“Individuals who have acute infections can look normal by MRI and echocardiography, but when we delved into the molecular level, we saw that something very dangerous could occur,” Smyth said. “In terms of diagnostics, we can now work with our colleagues here to start looking ways to analyze blood for a biomarker of the more serious problem. People get cardiac infections all the time and they recover. But can we identify what’s different about individuals that are at a higher risk to have the arrhythmia, possibly through a simple blood test in the doctor’s office.”
The work was supported in part by grants from the National Institutes of Health, American Heart Association, Fralin Biomedical Research Institute Seale Innovation Fund and Lyerly Postdoctoral Excellence Award.

In a new study, neuroscientists show how decision-making processes are controlled in the primate brain during foraging. The team, including a researcher from the German Primate Center (DPZ) — Leibniz Institute for Primate Research in Göttingen, trained two rhesus monkeys to search for food in an experimental room.
The animals were able to move freely and receive food pellets from two food boxes by pressing a button. In the course of the experiment, the monkeys learned that the amount of pellets dispensed from the boxes increased the longer they waited until the next button was pressed. If they were not rewarded with pellets after pressing the button, the monkeys waited longer the next time or switched to the other box. During the experiment, the researchers measured the neuronal activity in the front part of the brains of the two monkeys and decomposed it with the help of a mathematical model. By decoding monkeys’ reward expectations from the neural activity, they were able to predict how long the rhesus monkeys were willing to wait for a higher reward and when they decided to choose another option. The results advance our understanding of self-paced actions, eventually contributing to a better understanding of neurological diseases such as Parkinson’s (Nature Neuroscience).
Imagine a fisherman on a boat casting fish traps into a murky lake. To be successful, he has to check the traps regularly. But when is the best time to do this? If he checks the traps too often, it is unnecessary work and he scares the fish away. If he checks too late, he has a better chance, but may be wasting time. It is also tiring to paddle from one trap to another to check them one after the other, so the fisherman has to keep deciding whether and when it is worthwhile.
For decades, neuroscientists have been trying to understand how we manage to make the best possible decisions. Due to technical limitations, researchers have so far had to rely on experiments in which monkeys perform tasks on computer screens while the activity of their brain cells is measured. The animals are trained to sit still in a chair and are therefore restricted in their natural freedom of movement. Since it is now possible to wirelessly record the activity of several individual nerve cells, decision-making in scenarios with natural movement sequences can be investigated.
For the study, a team of researchers from Germany and the USA trained two rhesus monkeys to explore an experimental room with two button-controlled food boxes. Each time the monkeys pressed a button on one of the boxes, they had the chance to receive food pellets. The two boxes were set in such a way that the time intervals between the individual food dispenses became longer and longer during an experimental run. The longer the monkeys waited until they pressed the button again, the more pellets they received.
“When we started the experiment, we expected that our monkeys would simply choose the box based on how successful they had been with that box before,” explains first author Neda Shahidi, now a junior research group leader at the Collaborative Research Center 1528 at the University of Göttingen and the German Primate Center in Göttingen. “After a while, however, they had learned to pay attention to the time since the last keystroke and also to their previous success at a box. If they had waited a while but not received any pellets, they waited even longer before pressing the next time. However, if they were not rewarded too many times in a row after pressing the button, they moved to the other box. They had apparently decided that this food box was not worth the wait and it was better to look elsewhere.”
To analyze the underlying neuronal processes, the researchers wirelessly recorded the activity of 96 neurons in the prefrontal cortex. This brain area is involved in the control of goal-directed behavior and is activated in many aspects of the foraging task, for example in the evaluation of options, the expectation of a reward, the preparation of actions, and the perception of the outcome.
