Epilepsy, where patients suffer from unexpected seizures, affects roughly 1% of the population. These seizures often involve repetitive and excessive neuronal firing, with the trigger behind this still poorly understood.
Now, researchers at Tohoku University have monitored astrocyte activity using fluorescence calcium sensors, discovering that astrocyte activity starts approximately 20 seconds before the onset of epileptic neuronal hyperactivity. This suggests that astrocytes play a significant part in triggering epileptic seizures, facilitating the hyper-drive of the neural circuit.
The findings were detailed in the journal Glia on April 9, 2024.
Astrocytes are non-neuronal glial cells that occupy almost half of the brain. They have been shown to control the local ionic and metabotropic environment in the brain. Yet, since they do not exhibit electrical activity that can be easily monitored, their role in the function of the brain has largely been neglected. Fluorescence sensor proteins are changing this, revealing more about the mesmerizing activity of astrocytes.
“Astrocytes appear to have a determinant role in controlling the state of neuronal activity and synaptic plasticity both in physiological and pathophysiological situations,” says Professor Ko Matsui of the Super-network Brain Physiology lab at Tohoku University, who led the research. “Therefore, astrocytes could be considered as a new therapeutic target for epilepsy treatment.”
When brain tissue makes contact with metals such as copper, it is known to induce inflammation that leads to acute symptomatic seizures, which occurs a few times per day in mice. Matsui and his team observed these events, where they discovered that astrocyte activity may be the trigger for neuronal hyperactivity. Astrocytes can also be activated by low-amplitude direct current stimulation. The researchers noticed that such a stimulation induced a robust increase in the astrocyte calcium, which was followed by an epileptic neuronal hyperactivity episode. When the metabolic activity of the astrocytes was blocked by applying fluorocitrate, the magnitude of the epileptic neuronal hyperactivity was significantly reduced. These all point to the fact that astrocytes have the potential to control neuronal activity.
Lead study investigator Shun Araki emphasizes that with appropriate guidance, astrocytes’ functions could be harnessed to address a range of neurological conditions. This includes not only epilepsy but also potentially enhancing cognitive abilities beyond natural limitations.

Researchers at the Institute for Atmospheric and Earth System Research (INAR) at the University of Helsinki have found that modern weather models can accurately predict the energy that Earth emits and reflects into space, which directly affects the movements of low Earth-orbiting (LEO) satellites. By leveraging these models, the researchers gained insights into how LEO satellites respond to weather events below, such as tropical cyclones with tall and reflective clouds. The results were published in the Journal of Geophysical Research in April.
In the study, the researchers utilized numerical weather models. They are sophisticated computer simulators that predict future atmospheric conditions based on current observations and laws of physics.
“Numerical weather models not only simulate weather patterns but also calculate various parameters, including the Earth’s energy emissions and reflections under various weather conditions. By analysing these simulations, we sought to understand how changes in weather, such as cloud cover and storms, influence the movement of satellites, affecting their ability to fulfil their intended duties,” says Sanam Motlaghzadeh, lead author of the study and doctoral researcher at INAR, funded by the Nessling Foundation.
Improved satellite operations
The significance of the findings lies in their potential to enhance satellite tracking and control, improving the efficiency and reliability of satellite operations.
“Understanding how weather affects satellites also enhances the accuracy of satellite-based measurements used in climate studies. These findings address a critical challenge in satellite data reliability, namely, determining the precise orbits of satellites, on which the weather events have effect,” Motlaghzadeh explains.
Satellites play a crucial role in monitoring vegetation, tracking water resources, and observing glacier evolution through various measurement techniques. These measurements, including image capture and height and gravity field measurements, are essential for studying climate change and its impacts.
A better understanding of satellite movements can also aid in climate monitoring and disaster management. Utilizing advanced weather models can further refine satellite-based measurements, facilitating more effective study and mitigation of environmental issues.
“Understanding how satellites interact with Earth’s atmosphere offers valuable insights into our planet and how it changes over time. The findings contribute to more accurate satellite-based monitoring of terrestrial water resources, and hence to food security, Motlaghzadeh says.

