Category: Health

{New findings suggest risk may not be limited to fetuses of pregnant women.}

Concerns over the Zika virus have focused on pregnant women due to mounting evidence that it causes brain abnormalities in developing fetuses. However, new research in mice from scientists at The Rockefeller University and La Jolla Institute for Allergy and Immunology suggests that certain adult brain cells may be vulnerable to infection as well. Among these are populations of cells that serve to replace lost or damaged neurons throughout adulthood, and are also thought to be critical to learning and memory.

“This is the first study looking at the effect of Zika infection on the adult brain,” says Joseph Gleeson, adjunct professor at Rockefeller, head of the Laboratory of Pediatric Brain Disease, and Howard Hughes Medical Institute investigator. “Based on our findings, getting infected with Zika as an adult may not be as innocuous as people think.”

Although more research is needed to determine if this damage has long-term biological implications or the potential to affect behavior, the findings suggest the possibility that the Zika virus, which has become widespread in Central and South America over the past eight months, may be more harmful than previously believed. The new findings were published in Cell Stem Cell on August 18.

“Zika can clearly enter the brain of adults and can wreak havoc,” says Sujan Shresta, a professor at the La Jolla Institute of Allergy and Immunology. “But it’s a complex disease — it’s catastrophic for early brain development, yet the majority of adults who are infected with Zika rarely show detectable symptoms. Its effect on the adult brain may be more subtle, and now we know what to look for.”

Neuronal progenitors

Early in gestation, before our brains have developed into a complex organ with specialized zones, they are comprised entirely of neural progenitor cells. With the capability to replenish the brain’s neurons throughout its lifetime, these are the stem cells of the brain. In healthy individuals, neural progenitor cells eventually become fully formed neurons, and it is thought that at some point along this progression they become resistant to Zika, explaining why adults appear less susceptible to the disease.

But current evidence suggests that Zika targets neural progenitor cells, leading to loss of these cells and to reduced brain volume. This closely mirrors what is seen in microcephaly, a developmental condition linked to Zika infection in developing fetuses that results in a smaller-than-normal head and a wide variety of developmental disabilities.

The mature brain retains niches of these neural progenitor cells that appear to be especially impacted by Zika. These niches — in mice they exist primarily in two regions, the subventricular zone of the anterior forebrain and the subgranular zone of the hippocampus — are vital for learning and memory.

Gleeson and his colleagues suspected that if Zika can infect fetal neural progenitor cells, it wouldn’t be a far stretch for them to also be able to infect these cells in adults. In a mouse model engineered by Shresta and her team to mimic Zika infection in humans, fluorescent biomarkers illuminated to reveal that adult neural progenitor cells could indeed be hijacked by the virus.

“Our results are pretty dramatic — in the parts of the brain that lit up, it was like a Christmas tree,” says Gleeson. “It was very clear that the virus wasn’t affecting the whole brain evenly, like people are seeing in the fetus. In the adult, it’s only these two populations that are very specific to the stem cells that are affected by virus. These cells are special, and somehow very susceptible to the infection.”

Beyond fetal brain infection

The researchers found that infection correlated with evidence of cell death and reduced generation of new neurons in these regions. Integration of new neurons into learning and memory circuits is crucial for neuroplasticity, which allows the brain to change over time. Deficits in this process are associated with cognitive decline and neuropathological conditions, such as depression and Alzheimer’s disease.

Gleeson and colleagues recognize that healthy humans may be able to mount an effective immune response and prevent the virus from attacking. However, they suggest that some people, such as those weakened immune systems, may be vulnerable to the virus is a way that has not yet been recognized.

“In more subtle cases, the virus could theoretically impact long-term memory or risk of depression,” says Gleeson, “but tools do not exist to test the long-term effects of Zika on adult stem cell populations.”

In addition to microcephaly, Zika has been linked to Guillain-Barré syndrome, a rare condition in which the immune system attacks parts of the nervous system, leading to muscle weakness or even paralysis. “The connection has been hard to trace since Guillain-Barré usually develops after the infection has cleared,” says Shresta. “We propose that infection of adult neural progenitor cells could be the mechanism behind this.”

There are still many unanswered questions, including exactly how translatable findings in this mouse model are to humans. Gleeson’s findings in particular raise questions such as: Does the damage inflicted on progenitor cells by the virus have lasting biological consequences, and can this in turn affect learning and memory? Or, do these cells have the capability to recover? Nonetheless, these findings raise the possibility that Zika is not simply a transient infection in adult humans, and that exposure in the adult brain could have long-term effects.

