Medicare Advantage plans say it reduces waste and inappropriate care. Critics say it often restricts coverage unnecessarily.Slowly but steadily, Marlene Nathanson was recovering. She had suffered a stroke in November 2022 at her home in Minneapolis and spent a week in a hospital; afterward, when she arrived at Episcopal Homes in St. Paul for rehabilitation, she couldn’t walk. Weakness in her right arm and hand left her unable to feed herself, and her speech remained somewhat garbled.But over three weeks of physical, occupational and speech therapy, “she was making good progress,” her husband, Iric Nathanson, said. “Her therapists were very encouraging.” Ms. Nathanson, then 85, had begun to get around using a walker. Her arm was growing stronger and her speech had nearly returned to normal.Then, on a Wednesday afternoon, one of her therapists told the Nathansons that their Medicare Advantage plan had refused a request to cover further treatment. “She has to leave our facility by Friday,” the therapist said, apologetically.Mr. Nathanson, then 82, felt anxious and angry. He didn’t see how he could arrange for home care aides and equipment in 48 hours. Besides, he said, “it didn’t seem right that the therapists and professionals couldn’t determine the course of her care” and had to yield to an insurance company’s dictates. “But apparently it happens a lot.”It does. Traditional Medicare rarely requires so-called prior authorization for services. But virtually all Medicare Advantage plans invoke it before agreeing to cover certain services, particularly those carrying high price tags, such as chemotherapy, hospital stays, nursing home care and home health.“Most people come across this at some point if they stay in a Medicare Advantage plan,” said Jeannie Fuglesten Biniek, associate director of the program on Medicare policy at KFF, the nonprofit health policy research organization. After years of steep growth, more than half of Medicare beneficiaries are now enrolled in Advantage plans, which are administered by private insurance companies.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.

Scientists have pinpointed genetic changes that can leave children born with little to no immune defence against infection.
In a new study of 11 affected individuals, researchers from Newcastle University, the Wellcome Sanger Institute, the Great North Children’s Hospital, and their collaborators were able to link mutations in the NUDCD3 gene to Severe Combined Immunodeficiency and Omenn syndrome1 – rare and life-threatening immunodeficiency disorders. These mutations prevented the normal development of diverse immune cells needed to combat different pathogens2.
The findings, published today (24 May) in Science Immunology, open opportunities for early diagnosis and intervention for this condition.
Severe Combined Immunodeficiency (SCID) and Omenn syndrome are both rare genetic disorders that leave children without a functional immune system and at risk of life-threatening infections. Without urgent treatment, such as stem cell transplants to replace the faulty immune system, many affected will not survive their first year.
While newborn screening methods can flag T cell deficiency, knowledge of the specific genetic cause increases confidence in the diagnosis of SCID and informs the choice of curative therapy. Currently this remains out of reach for at least 1 in 10 affected families.
In this new study, researchers from Newcastle University, the Wellcome Sanger Institute and their collaborators studied 11 children across four families, two of whom had SCID while the other nine had Omenn syndrome. All had inherited mutations that disrupted the function of the NUDCD3 protein, which had not previously been linked to the immune system.
Using detailed studies of patient-derived cells and mouse models, the team demonstrated that NUDCD3 mutations impair a crucial gene-rearranging process called V(D)J recombination, essential for generating the diverse T cell receptors and antibodies needed to recognise and fight different pathogens.

While mice engineered with the same NUDCD3 mutations had milder immune problems, the human patients faced severe, life-threatening consequences. Two patients did survive, however, after receiving a stem cell transplant — reinforcing the importance of early diagnosis and intervention.
Dr Gosia Trynka, author of the study at the Wellcome Sanger Institute and science director at Open Targets, said: “For babies born with high-risk immunodeficiencies, early detection can mean the difference between life and death. These diseases leave newborns essentially defenceless against pathogens that most of us can easily fend off. The identification of this new disease gene will help clinicians to make a prompt molecular diagnosis in affected patients, meaning they can receive life-saving treatments more quickly.”
Professor Sophie Hambleton, senior author of the study at Newcastle University and practicing paediatric immunologist at the Great North Children’s Hospital, said: “SCID and Omenn syndrome are devastating disorders, requiring complex and timely treatments. The more we can understand about its underlying causes, the better we can look after affected babies. Our research is aimed at filling in the gaps so that families can achieve a molecular diagnosis while we continue learning more about how the immune system works in health and disease. We are deeply grateful to the families whose invaluable participation in this study will help future generations.”
Notes
1. Children with severe combined immunodeficiency disorder completely lack the T cells needed to combat infections, while those with Omenn syndrome have abnormal T cells that not only fail to combat infections but also mount attacks on the body’s own tissues. They require urgent infection management and treatment.
2. Specifically, the mutant NUDCD3 could not regulate RAG1, a key enzyme needed in V(D)J recombination. This caused RAG1 to get trapped within cell nucleoli instead of facilitating the gene rearrangements that build immune diversity.