“However, characterizing the activity patterns of individual neurons does not always reveal the whole story when we study complex decision-making processes,” Shahidi explains. “Complex behaviors consist of different components that are sometimes processed simultaneously in the same brain area.” To separate these components, the researchers developed a mathematical model that first identified components of neural activity, mainly consist of groups of neurons that were more strongly active when the animals waited longer before pressing a button or when the button has been more rewarding in last few presses. Since the animals cannot know in advance whether a button press will be rewarded, the researchers assume that these neurons represent the animals’ subjective expectations.
The researchers also tested whether the neuronal activity could be used to predict when the animals would press the button and whether they would decide to switch between the boxes. “We were surprised at how well our model could predict what the monkeys would do in the next few seconds,” says Shahidi. “Our results show not only how the development of wireless recording technologies can improve our understanding of brain mechanisms in natural movement scenarios, but also how advances in data science are transforming neuroscience by extracting the computational components of the brain from the collective activity of neurons. We hope that in the long term, such advances will help to better understand abnormalities in cognitive processes such as self-pacing in Parkinson’s or self-initiating actions in apathy” says Shahidi.

A surge of a neural-specific protein in the brain is the earliest-yet biomarker for Alzheimer’s disease, report University of Illinois Urbana-Champaign researchers studying a mouse model of the disease. Furthermore, the increased protein activity leads to the seizures associated with the earliest stages of neurodegeneration, and inhibiting the protein in the mice slowed the onset and progression of seizure activity.
The neural-specific protein, PSD-95, could pose a new target for Alzheimer’s research, early diagnosis and treatment, said study leader Nien-Pei Tsai, an Illinois professor of molecular and integrative physiology.
Tsai’s group studies mice that make more of the proteins that form amyloid-beta, which progressively aggregates in Alzheimer’s disease to form plaques in the brain that hamper neural activity. However, in the new work, the group focused on a time frame much earlier in the mouse lifespan than others have studied — when no other markers or abnormalities have been reported, Tsai said.
“We were thinking, if we can catch anything that is happening early enough, maybe we can find a way to diagnose the disease earlier or slow down the progression,” Tsai said. “We know that Alzheimer’s is irreversible. But if we can slow down the progression or even delay the onset of the disease, we can improve the quality of life for patients.”
While watching early neural development, first in neuron cultures and then in live mice, the researchers saw an elevation in PSD-95 levels. The PSD-95 protein’s job is to attract and pull other receptors to the synaptic surface — the space where two neurons pass signals to one another.
“Our data suggests that the elevated PSD-95 is contributing to hyperexcitability in the brain. That’s a common phenotype is some of the early stages of Alzheimer’s disease patients: They tend to have hyperexcitability or elevated seizure susceptibility in the brain, preceding and exacerbating the neurodegeneration that follows,” said Tsai, who also is affiliated with the Beckman Institute of Advanced Science and Technology at the U. of I.
To confirm that increased PSD-95 was a driving force behind the seizure activity, the researchers inhibited PSD-95 in a mouse cohort. They saw reduced receptor activity at the synapse, fewer seizures in the mice and reduced mortality from seizures.

“Our findings show that PSD-95 is a critical contributor to the hyperexcitability in the earliest stages of Alzheimer’s. So we think that PSD-95 can be an early biomarker to indicate that a patient could have Alzheimer’s disease or elevated seizure susceptibility. In terms of treatment, antibody inhibitors for PSD-95 could be useful in the early onset of Alzheimer’s, with more clinical study.”
The group published its findings in the journal EMBO Reports.
The researchers hope to partner with clinical research teams to determine whether their findings in mice correlate with samples from human patients. They also plan to study other receptors that PSD-95 interacts with on the synaptic surface to see if it plays a role in other symptoms of the disease or stages of its progression.
“For example, the NMDA receptor has been shown to contribute to neural cell death in Alzheimer’s disease. So we’re trying to see whether by inhibiting PSD-95, we also can inhibit this particular NMDA receptor to slow down cell death.”
The National Institutes of Health and the Alzheimer’s Association supported this work.
The National Institute of Health supported this work through grants R01NS105615, R01MH124827 and R21AG071278.