Toxic chemicals used to flame-proof plastic materials can be absorbed into the body through skin, via contact with microplastics, new research shows.
The study offers the first experimental evidence that chemicals present as additives in microplastics can leach into human sweat, and then be absorbed through the skin, into the bloodstream.
Many chemicals used as flame retardants and plasticisers have already been banned, due to evidence of adverse health effects including damage to the liver or nervous system, cancer, and risks to reproductive health. However, these chemicals are still present in the environment in older electronics, furniture, carpets, and building materials.
While the harm caused by microplastics is not fully understood, there is increasing concern over their role as conduits of human exposure to toxic chemicals.
The research team demonstrated in a study published last year, that chemicals were leached from microplastics into human sweat. The current study now shows that those chemicals can also be absorbed from sweat across the skin barrier into the body.
In their experiments, the team used innovative 3D human skin models as alternatives to laboratory animals and excised human tissues. The models were exposed over a 24-hour period to two common forms of microplastics containing polybrominated diphenyl ethers (PBDEs), a chemical group commonly used to flame retard plastics.
The results, published in Environment International, showed that as much as 8% of the chemical exposed could be taken up by the skin, with more hydrated — or ‘sweatier’ — skin absorbing higher levels of chemical. The study provides the first experimental evidence into how this process contributes to levels of toxic chemicals found in the body.

Dr Ovokeroye Abafe, now at Brunel University, carried out the research while at the University of Birmingham. He said: “Microplastics are everywhere in the environment and yet we still know relatively little about the health problems that they can cause. Our research shows that they play a role as ‘carriers’ of harmful chemicals, which can get into our bloodstream through the skin. These chemicals are persistent, so with continuous or regular exposure to them, there will be a gradual accumulation to the point where they start to cause harm.”
Dr Mohamed Abdallah, Associate Professor of Environmental Sciences at the University of Birmingham, and principal investigator for the project, said: “These findings provide important evidence for regulators and policymakers to improve legislation around microplastics and safeguard public health against harmful exposure.”
Professor Stuart Harrad, co-author of the paper, added “the study provides an important step forward in understanding the risks of exposure to microplastics on our health. Building on our results, more research is required to fully understand the different pathways of human exposure to microplastics and how to mitigate the risk from such exposure.”
In future research, the team plan to investigate other routes through which microplastics could be responsible for toxic chemicals entering the body, including inhalation and ingestion. The work is funded by a Marie Curie Research Fellowship, within the European Union’s Horizon 2020 Research and Innovation Programme.