UC Santa Cruz researchers have discovered a peptide in human RNA that regulates inflammation and may provide a new path for treating diseases such as arthritis and lupus. The team used a screening process based on the powerful gene-editing tool CRISPR to shed light on one of the biggest mysteries about our RNA-the molecule responsible for carrying out genetic information contained in our DNA.
This peptide originates from within a long non-coding RNA (lncRNA) called LOUP. According to the researchers, the human genome encodes over 20,000 lncRNAs, making it the largest group of genes produced from the genome. But despite this abundance, scientists know little about why lncRNAs exist or what they do. This is why lncRNA is sometimes referred to as the “dark matter of the genome.”
The study, published May 23 in the Proceedings of the National Academy of Sciences (PNAS), is one of the very few in the existing literature to chip away at the mysteries of lncRNA. It also presents a new strategy for conducting high-throughput screening to rapidly identify functional lncRNAs in immune cells. The pooled-screen approach allows researchers to target thousands of genes in a single experiment, which is a much more efficient way to study uncharacterized portions of the genome than traditional experiments which focus on one gene at a time.
The research was led by immunologist Susan Carpenter, a professor and Sinsheimer Chair of UC Santa Cruz’s Molecular, Cell, and Developmental Biology Department. She studies the molecular mechanisms involved in protection against infection. Specifically, she focuses on the processes that lead to inflammation to determine the role that lncRNAs play in these pathways.
“Inflammation is a central feature of just about every disease,” she said. “In this study, my lab focused on trying to determine which lncRNA genes are involved in regulating inflammation.”
This meant studying lncRNAs in a type of white blood cell known as a monocyte. They used a modification of the CRISPR/Cas9 technology, called CRISPR inhibition (CRISPRi), to repress gene transcription and find out which of a monocyte’s lncRNAs play a role in whether it differentiates into a macrophage — another type of white blood cell that’s critical to a well-functioning immune response.
In addition, the researchers used CRISPRi to screen macrophage lncRNA for involvement in inflammation. Unexpectedly, they located a region that is multifunctional and can work as an RNA as well as containing an undiscovered peptide that regulates inflammation.
Understanding that this specific peptide regulates inflammation gives drugmakers a target to block the molecular interaction behind that response in order to suppress it, Carpenter said. “In an ideal world, you would design a small molecule to disrupt that specific interaction, instead of, say, targeting a protein that might be expressed throughout the body,” she explained. “We’re still a long way from targeting these pathways with that level of precision, but that’s definitely the goal. There’s a lot of interest in RNA therapeutics right now.”
Co-authors of the study from UC Santa Cruz include Haley Halasz, Eric Malekos, Sergio Covarrubias, Samira Yitiz, Christy Montano, Lisa Sudek, and Sol Katzman, along with researchers at UCSF and MIT. The research was supported with funding from the National Institute of General Medical Sciences (R35GM137801 to Carpenter) and the National Institute of Allergy and Infectious Diseases (F31AI179201 to Malekos).

