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Human brain diseases, such as Parkinson’s disease, involve damage in more than one region of the brain, requiring technology that could precisely and flexibly address all affected regions simultaneously. Researchers at Washington University in St. Louis have developed a noninvasive technology combining a holographic acoustic device with genetic engineering that allows them to precisely target affected neurons in the brain, creating the potential to precisely modulate selected cell types in multiple diseased brain regions.
Hong Chen, associate professor of biomedical engineering in the McKelvey School of Engineering and of neurosurgery in the School of Medicine, and her team created AhSonogenetics, or Airy-beam holographic sonogenetics, a technique that uses a noninvasive wearable ultrasound device to alter genetically selected neurons in the brains of mice. Results of the proof-of-concept study were published in Proceedings of the National Academy of Sciences June 17.
AhSonogenetics brings together several of Chen’s group’s recent advances into one technology. In 2021, she and her team launched Sonogenetics, a method that uses focused ultrasound to deliver a viral construct containing ultrasound-sensitive ion channels to genetically selected neurons in the brain. They use low-intensity focused ultrasound to deliver a small burst of warmth, which opens the ion channels and activates the neurons. Chen’s team was the first to show that sonogenetics could modulate the behavior of freely moving mice.
In 2022, she and members of her lab designed and 3D-printed a flexible and versatile tool known as an Airy beam-enabled binary acoustic metasurface that allowed them to manipulate ultrasound beams. She also is developing Sonogenetics 2.0, which combines the advantage of ultrasound and genetic engineering to modulate defined neurons noninvasively and precisely in the brains of humans and animals. AhSonogenetics brings them together as a potential method to intervene in neurodegenerative diseases.
“By enabling precise and flexible cell-type-specific neuromodulation without invasive procedures, AhSonogenetics provides a powerful tool for investigating intact neural circuits and offers promising interventions for neurological disorders,” Chen said.
Sonogenetics gives researchers a way to precisely control the brains, while airy-beam technology allows researchers to bend or steer the sound waves to generate arbitrary beam patterns inside the brain with a high spatial resolution. Yaoheng (Mack) Yang, a postdoctoral research associate who earned a doctorate in biomedical engineering from McKelvey Engineering in 2022, said the technology gives the researchers three unique advantages.
“Airy beam is the technology that can give us precise targeting of a smaller region than conventional technology, the flexibility to steer to the targeted brain regions, and to target multiple brain regions simultaneously,” Yang said.

Chen and her team, including first authors Zhongtao Hu, a former postdoctoral research associate, and Yang, designed each Airy-beam metasurface individually as the foundation for wearable ultrasound devices that were tailored for different applications and for precise locations in the brain.
Chen’s team tested the technique on a mouse model of Parkinson’s disease. With AhSonogenetics, they were able to stimulate two brain regions simultaneously in a single mouse, eliminating the need for multiple implants or interventions. This stimulation alleviated Parkinson’s-related motor deficits in the mouse model, including slow movements, difficulty walking and freezing behaviors.
The team’s Airy-beam device overcomes some of the limits of sonogenetics, including tailoring the design of the device to target specific brain locations, as well as incorporating the flexibility to adjust target locations in a single brain.
Hu said the device, which costs roughly $50 to make, can be tailored in size to fit various brain sizes, expanding its potential applications.
“This technology can be used as a research platform to speed neuroscience research because of the capability to flexibly target different brain regions,” Hu said. “The affordability and ease of fabrication lower the barriers to the widespread adoption of our proposed devices by the research community for neuromodulation applications.”