His groundbreaking research, which he performed with Yvonne Barr, his doctoral student, uncovered the first virus capable of causing cancer in humans.In March of 1961, Dr. Anthony Epstein, a pathologist at Middlesex Hospital in London, almost skipped a visiting physician’s afternoon lecture about children with exceptionally large facial tumors in Uganda.The physician, Dr. Denis Burkitt, a native of Ireland who called himself a bush surgeon, showed slides of bulbous tumors that emerged along the jawline and occurred in tropical African regions where rainfall was high. During his lecture, Dr. Burkitt mapped a veritable pediatric cancer belt that extended across equatorial Africa.Despite Dr. Epstein’s initial reluctance to attend the talk — he sat in the rear to make a quick escape — his excitement grew the longer Dr. Burkitt spoke. By the time the lecture was over, he knew that he would drop all of his ongoing projects to find the cause of the unusual malignancy. His doctoral student, Yvonne Barr, soon joined him and, by 1964, their groundbreaking research uncovered the first virus capable of causing cancer in humans.He rocked the scientific world with the announcement. Some physicians and scientists applauded the discovery; others refused to accept it.Dr. Epstein died on Feb. 6 at his home in London. He was 102. His death was confirmed by the University of Bristol, where Dr. Epstein was a professor of pathology from 1968 to 1985, and had also served as the head of the department for 15 years.The pathogen that came to bear his and Dr. Barr’s names — Epstein-Barr virus — belongs to the herpes family and is one of the most ubiquitous on the planet. An estimated 90 percent of the world’s adult population carries the virus, which is also known as E.B.V.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

A large study of “discordant twins,” in which only one suffered abuse or neglect, adds to evidence linking childhood trauma to adult illness.Twins are a bonanza for research psychologists. In a field perpetually seeking to tease out the effects of genetics, environment and life experience, they provide a natural controlled experiment as their paths diverge, subtly or dramatically, through adulthood.Take Dennis and Douglas. In high school, they were so alike that friends told them apart by the cars they drove, they told researchers in a study of twins in Virginia. Most of their childhood experiences were shared — except that Dennis endured an attempted molestation when he was 13.At 18, Douglas married his high school girlfriend. He raised three children and became deeply religious. Dennis cycled through short-term relationships and was twice divorced, plunging into bouts of despair after each split. By their 50s, Dennis had a history of major depression, and his brother did not.Why do twins, who share so many genetic and environmental inputs, diverge as adults in their experience of mental illness? On Wednesday, a team of researchers from the University of Iceland and Karolinska Institutet in Sweden reported new findings on the role played by childhood trauma.Their study of 25,252 adult twins in Sweden, published in JAMA Psychiatry, found that those who reported one or more trauma in childhood — physical or emotional neglect or abuse, rape, sexual abuse, hate crimes or witnessing domestic violence — were 2.4 times as likely to be diagnosed with a psychiatric illness as those who did not.If a person reported one or more of these experiences, the odds of being diagnosed with a mental illness climbed sharply, by 52 percent for each additional adverse experience. Among participants who reported three or more adverse experiences, nearly a quarter had a psychiatric diagnosis of depressive disorder, anxiety disorder, substance abuse disorder or stress disorder.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Media accounts of a German man’s extreme vaccination history spurred researchers to analyze his immune responses.Two years ago, German doctors stumbled across news reports of a man being investigated for receiving scores of coronavirus vaccines with no medical explanation.Then followed a flurry of speculation about what he had been up to. As it turned out, prosecutors were looking into whether he had been receiving so many extra doses as part of a scheme to collect stamped immunization cards that he could later sell to people who wanted to skirt vaccine mandates.But to the doctors, the man was a medical anomaly, someone who had defied official recommendations and turned himself into a guinea pig for measuring the outer limits of an immune response. Last year, they asked prosecutors investigating his vaccine splurge to pass along a request: Would he like to join a research project?Once prosecutors closed their fraud investigation without criminal charges, the man agreed.By the time the doctors first saw him, the 62-year-old man had received 215 doses of coronavirus vaccine, they said. Flouting their pleas to stop, he received another two shots in the next months, expanding his immunological stockpile to a combined 217 doses of eight different Covid vaccine types over two and a half years.After months of studying him, the doctors, led by Dr. Kilian Schober, an immunologist at the University of Erlangen-Nuremberg in the German state of Bavaria, reported their findings this week in The Lancet Infectious Diseases, a medical journal.The man had seemingly never been infected with the coronavirus. He reported no vaccine side effects. And, most interestingly to the researchers, his repertoire of antibodies and immune cells was considerably larger than that of a typical vaccinated person, even if the precision of those immune responses remained effectively unchanged.We are having trouble retrieving the article content.Please enable JavaScript in your browser settings.Thank you for your patience while we verify access. If you are in Reader mode please exit and log into your Times account, or subscribe for all of The Times.Thank you for your patience while we verify access.Already a subscriber? Log in.Want all of The Times? Subscribe.