Undergoing surgery is seldom a pleasant experience, and it can sometimes be highly invasive. Surgical procedures have evolved steadily over the centuries, growing with the knowledge of anatomy and biology.
Innovative methods have also been bolstered with new tools, and a growth in the use of robotics since the 1980s has moved health care forward significantly. Assistant Professor Zhenhua Tian has pressed forward another step in the march of progress using robotics and noninvasive acoustics, and his team’s work has been published in Science Advances.
Robot-assisted surgery
Surgery using robots has been invasive since its invention because cutting is involved and often other instruments are inserted into the incision. However, because robotic-assisted tools can be smaller, the cuts also tend to be smaller than traditional surgeries, making robotics a preferred choice. This form of surgery has proven its benefits and has grown in use over time, with advantages to patients including Less discomfort and bleeding Less time in the hospital Faster recovery periodsIn fact, according to the American College of Surgeons, 1.8 percent of surgeries included a robot in 2012. By 2018, that percentage had risen to 15.1 percent and continues to rise through advancements in robotics. Some of the most common procedures involving robotics include appendectomies, hysterectomies, and gastric bypasses.
Noninvasive sound treatment
While robotic-assisted surgery has its share of advantages, Tian’s team has taken that idea a step beyond its current state: Team members are developing a method of moving small targets, such as cells and medicine, within a body that is noninvasive. That means the method requires no cuts.

The secret is found in acoustic energy emitters that Tian’s team uses to surround and capture particles, working like invisible tweezers. The emitters create 3D acoustic vortex fields that can pass through barriers such as bone and tissue, crossing over one another to form tiny ring-shaped acoustic traps. Micro- to millimeter-sized objects caught at the center of an acoustic trap can be moved and rotated. Tian received a 2024 National Science Foundation Faculty Early Career Development Program (CAREER) award for the acoustic vortex development.
“The ability to move cells and drugs around inside veins without breaking the skin creates new opportunities in medicine,” said Tian. “As we continue the work on this research, I anticipate we will find a host of new applications.”
By mounting an acoustic vortex emitter onto a robotic platform, the acoustic vortex beam can be moved at the micrometer scale. Accordingly, the particle trapping area can be precisely set in a 3D space, and moving a particle after its capture can be engineered. When moving a tiny object along the winding path of a blood vessel, this can be a critical feature.
More than medicine
While Tian’s team is able to move a small object behind a solid structure, the acoustic vortex beams can move particles within both gases and liquids as well. Although the current approach targets small particles within those substances, integrating the acoustic energy emitters together with robotics has applications beyond surgery and very small particles. Contactless, robotic manipulation has potential in many other applications across engineering, biology, and chemistry research. Some of those include Controlling microrobots Handling delicate bioparticles, such as exosomes and cells Transporting hazardous reagent droplets Controlling self-assembly of colloidal materials Arranging nanomaterials for composite fabrication”When we were recently participating in a STEM expo, the children who visited us enjoyed putting small beads into the invisible acoustic fields generated by our devices, but we would like to offer the opportunity for them to move larger objects,” said Tian. “Next year, we hope to have a larger emitter that can hold a ping pong ball. It will be interesting to see how we plug that approach into our other research.”

The stress of heart failure is remembered by the body and appears to lead to recurrent failure, along with other related health issues, according to new research. Researchers have found that heart failure leaves a “stress memory” in the form of changes to the DNA modification of hematopoietic stem cells, which are involved in the production of blood and immune cells called macrophages. These immune cells play an important role in protecting heart health. However, a key signaling pathway (a chain of molecules which relays signals inside a cell), called transforming growth factor beta (TGF-β), in the hematopoietic stem cells was suppressed during heart failure, negatively affecting macrophage production. Improving TGF-β levels could be a new avenue for treating recurrent heart failure, while detecting accumulating stress memory could provide an early warning system before it occurs.
Healthier lives and improved well-being are among the United Nations’ global Sustainable Development Goals. Positively, a recent study shows that life expectancy worldwide is projected to increase by about 4.5 years by 2050. Much of this is thanks to public health efforts to prevent disease and improved survival from illnesses, such as cardiovascular disorders. However, heart disease is still the leading cause of death worldwide, with 26 million people estimated to be affected by heart failure.
Once heart failure has occurred, it has a tendency to reoccur along with other health issues, such as kidney and muscle problems. Researchers in Japan wanted to understand what causes this recurrence and the deterioration of other organs, and whether it can be prevented.
“Based on our earlier research, we hypothesized that recurrence may be caused by stress experienced during heart failure accumulating in the body, particularly in hematopoietic stem cells,” explained Project Professor Katsuhito Fujiu from the Graduate School of Medicine at the University of Tokyo. Hematopoietic stem cells are found in bone marrow and are the source of blood cells and a type of immune cell called macrophages, which help to protect heart health.
By studying mice with heart failure, the researchers found evidence of stress imprinting on the epigenome, that is, chemical changes occurred to the mice’s DNA. An important signaling pathway, called the transforming growth factor beta, which is involved in regulating many cellular processes, was suppressed in the hematopoietic stem cells of mice with heart failure, leading to the production of dysfunctional immune cells.
This change persisted over an extended period of time, so when the team transplanted bone marrow from mice with heart failure into healthy mice, they found that the stem cells continued to produce dysfunctional immune cells. The latter mice later developed heart failure and became prone to organ damage.
“We termed this phenomenon stress memory because the stress from heart failure is remembered for an extended period and continues to affect the entire body. Although various other types of stress might also imprint this stress memory, we believe that the stress induced by heart failure is particularly significant,” said Fujiu.
The good news is that by identifying and understanding these changes to the TGF-β signaling pathway, new avenues are now open for potential future treatments. “Completely new therapies could be considered to prevent the accumulation of this stress memory during hospitalization for heart failure,” said Fujiu. “In animals with heart failure, supplementing additional active TGF-β has been shown to be a potential treatment. Correcting the epigenome of hematopoietic stem cells could also be a way to deplete stress memory.”
Now that it has been identified, the team hopes to develop a system that can detect and prevent the accumulation of stress memory in humans, with a long-term goal of being able to not only prevent the recurrence of heart failure, but also catch the condition before it can fully develop.