The ketogenic diet has its fanatics and detractors among dieters, but either way, the diet has a scientifically documented impact on memory in mice. Whlie uncovering how the high fat, low carbohydrate diet boosts memory in older mice, Buck scientists and a team from the University of Chile identified a new molecular signaling pathway that improves synapse function and helps explain the diet’s benefit on brain health and aging. Published in the June 5, 2024 issue of Cell Reports Medicine, the findings provide new directions for targeting the memory effects on a molecular level, without requiring a ketogenic diet or even the byproducts of it.
“Our work indicates that the effects of the ketogenic diet benefit brain function broadly, and we provide a mechanism of action that offers a strategy for the maintenance and improvement of this function during aging,” said the study’s senior author, Christian González-Billault, PhD, who is a professor at the Universidad de Chile and director of their Geroscience Center for Brain Health and Metabolism, and adjunct professor at the Buck Institute.
“Building off our previous work showing that a ketogenic diet improves healthspan and memory in aging mice, this new work indicates that we can start with older animals and still improve the health of the aging brain, and that the changes begin to happen relatively quickly,” said John Newman, MD, PhD, whose laboratory at Buck collaborated with Dr. González-Billault on the study. Newman is both an assistant professor at the Buck Institute, and a geriatrician at University of California, San Francisco. “It is the most detailed study to date of the ketogenic diet and aging brain in mice.”
More than a century ago, researchers observed that rats that consumed less food lived longer. “We now know that being able to manipulate lifespan is not about specifically eating less,” said Newman, but actually is related to signals inside cells that turn on and off specific pathways in response to available nutrients. Many of those pathways are related to aging, such as controlling protein turnover and metabolism.
Some of those signals are the ketone bodies, which consist of acetoacetate (AcAc), β-hydroxybutyrate (BHB) and to a much lesser extent, acetone. These molecules are routinely produced in the liver. They ramp up when glucose is in short supply, whether due to caloric restriction, intense exercise or low carbohydrate intake, such as with a ketogenic diet.
Seven years ago, Newman led a team that published the first proof of the concept that if a ketogenic diet exposes mice to increased levels of ketone bodies over much of their adult life, it helps them to live longer and age in a more healthy way. “The most striking effect on their health as they aged was that their memory was preserved; it was possibly even better than when they were younger,” he said.
The current study, designed to answer what part of the ketogenic diet was having the effect and how it was affecting the brain on a molecular level to improve memory, was led by González-Billault in a collaboration with scientists at the Buck. Mice on a ketogenic diet are fed a ratio of 90 percent calories from fat and 10 percent from protein, while mice on a control diet received the same amount of protein but only 13 percent fat. The test mice, of “advanced age” of more than two years old, received one week of the ketogenic diet, cycled with one week of the control diet, to keep the mice from overeating and becoming obese.

The benefits of the ketogenic diet, said, González-Billault, were demonstrated through neurophysiological and behavioral experiments with the mice that test how well the mechanisms involved in memory generation, storage, and retrieval function in aged animals. When these showed that the ketogenic diet appeared to benefit how well the synapses responsible for memory worked, they took a deep dive into the protein composition at these synapses in the hippocampus, in a collaboration with Buck professor Birgit Schilling, PhD, who directs the Proteomics and Mass Spectrometry Center.
“Surprisingly, we saw that the ketogenic diet caused dramatic changes in the proteins of the synapse,” said Schilling. Even more surprising, she said, was that the changes started after a relatively brief exposure to the diet (tested after only one week on the diet) and only became more pronounced over time (tested again after six weeks and a year).
Further testing indicated that in synapses, a particular signaling pathway (protein kinase A, which is critical to synapse activity) was activated by the ketogenic diet. In isolated cells, the team then showed that it appears that BHB, the main ketone body produced in a ketogenic diet, is activating this pathway. This leads to the idea, said González-Billault, that ketone bodies (specifically BHB) play a crucial role not only as an energy source, but also as a signaling molecule.
“BHB is almost certainly not the only molecule in play, but we think this is an important part of understanding how the ketogenic diet and ketone bodies work,” said Newman “This is the first study to really connect deep molecular mechanisms of ketone bodies all the way through to improving the aging brain.”
Looking forward, he said, the next step would be to see if the same memory protection could be achieved by using BHB alone, or possibly going even more targeted than that by manipulating the protein kinase A signaling pathway directly. “If we could recreate some of the big-picture effects on synapse function and memory just by manipulating that signaling pathway in the right cells,” he said, “we wouldn’t even need to eat a ketogenic diet in the end.”