Patients undergoing chemotherapy often experience cognitive effects such as memory impairment and difficulty concentrating — a condition commonly known as “chemo brain.”
MIT researchers have now shown that a noninvasive treatment that stimulates gamma frequency brain waves may hold promise for treating chemo brain. In a study of mice, they found that daily exposure to light and sound with a frequency of 40 hertz protected brain cells from chemotherapy-induced damage. The treatment also helped to prevent memory loss and impairment of other cognitive functions.
This treatment, which was originally developed as a way to treat Alzheimer’s disease, appears to have widespread effects that could help with a variety of neurological disorders, the researchers say.
“The treatment can reduce DNA damage, reduce inflammation, and increase the number of oligodendrocytes, which are the cells that produce myelin surrounding the axons,” says Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory and the Picower Professor in the MIT Department of Brain and Cognitive Sciences. “We also found that this treatment improved learning and memory, and enhanced executive function in the animals.”
Tsai is the senior author of the new study, which appears today in Science Translational Medicine. The paper’s lead author is TaeHyun Kim, an MIT postdoc.
Protective brain waves
Several years ago, Tsai and her colleagues began exploring the use of light flickering at 40 hertz (cycles per second) as a way to improve the cognitive symptoms of Alzheimer’s disease. Previous work had suggested that Alzheimer’s patients have impaired gamma oscillations — brain waves that range from 25 to 80 hertz (cycles per second) and are believed to contribute to brain functions such as attention, perception, and memory.

Tsai’s studies in mice have found that exposure to light flickering at 40 hertz or sounds with a pitch of 40 hertz can stimulate gamma waves in the brain, which has many protective effects, including preventing the formation of amyloid beta plaques. Using light and sound together provides even more significant protection. The treatment also appears promising in humans: Phase 1 clinical trials in people with early-stage Alzheimer’s disease have found the treatment is safe and does offer some neurological and behavioral benefits.
In the new study, the researchers set out to see whether this treatment could also counteract the cognitive effects of chemotherapy treatment. Research has shown that these drugs can induce inflammation in the brain, as well as other detrimental effects such as loss of white matter — the networks of nerve fibers that help different parts of the brain communicate with each other. Chemotherapy drugs also promote loss of myelin, the protective fatty coating that allows neurons to propagate electrical signals. Many of these effects are also seen in the brains of people with Alzheimer’s.
“Chemo brain caught our attention because it is extremely common, and there is quite a lot of research on what the brain is like following chemotherapy treatment,” Tsai says. “From our previous work, we know that this gamma sensory stimulation has anti-inflammatory effects, so we decided to use the chemo brain model to test whether sensory gamma stimulation can be beneficial.”