Mount Sinai scientists, in collaboration with researchers from the Carlos III Health Institute (ISCIII) in Madrid, Spain, have located and identified alterations in the monkeypox virus genome that potentially correlate with changes in the virus’s transmissibility observed in the 2022 outbreak. The findings were published April 18 in Nature Communications.
Monkeypox virus (MPXV) is a double-stranded DNA virus that can infect animals and humans. MPXV causes a disease known as mpox, with symptoms that include fever, swollen lymph nodes, and a rash. Most cases are mild and tend to get better on their own; however, mpox can be very painful and may lead to permanent scarring. First encountered in 1958 in crab-eating macaque monkeys imported to Belgium, MPXV has caused sporadic human disease outbreaks since the 1970s in Central and Western Africa. In May 2022, multiple countries, including the United States, reported an increasing number of MPXV infections and associated disease, including clusters in cases potentially linked to super-spreading events in Belgium, Spain, and the United Kingdom. While the number of new cases associated with the 2022 spillover has decreased over time, cases of the disease are still occurring among unvaccinated individuals, including a current increase in Central Africa due to a new spillover. As the virus’s circulation in humans increases, the risk of emergence of a more transmissible variant capable of becoming endemic in the human population increases.
“Biopreparedness and virological surveillance involves studying the causes that favor zoonotic spillover and facilitates human-to-human transmission. When we observe significant changes in basic epidemiological features of a viral agent like monkeypox, it should reinvigorate our interest in understanding those transmission conditions. The increasing number of cases currently happening in Africa, and the 2022 epidemic, should be clear alert signals,” says Gustavo Palacios, PhD, Professor of Microbiology at the Icahn School of Medicine at Mount Sinai and a senior author of the study.
To carry out the study, researchers analyzed samples from 46 patients infected with MPXV whose diagnosis and sequencing were carried out at the ISCIII at the beginning of the 2022 mpox outbreak. The team performed high-quality sequencing of each study participant’s complete monkeypox virus genome to determine possible correlations between genomic variations in the different groups of sequences and epidemiological links associated with the virus’s ability to evolve, transmit, and infect.
According to the research team, recurrent observed genomic changes were located in areas of the genome that could be related to viral adaptation. Those specific locations would contribute to modulating the viral replication cycle, adaptability, and path of entry and egress. These alterations appear in areas known as low complexity genomic regions, which are particularly difficult to sequence and analyze, explaining why they were overlooked before. This highly sophisticated complete genome sequencing was made possible through the use of two advanced sequencing technologies: single-molecule long-read sequencing (to cover highly repetitive regions) and deep short sequencing reads (to provide accuracy and depth).
By detailing the genomic alterations within these repetitive genomic sequences and linking them to critical viral functions, researchers provide a plausible explanation for the heightened transmissibility observed during the 2022 mpox outbreak.
“These findings might be offering the first hints to help us understand the unique features of the strains associated with sustained human-to-human transmission, which has not ever been observed in these agents,” says Dr. Palacios. “Better understanding of the doors that facilitate transmission of viral agents and impact their clinical presentations will enable us to develop more effective prevention and treatment strategies.”

Dietary treatment is more effective than medications in irritable bowel syndrome (IBS). These are the findings of a study conducted at the University of Gothenburg. With dietary adjustments, more than seven out of ten patients had significantly reduced symptoms.
Irritable bowel syndrome (IBS) is a common diagnosis that causes abdominal pain, gas and abdominal bloating, diarrhea, and constipation, in various combinations and with varying degrees of severity.
Treatment often consists of dietary advice such as eating small and frequent meals and avoiding excessive intake of food triggers such as coffee, alcohol and fizzy drinks. Patients may also be given medications to improve specific symptoms, such as gas or constipation, diarrhea, bloating or abdominal pain. Antidepressants are sometimes used to improve symptoms in IBS.
The current study, published in The Lancet Gastroenterology & Hepatology, compared three treatments: two dietary and one based on use of medications. The participants were adult patients with severe or moderate IBS symptoms at Sahlgrenska University Hospital in Gothenburg.
More symptom relief after dietary adjustment
The first group was given traditional IBS dietary advice, focusing on eating behavior combined with low intake of fermentable carbohydrates, known as FODMAPs. These include e.g. products with lactose, legumes, onions, and grains, which ferment in the colon and can cause pain in IBS.
The second group received a dietary treatment low in carbohydrates and proportionally high in protein and fat. In the third group, the best possible medication was given based on the patient’s most troublesome IBS symptoms.

Each group included around 100 participants and the treatment periods lasted four weeks. When the researchers then examined how well the participants responded to the treatments, using an established IBS symptom scoring scale, the results were clear.
Of those who received traditional IBS dietary advice and low content of FODMAPs, 76% had significantly reduced symptoms. In the group receiving low carbohydrates and high protein and fat, the proportion was 71%, and in the medication group 58%.
All groups reported significantly better quality of life, less physical symptoms and less symptoms of anxiety and depression.
The importance of personalization
At a six-month follow-up, when participants in the dietary groups had partially returned to their previous eating habits, a large proportion still had clinically significant symptom relief; 68% in the traditional dietary advice and low FODMAP group, and 60% in the low-carbohydrate diet group.
The study was led by Sanna Nybacka, Researcher and Dietician, Stine Störsrud, Associate Professor, and Magnus Simrén, Professor and Senior Consultant, all at Sahlgrenska Academy, University of Gothenburg.
“With this study, we can show that diet plays a central role in the treatment of IBS, but that there are several alternative treatments that are effective,” says Sanna Nybacka.
“We need more knowledge about how to best personalize the treatment of IBS in the future and we will further investigate whether there are certain factors that can predict whether individuals will respond better to different treatment options,” she concludes.