“The virus seems to be traveling quite a bit as people move around the world,” says Gleeson. “Given this study, I think the public health enterprise should consider monitoring for Zika infections in all groups, not just pregnant women.”

{A high-fat, high-sugar diet during pregnancy may be linked to symptoms of ADHD in children who show conduct problems early in life, new research indicates.}

New research led by scientists from King’s College London and the University of Bristol has found that a high-fat, high-sugar diet during pregnancy may be linked to symptoms of ADHD in children who show conduct problems early in life.

Published in the Journal of Child Psychology and Psychiatry, this study is the first to indicate that epigenetic changes evident at birth may explain the link between unhealthy diet, conduct problems and ADHD.

Early onset conduct problems (e.g. lying, fighting) and attention-deficit/hyperactivity disorder (ADHD) are the leading causes of child mental health referral in the UK. These two disorders tend to occur in tandem (more than 40 per cent of children with a diagnosis of conduct disorder also have a diagnosis of ADHD) and can also be traced back to very similar prenatal experiences such as maternal distress or poor nutrition.

In this new study of participants from the Bristol-based ‘Children of the 90s’ cohort, 83 children with early-onset conduct problems were compared with 81 children who had low levels of conduct problems. The researchers assessed how the mothers’ nutrition affected epigenetic changes (or DNA methylation) of IGF2, a gene involved in fetal development and the brain development of areas implicated in ADHD — the cerebellum and hippocampus. Notably, DNA methylation of IGF2 had previously been found in children of mothers who were exposed to famine in the Netherlands during World War II.

The researchers from King’s and Bristol found that poor prenatal nutrition, comprising high fat and sugar diets of processed food and confectionary, was associated with higher IGF2 methylation in children with early onset conduct problems and those with low conduct problems.

Higher IGF2 methylation was also associated with higher ADHD symptoms between the ages of 7 and 13, but only for children who showed an early onset of conduct problems.

Dr Edward Barker from King’s College London said: ‘Our finding that poor prenatal nutrition was associated with higher IGF2 methylation highlights the critical importance of a healthy diet during pregnancy.

‘These results suggest that promoting a healthy prenatal diet may ultimately lower ADHD symptoms and conduct problems in children. This is encouraging given that nutritional and epigenetic risk factors can be altered.’

Dr Barker added: ‘We now need to examine more specific types of nutrition. For example, the types of fats such as omega 3 fatty acids, from fish, walnuts and chicken are extremely important for neural development.

‘We already know that nutritional supplements for children can lead to lower ADHD and conduct problems, so it will be important for future research to examine the role of epigenetic changes in this process.’

{The term “healthy obesity” has gained traction over the past 15 years, but scientists have recently questioned its very existence. A study published August 18 in Cell Reports provides further evidence against the notion of a healthy obese state, revealing that white fat tissue samples from obese individuals classified as either metabolically healthy or unhealthy actually show nearly identical, abnormal changes in gene expression in response to insulin stimulation.}

“The findings suggest that vigorous health interventions may be necessary for all obese individuals, even those previously considered to be metabolically healthy,” says first author Mikael Rydén of the Karolinska Institutet. “Since obesity is the major driver altering gene expression in fat tissue, we should continue to focus on preventing obesity.”

Obesity has reached epidemic proportions globally, affecting approximately 600 million people worldwide and significantly increasing the risk of heart disease, stroke, cancer, and type 2 diabetes. Since the 1940s, evidence supporting the link between obesity and metabolic and cardiovascular diseases has been steadily growing. But in the 1970s and 80s, experts began to question the extent to which obesity increases the risk for these disorders. Subsequent studies in the late 90s and early 2000s showed that some obese individuals display a relatively healthy metabolic and cardiovascular profile.

Recent estimates suggest that up to 30% of obese individuals are metabolically healthy and therefore may need less vigorous interventions to prevent obesity-related complications. A hallmark of metabolically healthy obesity is high sensitivity to the hormone insulin, which promotes the uptake of blood glucose into cells to be used for energy. However, there are currently no accepted criteria for identifying metabolically healthy obesity, and whether or not such a thing exists is now up for debate.

To address this controversy, Rydén, Carsten Daub, and Peter Arner of the Karolinska Institutet assessed responses to insulin in 15 healthy, never-obese participants and 50 obese subjects enrolled in a clinical study of gastric bypass surgery. The researchers took biopsies of abdominal white fat tissue before and at the end of a two-hour period of intravenous infusion of insulin and glucose. Based on the glucose uptake rate, the researchers classified 21 obese subjects as insulin sensitive and 29 as insulin resistant.