Negotiators plan to ask for more time. Among the sticking points are equitable access to vaccines and financing to set up surveillance systems.Countries around the globe have failed to reach consensus on the terms of a treaty that would unify the world in a strategy against the inevitable next pandemic, trumping the nationalist ethos that emerged during Covid-19.The deliberations, which were scheduled to be a central item at the weeklong meeting of the World Health Assembly beginning Monday in Geneva, aimed to correct the inequities in access to vaccines and treatments between wealthier nations and poorer ones that became glaringly apparent during the Covid pandemicAlthough much of the urgency around Covid has faded since the treaty negotiations began two years ago, public health experts are still acutely aware of the pandemic potential of emerging pathogens, familiar threats like bird flu and mpox, and once-vanquished diseases like smallpox.“Those of us in public health recognize that another pandemic really could be around the corner,” said Loyce Pace, an assistant secretary at the Department of Health and Human Services, who oversees the negotiations in her role as the United States liaison to the World Health Organization.Negotiators had hoped to adopt the treaty next week. But canceled meetings and fractious debates — sometimes over a single word — stalled agreement on key sections, including equitable access to vaccines.The negotiating body plans to ask for more time to continue the discussions.“I’m still optimistic,” said Dr. Jean Kaseya, director general of Africa Centers for Disease Control and Prevention. “I think the continent wants this agreement. I think the world wants this agreement.”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.

Muscle from a sick dairy cow tested positive for the virus. The meat did not enter the commercial food supply, which officials said remained safe.Beef tissue from a sick dairy cow has tested positive for the bird flu virus, federal officials said on Friday.The cow had been condemned to be culled because it was sick, and the meat did not enter the food supply, according to the U.S. Department of Agriculture. The department continued to stress that the commercial food supply remained safe.But the positive test, which came as part of an ongoing federal study of beef safety, raises concerns about whether the virus might make its way into the commercial beef supply, posing a health risk to humans.So far, the U.S.D.A’s Food Safety and Inspection Service has tested tissue samples from 96 dairy cows that had been condemned because of signs of disease. Just one cow tested positive, the department said. Meat from condemned cows is not allowed in the commercial food supply.The agency is in the process of testing additional muscle samples.It has not found virus in ground beef samples collected from retail outlets in states where cows have tested positive.Earlier this month, the agency released results from an experimental study in which high concentrations of the virus were put into very large beef patties — 300 grams, compared to a typical burger size of 113 grams. The researchers found no virus present in the meat when they cooked the burger to 160 degrees Fahrenheit, the internal temperature of a well-done burger, or 145 degrees Fahrenheit, the temperature of a burger cooked to medium.However, there was virus present in rare burgers, cooked to 120 degrees, although at greatly reduced levels; the agency said cooking to that temperature “substantially inactivated the virus.”“All indications are: You cook your food, even if there’s virus in there, it will kill it,” said Stacey Schultz-Cherry, a virologist and influenza expert at St. Jude Children’s Research Hospital. Food safety experts have expressed particular concern about the risk of transmission through raw milk.Food safety experts recommend always thoroughly cooking meat to prevent infection from other more common pathogens such as salmonella, listeria and E.coli. “Those food safety recommendations were in store long before H5N1 became an issue, and they should always be our basic standard,” said Dr. Keith Poulsen, director of the Wisconsin Veterinary Diagnostic Laboratory at the University of Wisconsin-Madison.