A new study by investigators from Mass General Brigham suggests that whether a person inherits risk of Alzheimer’s disease from their mother or father influences risk of biological changes in the brain that lead to disease. By evaluating 4,400 cognitively unimpaired adults ages 65-85, the team found those with a history of Alzheimer’s disease (AD) on either their mother’s side or both parents’ sides had increased amyloid in their brains. Their results are published in JAMA Neurology.
“Our study found if participants had a family history on their mother’s side, a higher amyloid level was observed,” said senior corresponding author Hyun-Sik Yang, MD, a neurologist at Mass General Brigham and behavioral neurologist in the Division of Cognitive and Behavioral Neurology at Brigham and Women’s Hospital. He is also a physician investigator of Neurology for the Mass General Research Institute.
Yang collaborated with other researchers from Mass General Brigham, as well as investigators from Vanderbilt and Stanford University. He said previous smaller studies have investigated the role family history plays in Alzheimer’s disease. Some of those studies suggested maternal history represented a higher risk of developing Alzheimer’s, but the group wanted to revisit the question with cognitively normal participants and access to a larger clinical trial data set.
The team examined the family history of older adults from the Anti-Amyloid Treatment in Asymptomatic Alzheimer’s (A4) study, a randomized clinical trial aimed at AD prevention. Participants were asked about memory loss symptom onset of their parents. Researchers also asked if their parents were ever formally diagnosed or if there was autopsy confirmation of Alzheimer’s disease.
“Some people decide not to pursue a formal diagnosis and attribute memory loss to age, so we focused on a memory loss and dementia phenotype,” Yang said.
Researchers then compared those answers and measured amyloid in participants. They found maternal history of memory impairment at all ages and paternal history of early-onset memory impairment was associated with higher amyloid levels in the asymptomatic study participants. Researchers observed that having only a paternal history of late-onset memory impairment was not associated with higher amyloid levels.
“If your father had early onset symptoms, that is associated with elevated levels in the offspring,” said Mabel Seto, PhD, first author and a postdoctoral research fellow in the Department of Neurology at the Brigham. “However, it doesn’t matter when your mother started developing symptoms — if she did at all, it’s associated with elevated amyloid.”
Seto works on other projects related to sex differences in neurology. She said the results of the study are fascinating because Alzheimer’s tends to be more prevalent in women. “It’s really interesting from a genetic perspective to see one sex contributing something the other sex isn’t,” Seto said. She also noted the findings were not affected by whether study participants were biologically male or female.

Yang noted one limitation of the study is some participants’ parents died young, before they could potentially develop symptoms of cognitive impairment. He said social factors like access to resources and education may have also played a role in when someone acknowledged cognitive impairment and if they were ever formally diagnosed.
“It’s also important to note a majority of these participants are non-Hispanic white,” Seto added. “We might not see the same effect in other races and ethnicities.”
Seto said the next steps are to expand the study to look at other groups and examine how parental history affects cognitive decline and amyloid accumulation over time and why DNA from the mother plays a role.
Reisa Sperling, MD, a co-author on the paper, principal investigator of the A4 Study and a neurologist at Mass General Brigham, said the findings could be used soon in clinical translation.
“This work indicates that maternal inheritance of Alzheimer’s disease may be an important factor in identifying asymptomatic individuals for ongoing and future prevention trials,” Sperling said.

Many bedtime battles stem from children’s after dark worries, suggests a new national poll.
And while most families have bedtime rituals to help their little ones ease into nighttime, many rely on strategies that may increase sleep challenges long term, according to the University of Michigan Health C.S. Mott Children’s Hospital National Poll on Children’s Health.
Overall, one in four parents describe getting their young child to bed as difficult — and these parents are less likely to have a bedtime routine, more likely to leave on a video or TV show, and more likely to stay with their child until they’re asleep.
“Our report reinforces the common struggle of getting young children to sleep. When this transition to bedtime becomes a nightly conflict, some parents may fall into habits that work in the moment but could set them up for more sleep issues down the road,” said Mott Poll co-director Sarah Clark, M.P.H.
“Establishing a consistent bedtime routine is crucial. When children don’t get enough rest, it can impact their physical development, emotional regulation and behavior.”
Nearly one in five parents say they have given their kids melatonin to help with sleep while a third stay in the room until their child completely dozes off, according to the nationally representative poll that includes responses from 781 parents of children ages one to six surveyed in February.
Nighttime worries interfere with sleep
Parents share common reasons behind bedtime struggles, with nearly a quarter saying their child’s sleep is often or occasionally delayed due to being worried or anxious.