Surprisingly, mRNA sequencing of white fat tissue samples revealed a clear distinction between never-obese participants and both groups of obese individuals. White fat tissue from insulin-sensitive and insulin-resistant obese individuals showed nearly identical patterns of gene expression in response to insulin stimulation. These abnormal gene expression patterns were not influenced by cardiovascular or metabolic risk factors such as waist-to-hip ratio, heart rate, or blood pressure. The findings show that obesity rather than other common risk factors is likely the primary factor determining metabolic health.

“Our study suggests that the notion of metabolically healthy obesity may be more complicated than previously thought, at least in subcutaneous adipose tissue,” Rydén says. “There doesn’t appear to be a clear transcriptomic fingerprint that differentiates obese subjects with high or low insulin sensitivity, indicating that obesity per se is the major driver explaining the changes in gene expression.”

One limitation of the study is that it examined gene expression profiles only in subcutaneous white fat tissue, not other types of fat tissue or other organs. Moreover, all of the obese subjects were scheduled to undergo bariatric surgery, so the findings may only apply to individuals with severe obesity.

In future research, Rydén and his collaborators will track the study participants after bariatric surgery to determine whether weight loss normalizes gene expression responses to insulin. They will also look for specific genes linked to improved metabolic health in these individuals.

In the meantime, the study has an important take-home message. “Insulin-sensitive obese individuals may not be as metabolically healthy as previously believed,” Rydén says. “Therefore, more vigorous interventions may be necessary in these individuals to prevent cardiovascular and metabolic complications.”

{A profound new level of complexity and interaction among genes within specific tissues responsible for mediating the inherited risk for cardiometabolic diseases have been identified by researchers, including processes that lead to heart attack and stroke.}

In a study being published in the August 19 issue of Science, researchers from the Icahn School of Medicine at Mount Sinai, in collaboration with scientists from Tartu University Hospital in Estonia, the Karolinska Institutet and Science for Life Laboratory (SciLifeLab) in Sweden, and AstraZeneca, have identified a profound new level of complexity and interaction among genes within specific tissues responsible for mediating the inherited risk for cardiometabolic diseases, including processes that lead to heart attack and stroke.

“By analyzing gene-expression data from multiple tissues in hundreds of patients with coronary artery disease, we were able to identify disease-causing genes that either were specific to single tissues or acted across multiple tissues in networks to cause cardiometabolic diseases,” said Johan Björkegren, MD, PhD, senior author of the study, Professor of Genetics and Genomic Sciences at the Icahn School of Medicine at Mount Sinai, visiting professor at the University of Tartu and senior investigator at the Karolinska Institutet.

The ground-breaking research was done as part of the STARNET study, the first systematic analysis of RNA sequence data from blood, vascular, and metabolic tissues from patients with coronary artery disease (CAD). RNA sequences are copies of the DNA in each cell that serve as templates for protein synthesis and determine whether a tissue remains healthy or becomes diseased.

“Genome-wide association studies (GWAS) have identified thousands of DNA variants increasing risk for common diseases like CAD,” said Dr. Björkegren. “However, while GWAS was an important first line of investigations of the genetics of CAD, in order to translate these risk markers into opportunities for new diagnostics and therapies, we must now move into a new phase of discovery and identify the genes perturbed by these DNA variants responsible for driving disease development. Furthermore, we also need to understand in which tissues, pathways, and molecular networks these disease genes are active. Unraveling disease-driving genes with their tissue-belonging, as we have started to achieve using STARNET, will also be a prerequisite for developing precision medicine with individualized diagnostics and therapies.”

STARNET was launched in 2007 by Dr. Björkegren and Arno Ruusalepp, MD, PhD, Chief Cardiac Surgeon at Tartu University Hospital and senior co-author on the study. Unlike similar studies, STARNET obtained samples of several key tissues from 600 clinically well-characterized patients with CAD during coronary artery bypass surgery. By using sophisticated data analysis techniques, the researchers found that the gene expression data from STARNET were highly informative in identifying causal disease genes and their activity in networks not only in CAD but also for other cardiometabolic diseases as well as Alzheimer’s disease.

“One unexpected and thus potentially important finding of the study was that besides the liver, abdominal fat emerged as a key site for regulation of blood lipid levels,” said Oscar Franzén, MSc, PhD, Postdoctoral Fellow at the Icahn School of Medicine at Mount Sinai, first author of the study, and computational biologist in Dr. Björkegren’s laboratory. “For example, a gene called PCSK9, which is implicated in controlling plasma levels of low-density lipoprotein (LDL) — the so-called bad cholesterol — was found to do so by acting in abdominal fat, not in the liver where blood levels of LDL are mainly regulated.” PCSK9 has lately gained substantial attention as the latest target for lipid-lowering drugs now reaching the market.