Mice administered raw milk samples from dairy cows infected with H5N1 influenza experienced high virus levels in their respiratory organs and lower virus levels in other vital organs, according to findings published in the New England Journal of Medicine. The results suggest that consumption of raw milk by animals poses a risk for H5N1 infection and raises questions about its potential risk in humans.
Since 2003, H5N1 influenza viruses have circulated in 23 countries, primarily affecting wild birds and poultry with about 900 human cases, primarily among people who have had close contact with infected birds. In the past few years, however, a highly pathogenic avian influenza virus called HPAI H5N1 has spread to infect more than 50 animal species, and in late March, the United States reported a viral outbreak among dairy cows in Texas. To date, 52 cattle herds across nine states have been affected, with two human infections detected in farm workers with conjunctivitis. Although the virus has so far shown no genetic evidence of acquiring the ability to spread from person-to-person, public health officials are closely monitoring the dairy cow situation as part of overarching pandemic preparedness efforts.
To assess the risk of H5N1 infection by consuming raw milk, researchers from the University of Wisconsin-Madison and Texas A&M Veterinary Medical Diagnostic Laboratory fed droplets of raw milk from infected dairy cattle to five mice. The animals demonstrated signs of illness, including lethargy, on day 1 and were euthanized on day 4 to determine organ virus levels. The researchers discovered high levels of virus in the animals’ nasal passages, trachea and lungs and moderate-to-low virus levels in other organs, consistent with H5N1 infections found in other mammals.
In addition to the mice studies, the researchers also tested to determine which temperatures and time intervals inactivate H5N1 virus in raw milk from dairy cows. Four milk samples with confirmed high H5N1 levels were tested at 63 degrees Celsius (145.4 degrees Fahrenheit) for 5, 10, 20 and 30 minutes, or at 72 degrees Celsius (161.6 degrees Fahrenheit) for 5, 10, 15, 20 and/or 30 seconds. Each of the time intervals at 63℃ successfully killed the virus. At 72℃, virus levels were diminished but not completely inactivated after 15 and 20 seconds. The authors emphasize, however, that their laboratory study was not identical to large-scale industrial pasteurization of raw milk and reflect experimental conditions that should be replicated with direct measurement of infected milk in commercial pasteurization equipment.
In a separate experiment, the researchers stored raw milk infected with H5N1 at 4℃ (39.2 degrees Fahrenheit) for five weeks and found only a small decline in virus levels, suggesting that the virus in raw milk may remain infectious when maintained at refrigerated temperatures.
To date, the U.S. Food and Drug Administration concludes that the totality of evidence continues to indicate that the commercial milk supply is safe. While laboratory benchtop studies provide important, useful information, there are limitations that challenge inferences to real world commercial processing and pasteurization. The FDA conducted an initial survey of 297 retail dairy products collected at retail locations in 17 states and represented products produced at 132 processing locations in 38 states. All of the samples were found to be negative for viable virus. These results underscore the opportunity to conduct additional studies that closely replicate real world conditions. FDA, in partnership with USDA, is conducting pasteurization validation studies — including the use of a homogenizer and continuous flow pasteurizer. Additional results will be made available as soon as they are available.
The National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, funded the work of the University of Wisconsin-Madison researchers.