Researchers have revealed the regulatory mechanism of a specific protein that plays a key role in balancing the immune response triggered by viral infections in mammal cells. These findings could help drive the development of antiviral therapies and nucleic acid medicines to treat genetic disorders.
For cells to protect themselves from viral infections, a series of immune responses typically occur, including programmed cell death called apoptosis and interferon signaling. While apoptosis is a normal process, which occurs with or without the presence of viral molecules, following a cascade of steps to end with the death of a cell — which might not sound advantageous to the host — it can help prevent the reproduction of abnormal cells, including those infected by viruses, and eliminate them from the body. Interferons, on the other hand, are proteins produced by animal cells in response to a viral infection to protect the cell against viral attacks and prevent the virus from replicating. The regulatory mechanism of how cells maintain a balance between apoptosis and interferon response to efficiently suppress viral replication during infection, however, remained unclear.
In the current study, a team including researchers from the University of Tokyo focused on a specific protein, TRBP, which is also classified as a type of protein called an RNA silencing factor.
RNA is a nucleic acid, an organic compound found in living cells and viruses, which controls protein synthesis and the genetic makeup of many viruses. RNA synthesizes proteins through a process known as translation, by reading genetic sequences and translating them into instructions for the cells to create proteins, which are mostly responsible for the overall structure and function of the organism, whether it’s a plant or animal.
RNA silencing, also known as RNA interference, is a way that plants and invertebrate animals can protect themselves from viruses by cleaving viral RNA to repress viral replication.
“This study provides a significant insight that clearly revealed the protein related to the RNA silencing mechanism, which is known to be an antiviral mechanism in a plant or invertebrate, is strongly related to antiviral response also in mammals by another mechanism,” said co-author Tomoko Takahashi, a visiting researcher at the University of Tokyo and assistant professor at Saitama University in Japan.
Though it is widely understood that RNA silencing is a mechanism that operates under normal conditions to control gene expression (if the gene is “turned on” to provide instructions for the cell to assemble the specific protein it encodes), it’s still unclear how this process occurs under the stress of viral infection.

So the researchers looked at TRBP (an abbreviation for TAR RNA-binding protein), which has shown a significant role in RNA silencing during a viral infection.
This protein interacts with a virus sensor protein early on in the phases of infection in human cells. In the later stages of viral infection, proteins called caspases are activated, and this type of protein is chiefly responsible for triggering cell death.
“RNA silencing and interferon signaling were previously considered as independent pathways, but multiple reports, including ours, have demonstrated crosstalk between them,” said Kumiko Ui-Tei, another co-author and associate professor from the University of Tokyo (at the time of the study).
This functional conversion of TRBP triggered by viral infection is the basis of regulating interferon response and apoptosis, with TRBP irreversibly increasing the programmed cell death of infected cells, while reducing interferon signaling. TRBP works on the cell by inducing cell death, stopping the viral replication entirely, in contrast to the interferon response pathway, which just subdues viral replication instead of eliminating the infected cells.
“The ultimate goal is understanding the molecular mechanism underlying the antiviral defense system, orchestrated through the interplay between internal and external RNA pathways in human cells,” said Takahashi.
By gaining a deeper understanding of how defenses against viruses work on a molecular level, the researchers aim to drive the development of nucleic acid medicines. These medicines utilize targeting and inhibition approaches similar to the antiviral response of RNA silencing, and they hold promise of being increasingly useful in treating a wider range of patients afflicted with viral infections, genetic mutations and genetic defects.
This study was conducted in collaboration with Saitama University, Chiba University, Kyoto University and Maebashi Institute of Technology in Japan.