A particular challenge, parents say, is when children don’t stay asleep. More than a third of parents say their child wakes up upset or crying, with more than 40% saying their child moves to their parents’ bed and about 30% saying children insist that the parent sleep in their room.
“Many young children go through stages when they become scared of the dark or worry that something bad might happen, causing them to delay bedtime or become distressed by parents leaving the room. Bad dreams or being awakened in the middle of the night can also disrupt sleep,” Clark said.
“Although this is a normal part of a child’s development, it can be frustrating when parents already feel tired themselves at the end of the day. Parents should find a balance between offering reassurance and comfort while maintaining some boundaries that help ensure everyone — both kids and adults — get adequate sleep.”
More findings from the report, plus Clark’s recommendations for helping young children fall and stay asleep:
Stick to a regular bedtime routine
Most parents polled report having a bedtime routine for their child, often including brushing teeth, reading bedtime stories and/or bathing. Less than half also say their child has a drink of water or snack, turns off devices, prays and talks about their day.

Other bedtime habits include holding a blanket or stuff animal or sucking a pacifier or fingers.
Not only does having a consistent bedtime routine help make the nighttime transition smoother, Clark says, it also provides one-on-one time, allowing the child to get their parent’s full attention.
“A predictable bedtime routine provides a sense of security and comfort and signals to the child that it’s time to slow down,” she said.
“Knowing what to expect next can reduce anxiety and help children feel safe and relaxed. Having this dedicated time with parents also promotes bonding and emotional connection, creating positive associations with bedtime.”
Nearly two-thirds of parents also said children staying up to play was a major factor in delaying sleep. Clark says, highlighting the need to wind down at least an hour before bed.
Promote an environment conducive to sleep
A little less than half of parents polled say their child sleeps in their own bedroom while less than a quarter share a bedroom with siblings or in the parents’ bedroom. One in 10 kids spend part the night in their own bedroom and part of the night with parents.
More than two-fifths of parents polled said noise from other rooms interfered with their child’s sleep.
“The sleep environment can have a major effect on a child’s sleep quality, including getting to sleep and staying asleep through the night,” Clark said.
“When possible, children should have their own bed in a room that is quiet, without a lot of noise from other family members.”
Many parents polled also use a nightlight or crack the bedroom door so the child isn’t in complete darkness, Clark says, but parents should make sure the light does not shine directly at the child’s face.
Some parents also play calming music or stories to help their child go to sleep, while others use a white noise machine or app. However, Clark cautions to keep white noise machines at no more than 50 decibels and placed at least seven feet from the child’s bed to prevent unintended damage to the child’s hearing.
Talk to a doctor before using aids like melatonin
Many types of melatonin products are advertised as being appropriate for children but these products have not undergone rigorous testing for safety and effectiveness, and their side effects and long term impact on a child’s growth and development are unknown, Clark says.
“Although melatonin is a natural hormone that regulates sleep-wake cycles and may be fine to use occasionally, parents shouldn’t rely on it as a primary sleep aid,” Clark said.
“Parents who are considering giving melatonin to their young child should consult with their pediatrician to discuss options and rule out other causes of sleep problems first.”
If using melatonin, parents should also start with the lowest dose possible.
In addition, it’s important to keep electronics such as tablets or televisions out of children’s bedroom, as the blue light emitted by many of these screens interferes with the natural production of melatonin.
Offer comfort but enforce boundaries
Parents can help ease little ones’ anxiety by allowing extra time to let them talk about their day, which might draw out specific worries and give parents a chance to provide compassion and reassurance, Clark said.
Rather than remaining in the room, parents can also offer to check on the child every few minutes, which acknowledges the child’s fears and offers a reassuring presence, but still maintains a calm sleep environment and promotes sleep independence.
“Families can incorporate comforting rituals to help transform nighttime fears into a calming experience,” Clark said.
Have a consistent approach when children wake up in the night
Some children are prone to vivid dreams or nightmares and may have difficulty getting back to sleep. Parents should decide on their approach to this situation and stick with it, Clark says, whether it’s taking the child back to bed or allowing them to stay in the parents’ room.
“Being consistent in carrying out that approach will help the child adjust and be more likely to return to sleep,” Clark said.
Ease into changes in sleep patterns, such as dropping naps
For young children, a major sleep-related transition is discontinuing daytime naps. In general, children ages one to two should get 11-14 hours of sleep with naps while the amount of recommended sleep decreases slightly from ages three to six.
If children are taking longer to fall asleep at nap time, resisting naps or suddenly having difficulty falling asleep at night or waking up earlier than usual in the morning, it may be time to drop the nap, Clark says.
“Parents may need to adjust sleep routines gradually to transition to changes to a child’s sleep patterns,” Clark said.
Other changes that can affect a child’s sleep include transitioning from a crib to a toddler bed, starting school, having a change in their daytime routine, or being outdoors for longer than usual.