Vaccinia viruses are therapeutic tools with different biomedical applications depending on the susceptibility characteristics. For example, the strain called MVA (modified vaccinia Ankara), which is unable to replicate in mammalian cells, triggers a potent immune system response and is used to develop vaccines against COVID-19 or AIDS. In contrast, other strains such as Western Reserve (WR) or Copenhagen (Cop), which replicate efficiently in tumour cells, are used to develop cancer treatments. For this reason, they are called immune-oncolytic viruses and are the basis of viral immunotherapy.
However, these viral strains have reduced immunogenicity, which makes them less effective in activating patients’ immune responses against tumours.
Now, a study led by the University of Barcelona, the Bellvitge Biomedical Research Institute (IBIDELL) and the University of Munich (Germany) has developed a new strain of vaccinia virus, which can replicate in tumour cells while maintaining increased immunogenicity. Specifically, it can to induce so-called immunogenic cell death in tumour cells.
The study, published in the journal Molecular Therapy, has been carried out with the support of the Spanish Association Against Cancer (AECC) and the collaboration of the State Research Agency (AEI). The new therapeutic tool, which has been tested in a wide variety of mouse models, has been shown to have reduced toxicity and a high capacity and efficiency to activate immune responses against tumours. The virus is also effective in different cancer treatments, such as melanoma, colon and kidney cancer.
“In addition, we achieved the total disappearance of tumours in a very significant way when we administered the virus repeatedly,” notes expert Juan J. Rojas, first author of the study and principal investigator of the Immunity, Inflammation and Cancer group of the Faculty of Medicine and Health Sciences of the UB and IBIDELL.
The discovery of this new viral strain represents a significant advance in viral immunotherapy research and demonstrates its therapeutic potential for treating cancer patients.

Scientists have known for years that a lattice of blood vessels nourishes cells in the retina that allow us to see — but it’s been a mystery how the intricate structure is created.
Now, researchers at UC San Francisco have found a new type of neuron that guides its formation.
The discovery, described in the May 23, 2024, issue of Cell, could one day lead to new therapies for diseases that are related to impaired blood flow in the eyes and brain.
“This is the first time anyone has seen retinal neurons using direct contact with blood vessels as a way of guiding them to form these precise 3-D lattices,” said Xin Duan, PhD, an associate professor of ophthalmology and senior author of the study. “This brings us closer to the possibility of repairing them when they’re damaged or rerouting them when they weren’t built right in the first place.”
A protein that senses the presence of nearby cells
The researchers worked with newborn mice, whose eyes still need several weeks to develop fully. Kenichi Toma, PhD, labeled the retinal neurons closest to the blood vessels with a protein that glows green under ultraviolet light so he could observe the lattice as it was forming.
The team then identified a subset of neurons, called perivascular neurons, which contact and then surround growing blood vessels, directing them to form the lattice. These perivascular neurons produce a protein called PIEZO2 that enables them to sense when they are touching another cell.

Perivascular neurons in mice that were unable to produce PIEZO2 could not maintain contact with blood vessels, and they grew in a tangled, disorganized way that disrupted blood flow.
Starved for oxygen, the surrounding nerve cells degraded, and the mutant mice were more vulnerable to stroke-like injuries.
Duan found that these neurons guide the formation of a similar network of blood vessels in the cerebellum, a part of the brain that is involved in coordination, language, and sense perception.
“The fact that we see this same pattern repeated in the brain means that damage to this lattice might have a role in multiple neurodegenerative diseases,” Toma said.
The team collaborated with developmental biologist Arnold Kriegstein, MD, PhD, to confirm that perivascular retinal neurons also exist in humans.
3-D view shows how the lattice forms
Most research to date on the connection between the vascular and nervous systems has been limited by technology that only allows scientists to take two-dimensional pictures.

But Duan and Toma benefited from a new technique, using multiphoton microscopy, that Tyson Kim, MD, PhD, an assistant professor of ophthalmology, had developed to make 3-D images of retinal blood networks without disturbing the eye.
Kim helped Toma create revolving movies that captured the lattice from every angle and showed how it broke down in the absence of PIEZO2.
“We had been wanting to collaborate for some time, and this was the perfect opportunity,” Kim said. “It was really a confluence of what we’re each passionate about.”
A new way to protect neurons
The discoveries could inspire new ways of treating neurodegenerative diseases by ensuring that neurons, which demand a lot of energy, maintain a healthy blood supply.
“There are lots of people trying to understand the ways we can grow neurons,” Duan said. “But how in the world do we grow the intricate networks of blood vessels required to support them? That’s the question we’re trying to answer.”