In a discovery that could hasten treatment for patients with multiple sclerosis (MS), UC San Francisco scientists have discovered a harbinger in the blood of some people who later went on to develop the disease.
In about 1 in 10 cases of MS, the body begins producing a distinctive set of antibodies against its own proteins years before symptoms emerge. These autoantibodies appear to bind to both human cells and common pathogens, possibly explaining the immune attacks on the brain and spinal cord that are the hallmark of MS.
The findings were published in Nature Medicine on April 19.
MS can lead to a devastating loss of motor control, although new treatments can slow the progress of the disease and, for example, preserve a patient’s ability to walk. The scientists hope the autoantibodies they have discovered will one day be detected with a simple blood test, giving patients a head start on receiving treatment.
“Over the last few decades, there’s been a move in the field to treat MS earlier and more aggressively with newer, more potent therapies,” said UCSF neurologist Michael Wilson, MD, a senior author of the paper. “A diagnostic result like this makes such early intervention more likely, giving patients hope for a better life.”
Linking infections with autoimmune disease
Autoimmune diseases like MS are believed to result, in part, from rare immune reactions to common infections.

In 2014, Wilson joined forces with Joe DeRisi, PhD, president of the Chan Zuckerberg Biohub SF and a senior author of the paper, to develop better tools for unmasking the culprits behind autoimmune disease. They took a technique in which viruses are engineered to display bits of proteins like flags on their surface, called phage display immunoprecipitation sequencing (PhIP-Seq), and further optimized it to screen human blood for autoantibodies.
PhIP-Seq detects autoantibodies against more than 10,000 human proteins, enough to investigate nearly any autoimmune disease. In 2019, they successfully used it to discover a rare autoimmune disease that seemed to arise from testicular cancer.
MS affects more than 900,000 people in the US. Its early symptoms, like dizziness, spasms, and fatigue, can resemble other conditions, and diagnosis requires careful analysis of brain MRI scans.
The phage display system, the scientists reasoned, could reveal the autoantibodies behind the immune attacks of MS and create new opportunities to understand and treat the disease.
The project was spearheaded by first co-authors Colin Zamecnik, PhD, a postdoctoral researcher in DeRisi’s and Wilson’s labs; and Gavin Sowa, MD, MS, former UCSF medical student and now internal medicine resident at Northwestern University.
They partnered with Mitch Wallin, MD, MPH, from the University of Maryland and a senior author of the paper, to search for autoantibodies in the blood of people with MS. These samples were obtained from the U.S. Department of Defense Serum Repository, which stores blood taken from armed service members when they apply to join the military.