As an experimental model, the researchers used mice that were given cisplatin, a chemotherapy drug often used to treat testicular, ovarian, and other cancers. The mice were given cisplatin for five days, then taken off of it for five days, then on again for five days. One group received chemotherapy only, while another group was also given 40-hertz light and sound therapy every day.
After three weeks, mice that received cisplatin but not gamma therapy showed many of the expected effects of chemotherapy: brain volume shrinkage, DNA damage, demyelination, and inflammation. These mice also had reduced populations of oligodendrocytes, the brain cells responsible for producing myelin.
However, mice that received gamma therapy along with cisplatin treatment showed significant reductions in all of those symptoms. The gamma therapy also had beneficial effects on behavior: Mice that received the therapy performed much better on tests designed to measure memory and executive function.

“A fundamental mechanism”
Using single-cell RNA sequencing, the researchers analyzed the gene expression changes that occurred in mice that received the gamma treatment. They found that in those mice, inflammation-linked genes and genes that trigger cell death were suppressed, especially in oligodendrocytes, the cells responsible for producing myelin.
In mice that received gamma treatment along with cisplatin, some of the beneficial effects could still be seen up to four months later. However, the gamma treatment was much less effective if it was started three months after the chemotherapy ended.
The researchers also showed that the gamma treatment improved the signs of chemo brain in mice that received a different chemotherapy drug, methotrexate, which is used to treat breast, lung, and other types of cancer.
“I think this is a very fundamental mechanism to improve myelination and to promote the integrity of oligodendrocytes. It seems that it’s not specific to the agent that induces demyelination, be it chemotherapy or another source of demyelination,” Tsai says.
Because of its widespread effects, Tsai’s lab is also testing gamma treatment in mouse models of other neurological diseases, including Parkinson’s disease and multiple sclerosis. Cognito Therapeutics, a company founded by Tsai and MIT Professor Edward Boyden, has finished a phase 2 trial of gamma therapy in Alzheimer’s patients, and plans to begin a phase 3 trial this year.
“My lab’s major focus now, in terms of clinical application, is Alzheimer’s; but hopefully we can test this approach for a few other indications, too,” Tsai says.
The research was funded by the JPB Foundation, the Ko Hahn Seed Fund, and the National Institutes of Health.

The gastrointestinal tract is already known to researchers as a major storage site for micro- and nanoplastic particles (MNPs) in the human body. A research consortium consisting of the University of Vienna, the Medical University of Vienna and other partners under the leadership of CBmed GmbH in Graz has now investigated the effects of the tiny plastic particles on cancer cells in the human gastrointestinal tract. The study showed that MNPs remain in the cell for much longer than previously assumed, as they are passed on to the newly formed cell during cell division. The first indications were also discovered that the plastic particles could promote the metastasis of tumours. The results of the study were recently published in the scientific journal “Chemospheres.”
Besides respiration, ingestion is the most important route for MNPs into the organism. Plastic particles up to the weight of a credit card (approx. five grams) enter the gastrointestinal tract every week. The team led by Verena Pichler (University of Vienna, CBmed) and Lukas Kenner (MedUni Vienna, CBmed, Vetmeduni Vienna) investigated the interactions between MNPs and various colon cancer cells.
In their analyses, they were not only able to show how MNPs enter the cell and where exactly they are deposited, but also observed their direct effects: The MNPs are taken up into lysosomes like other “waste products” in the body. Lysosomes are cell organelles that are also known as the “stomach of the cell” and break down foreign bodies in the cell. However, the researchers observed that, unlike foreign bodies of biological origin, the MNPs are not degraded due to their foreign chemical composition.
Depending on various factors, the MNPs are even passed on to the newly formed cell during cell division and are therefore likely to be more persistent in the human body than originally assumed. In addition, there are initial indications that MNPs increase the migration of cancer cells to other regions of the body and thus possibly promote the metastasis of tumours. This effect is now to be investigated further in a follow-up study.