A study led by Nagoya University Graduate School of Medicine in Japan has revealed a link between gut microbiota and Parkinson’s disease (PD). The researchers found a reduction in the gut bacteria of genes responsible for synthesizing the essential B vitamins B2 and B7. They also identified a relationship between the lack of these genes and low levels of agents that help maintain the integrity of the intestinal barrier. This barrier prevents toxins from entering the bloodstream, which causes the inflammation seen in PD. Their findings, published in npj Parkinson’s Disease, suggest that treatment with B vitamins to address these deficiencies can be used to treat PD.
PD is characterized by a variety of physical symptoms that hinder daily activities and mobility, such as shaking, slow movement, stiffness, and balance problems. While the frequency of PD may vary between different populations, it is estimated to affect approximately 1-2% of individuals aged 55 years or older.
Various physiological processes are heavily influenced by the microorganisms found in the gut, which are collectively known as gut microbiota. In ideal conditions, gut microbiota produce SCFAs and polyamines, which maintain the intestinal barrier that prevents toxins entering the bloodstream. Toxins in the blood can be carried to the brain where they cause inflammation and affect neurotransmission processes that are critical for maintaining mental health.
To better understand the relationship between the microbial characteristics of the gut in PD, Hiroshi Nishiwaki and Jun Ueyama from the Nagoya University Graduate School of Medicine conducted a metanalysis of stool samples from patients with PD from Japan, the United States, Germany, China, and Taiwan. They used shotgun sequencing, a technique that sequences all genetic material in a sample. This is an invaluable tool because it offers researchers a better understanding of the microbial community and genetic makeup of the sample.
They observed a decrease in the bacterial genes responsible for the synthesizing of riboflavin (vitamin B2) and biotin (vitamin B7) in patients diagnosed with PD. Riboflavin and biotin, derived from both food and gut microbiota, have anti-inflammatory properties, which may counteract the neuroinflammation seen in diseases like PD.
B vitamins play crucial roles in the metabolic processes that influence the production and functions of short-chain fatty acids (SCFAs) and polyamines, two agents that help maintain the integrity of the intestinal barrier, preventing toxins entering the bloodstream. An examination of fecal metabolites revealed decreases of both in patients with PD.
The findings indicate a potential explanation for the progression of PD. “Deficiencies in polyamines and SCFAs could lead to thinning of the intestinal mucus layer, increasing intestinal permeability, both of which have been observed in PD,” Nishiwaki explained. “This higher permeability exposes nerves to toxins, contributing to abnormal aggregation of alpha-synuclein, activating the immune cells in the brain, and leading to long-term inflammation.”
He added, “Supplementation therapy targeting riboflavin and biotin holds promise as a potential therapeutic avenue for alleviating PD symptoms and slowing disease progression.”
The results of the study highlight the importance of understanding the complex relationship among gut microbiota, metabolic pathways, and neurodegeneration. In the coming years, therapy could potentially be customized based on the unique microbiome profile of each patient. By altering bacterial levels in the microbiome, doctors can potentially delay the onset of symptoms associated with diseases like PD.
“We could perform gut microbiota analysis on patients or conduct fecal metabolite analysis,” Nishiwaki said. “Using these findings, we could identify individuals with specific deficiencies and administer oral riboflavin and biotin supplements to those with decreased levels, potentially creating an effective treatment.”