The group analyzed blood from 250 MS patients collected after their diagnosis, plus samples taken five or more years earlier when they joined the military. The researchers also looked at comparable blood samples from 250 healthy veterans.
Between the large number of subjects and the before-and-after timing of the samples, it was “a phenomenal cohort of individuals to look at to see how this kind of autoimmunity develops over the course of clinical onset of this disease,” said Zamecnik.
A consistent signature of MS
Using a mere one-thousandth of a milliliter of blood from each time point, the scientists thought they would see a jump in autoantibodies as the first symptoms of MS appeared.
Instead, they found that 10% of the MS patients had a striking abundance of autoantibodies years before their diagnosis.
The dozen or so autoantibodies all stuck to a chemical pattern that resembled one found in common viruses, including Epstein-Barr Virus (EBV), which infects more than 85% of all people, yet has been flagged in previous studies as a contributing cause for MS.
Years before diagnosis, this subset of MS patients had other signs of an immune war in the brain. Ahmed Abdelhak, MD, co-author of the paper and a postdoctoral researcher in the UCSF laboratory of Ari Green, MD, found that patients with these autoantibodies had elevated levels of neurofilament light (Nfl), a protein that gets released as neurons break down.
Perhaps, the researchers speculated, the immune system was mistaking friendly human proteins for some viral foe, leading to a lifetime of MS.
“When we analyze healthy people using our technology, everybody looks unique, with their own fingerprint of immunological experience, like a snowflake,” DeRisi said. “It’s when the immunological signature of a person looks like someone else, and they stop looking like snowflakes that we begin to suspect something is wrong, and that’s what we found in these MS patients.”
A test to speed patients toward the right therapies
To confirm their findings, the team analyzed blood samples from patients in the UCSF ORIGINS study. These patients all had neurological symptoms and many, but not all, went on to be diagnosed with MS.
Once again, 10% of the patients in the ORIGINS study who were diagnosed with MS had the same autoantibody pattern. The pattern was 100% predictive of an MS diagnosis. Across both the Department of Defense group and the ORIGINS group, every patient with this autoantibody pattern had MS.
“Diagnosis is not always straightforward for MS, because we haven’t had disease specific biomarkers,” Wilson said. “We’re excited to have anything that can give more diagnostic certainty earlier on, to have a concrete discussion about whether to start treatment for each patient.”
Many questions remain about MS, ranging from what’s instigating the immune response in some MS patients to how the disease develops in the other 90% of patients. But the researchers believe they now have a definitive sign that MS is brewing.
“Imagine if we could diagnose MS before some patients reach the clinic,” said Stephen Hauser, MD, director of the UCSF Weill Institute for Neurosciences and a senior author of the paper. “It enhances our chances of moving from suppression to cure.”

In a new study published today in Nature Biomedical Engineering, researchers at The University of Texas MD Anderson Cancer Center have designed a new method for developing immunotherapy drugs using engineered peptides to elicit a natural immune response inside the body.
In preclinical models of locally advanced and metastatic breast cancer, this method improved tumor control and prolonged survival, both as a monotherapy and in combination with immune checkpoint inhibitors.
“Amino acids are the building blocks of life and, when a few of them are linked together, they create a peptide. All the biological functions performed by our body are done by proteins and peptides, so our goal was to find a way to redesign these small molecules to possess the unique ability to activate our immune system,” said senior author Betty Kim, M.D., Ph.D., professor of Neurosurgery.
The body’s immune system is built to patrol and identify infected or diseased cells to eliminate, but cancer cells often exploit weaknesses in the immune system to avoid detection. The goal of immunotherapy is to bolster the body’s natural ability to identify and destroy cancer cells. Current immune checkpoint inhibitors are antibodies designed to block specific immune signaling pathways.
The engineered peptide improves the immune system’s ability to detect and destroy cancer cells in a unique way. Rather than using an external compound to initiate a response, or harvesting and modifying immune cells for cell therapies, the peptide serves as a messenger to activate specific signaling pathways in immune cells to boost their performance.
“These findings open a whole new avenue for developing immunotherapy drugs. By using designed polypeptides, we can potently activate immune signaling pathways to enhance anti-tumor responses. Additionally, since these are naturally derived agents, we anticipate the toxicity profile would be significantly better than with synthetic compounds,” said co-corresponding author Wen Jiang, M.D., Ph.D., associate professor of Radiation Oncology.
This study was supported by the National Cancer Institute (CA241070) and the U.S. Department of Defense.