The smaller, the more harmful
The altered behaviour of colorectal cancer cells in relation to cell migration was primarily observed as a result of interaction with plastic particles that are smaller than one micrometre (1 µm = 0.001 mm). Particles of this size are usually referred to as nanoplastics, which occur 10 to 100 times more frequently than microplastics in a water bottle, for example. It is undisputed that the smaller the plastic particles are, the more harmful they are. “This is once again consistent with the results of our analyses,” emphasises Verena Pichler. “Our study also confirms recent findings that indicate that MNPs can influence cell behaviour and possibly contribute to the progression of diseases,” adds Lukas Kenner.
“Given the ubiquity of plastics in the environment and the persistent exposure of even humans to the smallest plastic particles, further studies are urgently needed to investigate long-term effects in particular,” says Kenner. “It can be assumed that MNP causes chronic toxicity,” fears Pichler. The latest results and earlier studies show a high uptake and long retention in tissues and cells. The investigated particles therefore fulfil two of three characteristics in toxicology that are used to classify substances as being of concern under the EU Chemicals Regulation (“REACH”).

Early experiences in an animal’s life can have a significant impact on its capacity to thrive, even years or decades later, and DNA methylation may help record their effects. In a study of 256 wild baboons, researchers from the Max Planck Institute for Evolutionary Anthropology and Duke University found that resource limitation during early life was associated with many differences in DNA methylation, a small chemical mark on the DNA sequence that can affect gene activity.
Resource limitation was more important than other types of early environmental stressors, suggesting the particular importance of resource deprivation in the first years of life. However, the researchers also suggest that aspects of the environment at the time of sampling, such as social status, may be more important in explaining differences in DNA methylation between individuals, indicating that multiple pathways must connect early life effects on later life outcomes.
Adverse environmental conditions, especially early in life, can have long-term effects on an animal’s health and survival. For example, in rhesus monkeys, infants who are separated from their mothers soon after birth, are more susceptible to disease later in life. The idea that such differences arise from long-term changes in the animal’s biology is called “biological embedding.” Changes in DNA methylation, an “epigenetic” modification of the DNA sequence, have been proposed to contribute to biological embedding, particularly because these changes can be stable and affect gene activity, and potentially other traits. However, studies of early life adversity and DNA methylation in wild mammals are limited.
To investigate the associations between DNA methylation and early life adversity, an international team of researchers from the Max Planck Institute for Evolutionary Anthropology and Duke University studied a population of wild baboons in Kenya. “Our study included 256 baboons — 115 males and 141 females — and we combined DNA methylation data with ecological, behavioral, and life history data collected over the more than 50 years of this study site’s history,” says first author Jordan Anderson, a PhD researcher at Duke University. “This population was a good candidate for analysis because we already know that female baboons who experience a lot of early life adversity have elevated stress hormone levels in adulthood, weaker social bonds, and lower offspring survival.”
Early life resource deprivation can affect health across generations
Surprisingly, the study showed that the loss of a mother was not strongly associated with variation in DNA methylation — nor was early life social status or social isolation. Instead, the clearest results came from looking at drought and poor habitat quality, which limit the availability of food for the baboons. The researchers also found that multiple exposures to early adversity left particularly strong signatures. “Exposure to repeated early life adversity seems to have compounding effects on DNA methylation. For example, for those born into poor early life habitats, the impact of drought is greater,” says senior author and project leader Jenny Tung, director of the Department of Primate Behavior and Evolution at the Max Planck Institute for Evolutionary Anthropology. “This may be because different types of adversity can work through similar mechanisms, like affecting how much they have to eat.”
The authors emphasize that the importance of also examining whether, as predicted by biological embedding, differences in DNA methylation also affect gene activity. “We have taken a step in this direction by using genomic approaches to test whether DNA methylation can influence gene expression in isolated cells, but much more research is needed to understand how early life adversity influences animal physiology, health, and survival, including, but not limited to, its effects on DNA methylation,” says Tung.