Aphasia is a condition that affects a quarter of stroke survivors. It impairs communication abilities, including speaking, listening, reading, and writing. Aphasia can have a profound impact on social relationships, employment, and overall quality of life.
In current UK practice, 90% of speech and language therapists acknowledge the importance of discourse assessment and treatment. However, they face considerable barriers such as limited resources, time, and expertise. Addressing this critical need, the Language Underpins Narrative in Aphasia (LUNA) intervention used in the study offers a multi-level approach targeting words, sentences, and discourse macrostructure through personalised narratives. This aligns more closely with real-life communication needs.
The study, which was led by Professors Madeline Cruice and Lucy Dipper from the Centre for Language and Communication Sciences Research at City and funded by the Stroke Association, involved 28 participants with chronic aphasia, split equally into immediate treatment and delayed treatment (control) groups. Treatment was structured into 20 sessions over 10 weeks, each lasting an hour. Sessions were conducted via Zoom, making the therapy accessible during the COVID-19 pandemic. The LUNA treatment focused on personal narrative monologues, helping participants reconstruct their chosen narratives through structured language exercises targeting words, phrases, sentences, and discourse macrostructures.
It was seen that LUNA improved the narrative abilities of participants who received the treatment compared to the control group. Improvements were also seen in terms of language functioning and mood. These results underscore the potential of LUNA to effectively enhance communication skills among aphasia patients. The study has been published in the journal PLoS One.
Professor Dipper, Professor of Clinical Linguistics, said: “Traditional therapeutic approaches often focus on word and sentence-level treatments, but LUNA represents a shift in aphasia treatment to align more closely with real-life communication needs.”
Professor Cruice, Professor of Aphasia Rehabilitation and Recovery, said: “Our findings demonstrate the potential of narrative-based interventions to make a real difference in the lives of people with aphasia. We hope this study encourages further research and adoption of discourse-focused therapies, ultimately leading to more holistic and effective rehabilitation practices.”

The number of individuals in the U.S. who had chronic hypertension or chronic high blood pressure during pregnancy doubled between 2008 and 2021, while the prescribing and filling of antihypertensive medication during pregnancy remained low but stable at 60%, according to new research published today in Hypertension, a peer-reviewed journal of the American Heart Association.
Chronic hypertension in pregnancy is defined as high blood pressure diagnosed before pregnancy or before 20 weeks of pregnancy. Recent research has suggested that medication treatment of mild or moderate high blood pressure during pregnancy reduces the risk of severe hypertension and preeclampsia. Preeclampsia typically begins after 20 weeks of pregnancy, can cause liver or kidney damage, and may double a woman’s chances for future heart failure and other cardiovascular complications.
In 2017, clinical guideline from the American Heart Association and the American College of Cardiology revised the thresholds to diagnose high blood pressure from 140/90 mm Hg to 130/80 mm Hg for stage 1, and from 160/110 mm Hg to 140/90 mm Hg for stage 2 hypertension. The guideline recommends medication treatment for non-pregnant adults with stage 2 high blood pressure; for stage 1 high blood pressure in individuals with Type 1 or Type 2 diabetes, or kidney disease; and for stage 1 high blood pressure in individuals with established cardiovascular disease or without cardiovascular disease but with an estimated 10% or higher risk of developing atherosclerotic cardiovascular disease.
“We had hoped to see some impact from the 2017 guideline, which reduced the blood pressure threshold for treatment of hypertension. We were surprised to not find any meaningful changes from before and after the guideline,” said lead study author Stephanie Leonard, Ph.D., an epidemiologist and assistant professor in maternal-fetal medicine and obstetrics at Stanford University’s School of Medicine in Stanford, California. “While the rate of hypertension in pregnancy has doubled, the use of medication for treatment remained stable at only 60%, which we believe is likely below what it should be if patients are treated according to clinical guidelines.”
The researchers analyzed a database of private health insurance claims for 2007 to 2021 and found: The rate of high blood pressure diagnosis steadily increased from 1.8% to 3.7% among 1.9 million pregnancies between 2008 and 2021. Over the 14-year study period, this amounted to a doubling in the rate of high blood pressure in pregnancy. The frequency of high blood pressure during pregnancy continued to rise steadily, without a spike in new diagnoses after the 2017 ACC/AHA hypertension guideline, which lowered the threshold for stage 1 hypertension to blood pressure readings ≥130/80 mm Hg. A higher proportion of the individuals with high blood pressure were ages 35 or older, lived in the South (Alabama, Arkansas, Delaware, Florida, Georgia, Kentucky, Louisiana, Maryland, Mississippi, North Carolina, Oklahoma, South Carolina, Virginia, West Virginia, Tennessee, Oklahoma, Texas or the District of Columbia, according to the Census Bureau) and had other chronic health conditions, such as obesity, Type 1 or Type 2 diabetes, or kidney disease. The use of medication for high blood pressure treatment during pregnancy remained low and relatively stable, ranging from 57% to 60% over the 14-year study period. The number of pregnant individuals with high blood pressure treated with the medications methyldopa or hydrochlorothiazide, decreased from 29% to 2% and from 11% to 5%, respectively, over the study period. The proportion of patients treated with antihypertensive medications labetalol or nifedipine increased from 19% to 42% and from 9% to 17%, respectively. These are the currently recommended, first-line medications for chronic hypertension in pregnancy, Leonard said.”This study highlights the growing burden of chronic hypertension and poor cardiovascular health pre-pregnancy as critical targets to improve maternal health. These data are consistent with prior studies highlighting the increasing prevalence of hypertension from data from the National Vital Statistics System, which covers all births in the U.S.,” said Sadiya S. Khan, M.D., M.Sc., FAHA, chair of the writing group for the Association’s 2023 scientific statement, “Optimizing Prepregnancy Cardiovascular Health to Improve Outcomes in Pregnant and Postpartum Individuals and Offspring. Khan is the Magerstadt Professor of Cardiovascular Epidemiology and an associate professor of medicine and preventive medicine at the Northwestern University Feinberg School of Medicine and a preventive cardiologist at Northwestern Medicine, both in Chicago.
“Since nearly 1 in 3 individuals with chronic hypertension may face a pregnancy complication, the prevention and control of hypertension should be among the highest priorities for improving maternal health,” Khan added.