Although there are still some aspects pending confirmation for its use in the clinical setting, and its resolution needs to be improved slightly, a study by the UPV/EHU and Biobizkaia has shown that a method routinely used to carry out ophthalmological tests can also be used to monitor the neurodegeneration that occurs in Parkinson’s patients. In the course of the research it was found that the neurodegeneration of the retina probably precedes cognitive impairment.
When Parkinson’s or another neurodegenerative disease is diagnosed, patients always ask: “And now what? What will happen? What can be expected from the disease?” For neurologists, however, it is not possible to answer these questions precisely, as “the evolution of patients tends to be very varied: some experience no change over the years, while others end up with dementia or in a wheelchair,” explained Ane Murueta-Goyena, researcher in the UPV/EHU’s department of Neurosciences.
Today, identifying Parkinson’s patients at risk of cognitive impairment poses a major challenge, yet this is necessary when it comes to providing more effective clinical treatments and stepping up clinical trials. In fact, Dr Ane Murueta-Goyena, in collaboration with Biobizkaia’s research staff, wanted to see “whether the visual system can enable this deterioration to be predicted, in other words, what future the patient can expect within a few years.” The thickness of the retina was used for this purpose.
The retina is a membrane located at the back of the eyeball, it is related to the nervous system and comprises several layers. During the study, a cohort of Parkinson’s patients had the thickness of the innermost layer of their retinas measured using optical coherence tomography. This type of tomography is a routinely used instrument in ophthalmological tests, as it allows high-resolution, repeatable and accurate measurements to be made. So the evolution of this retinal layer was analysed and compared in people with and without Parkinson’s disease over the 2015-2021 period. The results of the analysis of the images of the retinal layers of Parkinson’s patients were also confirmed in a UK hospital.
The results showed that the retinal layer is noticeably thinner in Parkinson’s patients. It was also observed that “during the initial phases of the disease it is in the retina where the greatest neurodegeneration is detected, and, from a given moment onwards, when the layer is already very thin, a kind of stabilising of the neurodegeneration process takes place. Retinal thinning and cognitive impairment do not occur simultaneously. The initial changes in the retina are more evident and then, over the years, patients are observed to worsen clinically in both cognitive and motor terms,” explained Murueta-Goya. In other words, the slower retinal layer thickness loss is associated with faster cognitive decline; this slowness is linked to greater severity of the disease.”
The researcher has attached great importance to the results: “We have obtained information on the progression of the disease, and the tool we are proposing is non-invasive and available at all hospitals.” The results need to be validated internationally and “by slightly improving the resolution of the technology, we will be closer to validating the method for monitoring the neurodegeneration that takes place in Parkinson’s disease.” The researcher also revealed that they are continuing the research on another cohort of patients and that funding is the key.

The NewsFor parents struggling with mental health or substance use disorders, access to treatment can often mean the difference between keeping and losing their children. But a new analysis of health and child welfare records found that a significant portion of those who were eligible for Medicaid coverage for such treatment were not getting it.The analysis, published Friday by researchers at the nonprofit institute RTI International and the Department of Health and Human Services, found that fewer than half of parents on Medicaid who had substance use disorders and had been referred to authorities over suspicions of child abuse or neglect had received treatment.A temporary shelter in Brooklyn.Hiroko Masuike/The New York Times Some Context: Experts say bad situations can often be reversed with treatment.Both mental health and drug addiction crises have been roiling the country, and the effects of parental drug use and mental illness can quickly trickle down to their children. Public health experts say substance use disorders can incapacitate a previously diligent parent and lead to the involvement of child protective services.In 2021 alone, more than seven million children were referred to authorities over worries of maltreatment, according to a federal report, and more than 200,000 were removed from their homes. But research shows that when parents seek treatment for psychiatric and substance use disorders, they are far less likely to experience family separation.The Numbers: What the researchers found.To calculate treatment rates among parents on Medicaid, the health insurance program for low income people, Tami Mark, a health economist at RTI, who led the research, and her colleagues drew from a new publicly available data set that used de-identified social security numbers to link child welfare records in Florida and Kentucky with corresponding Medicaid claims records from 2020.For comparison, they also analyzed a random sample of Medicaid recipients who had no records in the child welfare system. (The study didn’t capture any counseling or medication given outside the Medicaid system, nor any cases of mental health or substance use disorders that were undiagnosed.)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.