Study design, background and details: The database used in the study includes private, or commercial, health insurance claims, as well as enrollment data from large employers and health plans across the U.S. that provide private health care coverage for employees, their spouses and dependents. The database has information for claims involving several million individuals annually in the United States. Researchers identified oral antihypertensive medications dispensed by outpatient pharmacies using a previously established list of medications. Patient characteristics, including age, region of residence in the U.S. and birth year were noted. The study examined treatment rates and type of medication use among people with conditions including obesity, kidney disease, Type 1 or Type 2 diabetes, lupus, thyroid disorder, and pregnancies involving more than one fetus (twins, triplets, etc.).The study had several limitations. First, the database only noted prescriptions that were filled, not if the prescription was taken as directed. The database also did not include blood pressure measurements, so chronic hypertension status was assessed by diagnosis codes; this meant the researchers could not analyze the severity of high blood pressure or assess blood pressure changes. In addition, the findings may not be generalizable to people who have Medicaid for health insurance, people without insurance or people who live in other countries with health care systems different from the U.S.
Co-authors, disclosures and funding sources are listed in the manuscript.
Studies published in the American Heart Association’s scientific journals are peer-reviewed. The statements and conclusions in each manuscript are solely those of the study authors and do not necessarily reflect the Association’s policy or position. The Association makes no representation or guarantee as to their accuracy or reliability. The Association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific Association programs and events. The Association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and biotech companies, device manufacturers and health insurance providers and the Association’s overall financial information are available here.

A pioneering study published today in the journal Nature Aging has unveiled significant heterogeneity in the risk factors affecting healthy aging in Latin America and emphasised the limitations of current models of brain health, which are primarily based on data from high-income countries. The research was conducted by researchers from Trinity College Dublin (Ireland), and by colleagues in Universidad Adolfo Ibanez (Chile) and Pontificia Universidad Javeriana (Colombia) among others.
The study developed a metanalytical approach with 146,000 participants and findings emphasise how current models of brain health may not apply to the diverse populations of Latin America.
Towards tailored and personalised models of healthy aging and brain health
Latin America faces unique challenges in promoting healthy brain aging, including genetic admixture (shaping genetic variation and disease risk), adverse childhood experiences, socioeconomic inequities, and health disparities. Both physical and social exposomes significantly influence brain health, differing from the patterns observed in high-income countries.
The study involved a comprehensive meta-analysis of multiple studies, ultimately including over 146,000 participants. Results highlighted significant but heterogeneous effects on cognition and functional ability, with varied impacts from demographics, mental health, health status, and social determinants.
This study revealed substantial variability in how risk factors impact cognition and functional ability across Latin American populations. This variability underscores the inadequacy of one-size-fits-all models developed from high-income countries. High heterogeneity, outliers, variations between countries, and lack of robust computational approaches have affected the reliability of existing data.
Toward a better science of healthy aging and brain health
Agustin Ibanez, first author of the study, Atlantic Fellow at the Global Brain Health Institute, Trinity College Dublin and Director of BrainLat UAI,.said:

“The study confirmed an emerging idea that global models of brain health, predominantly based on data from high-income countries, may not be universally applicable. Our work shows significant heterogeneity in risk factors affecting cognition and functional ability across Latin American populations, highlighting the inadequacy of current models based on data from high-income countries.”
There is an urgent need for comprehensive and harmonised data collection efforts to capture the diverse factors influencing healthy aging in Latin America.
Carlos Coronel, Atlantic Fellow at the Global Brain Health Institute, Trinity College Dublin, co-authorsaid:
“Developing predictive models tailored to the region’s unique demographic, genetic, and socioeconomic contexts is essential. Bridging this gap requires advanced computational approaches that integrate theories of brain function and its interaction with the exposome.”
The study recommends implementing robust methodological approaches, promoting data-driven and machine-learning techniques, and focusing on social determinants of health and other socioeconomic disparities. On those social factors,
Commenting on those social factors, Joaquin Migeot, co-author and postdoctoral researcher at BrainLat, said:
“The need to address the aggregated effect of various exposures throughout life entails a high dimensionality of variables. To manage this complexity and derive meaningful conclusions, the use of machine learning techniques is essential to facilitating a more comprehensive and accurate understanding of how multiple exposures impact brain health. These efforts will inform tailored policy and healthcare interventions, improving brain health and aging outcomes in Latin America.”

Sandra Baez, co-author and professor at Los Andes University (Colombia) and Atlantic Fellow at the Global Brain Health Institute, Trinity College Dublin, said:,
“This study is a significant step towards understanding the unique factors that impact aging and brain health in Latin America. Our findings advocate for a more nuanced and region-specific approach to developing brain health models tailored to diverse and underrepresented populations.”

Treatment outcomes for breast cancer have become better over the years, but proportion of breast cancers still recur even after long periods without signs of cancer remaining dormant in the body. Finnish cancer researchers discovered a mechanism that wakes up these dormant breast cancer cells and demonstrated that preventing the mechanism can significantly improve treatment outcomes in experimental models.
Although treatment outcomes for breast cancer have significantly improved through new research-based therapies, it remains the second most common fatal cancer in women. A particular challenge in breast cancer treatment is the recurrence of the disease. Even when treatment appears to be successful and the cancer is considered gone, it can return years later either locally or, in the worst case, by spreading to other parts of the body, such as the brain.
The reasons why dormant breast cancer cells awake even after several years are not well understood. However, identifying these reasons could provide an opportunity to develop new therapies to prevent cancer recurrence.
DUSP6 protein activity associated with awakening of the breast cancer cells
A newly-published Finnish study provides important new insights into how breast cancer cells belonging to the HER2-positive subtype are able to awaken during treatment.
The research group led by Jukka Westermarck, the Professor of Cancer Biology at the Turku Bioscience Centre and the InFLAMES research flagship of the University of Turku and Åbo Akademi University, approached this research question by treating breast cancer cells sensitive to treatment with HER2 inhibitor for nine months and by monitoring how these cancer cells were able to restart their growth during the treatment.
By sequencing the molecular changes in the cells, the group identified the DUSP6 protein, whose expression closely followed the development of therapy resistance. The leading researcher Majid Momeny was also able to show that when the activity of the DUSP6 protein was blocked during cancer treatment, breast cancer cells lost their ability to grow. Blocking the protein also made the previously treatment-resistant cancer cells more sensitive to HER2 inhibitors. Another important finding was that by inhibiting DUSP6, it was possible to slow the growth of breast cancer metastases in the brain in mouse models.
“Based on our findings, blocking the DUSP6 protein could therefore provide a basis for effective combination therapy also in HER2 breast cancer cases that have already lost response to treatment,” says Professor Westermarck.
The significance of the study is highlighted by the group’s access to experimental drug molecules that inhibit the DUSP6 protein. By administering the drug, the researchers demonstrated that the protein could be inhibited in mice without significant side effects. Importantly, the drug was shown to significantly enhance the therapeutic effect of several existing HER2 inhibitors.
“The molecules we used in this study are not yet suitable for patient treatment, but these newly-published basic research results provide important evidence that DUSP6 is a very promising target protein for future cancer drug development and worth investigating,” Westermarck continues.