“The STARNET project is fundamentally relevant for studies of the causes of CAD and other complex diseases,” said Eric Schadt, senior co-author on the paper and the Jean C. and James W. Crystal Professor of Genomics at the Icahn School of Medicine at Mount Sinai, and Founding Director of the Icahn Institute for Genomics and Multiscale Biology. “We were not only able to assign a high number of individual genes to DNA markers previously identified by GWAS but also, and quite unexpectedly, we found that many of these downstream genes appeared in disease-causal gene regulatory networks that were shared across tissues and diseases.”

In collaboration with AstraZeneca and the SciLifeLab team, Dr. Björkegren’s team has also used STARNET to try to improve drug target development. “We are excited about our joint project with Dr. Björkegren’s team at the Karolinska Institutet and AstraZeneca, which now with the Science report has delivered the first wave of ground-breaking data that we have supported for the past 3 years,” said Li-Ming Gan, MD, PhD, a co-author of the study, Senior Medical Director and collaboration lead at AstraZeneca. “During the course of our project we have found that Dr. Björkegren’s datasets including STARNET provide essential translation information to help us identify new drug targets, as well as informing on existing targets in cardiovascular and metabolic diseases, a main therapy area for AstraZeneca.”

“The PCSK9 finding together with the unexpected cross-tissue and even cross-disease activity of many disease-causing genes shows how little we currently understand about the cause of CAD,” said Dr. Ruusalepp. “As a cardiac surgeon actively treating CAD patients, I am confronted by the massive global burden of CAD and the toll it takes on our society every day. STARNET has opened the door to a new era of understanding in CAD, and brings exciting new hope for future therapies.”

{Nyagatare Hospital is holding 74 patients over failure to clear medical bills for various services they received at the hospital. Some of them have stayed in the hospital for almost two months.}

Patients held for almost two months have said that they are kept inside a house where they lack food while others live on handouts.

The direct of Nyagatare hospital, Dr Ngabire Nkunda Philippe has told media that the decision was taken by hospital management.

“We had 74 patients last week, some of who had Mituelle de santé related problems. We have got a particular room with beds where they sleep. Arriving at their accommodation one may think they are patients; they were healed but lacked money to pay the hospital after getting discharged. Some of them do not subscribe to Mituelle de santé. We also have others owning Mituelle de santé but lacked 10% of health service payments. In fact they are here on account of different problems,” he explained.

Dr. Nkunda explained that the number of such people increases every day, posing potential danger to the hospital coffers. “More than 70 people defaulting is too much. If they are left to go scot-free without clearing debts, the hospital would incur grave losses,” he said.

Retaining recovered patients at the hospital will motivate them to seek rescue from relatives. Patients owe the hospital more Rwf 8 million accumulated over the past three years,” added Dr Nkunda.

Among the retained patients are women who gave birth by caesarian operation, with some supposed to pay Rwf 200,000 each while others have to pay Rwf 100,000 and below.

IGIHE has talked to Nyagatare deputy vice mayor in charge of social welfare, Musabyemariya Domithile who said that they have arranged a meeting today to discuss the matter.

{A review looking at studies on the effect music interventions have on the treatment of cancer patients found treatment benefits for anxiety, pain, fatigue and overall quality of life.}

We’ve all heard of laughter being the best medicine, but what about music?

A systematic review published by the Cochrane Library found that there is significant evidence that music interventions help alleviate symptoms of anxiety, pain and fatigue in cancer patients, while also boosting their quality of life.

Led by Joke Bradt, PhD, associate professor in Drexel University’s College of Nursing and Health Professions, a team looked into studies that examined the impact of music therapy (a personalized music experience offered by trained music therapists) and music medicine (listening to pre-recorded music provided by a doctor or nurse) on psychological and physical outcomes in people with cancer.

“We found that music therapy interventions specifically help improve patients’ quality of life,” explained Bradt. “These are important findings as these outcomes play an important role in patients’ overall well-being.”

A total of 52 trials were examined in the review, constituting of 3,731 participants with cancer. Twenty-three of the trials were categorized as music therapy and the remaining 29 were classified as music medicine interventions.

Overall, one of the most impactful findings was that music interventions of all kinds resulted in a moderate-to-strong effect in reducing patients’ anxiety.

When it came to pain reduction, the researchers found a large treatment benefit; for fatigue, a small-to-moderate treatment effect was found.

Small reductions in heart and respiratory rates, as well as lowered blood pressure, were also linked to music interventions.

“The results of single studies suggest that music listening may reduce the need for anesthetics and analgesics, as well as decreased recovery time and duration of hospitalization, but more research is needed for these outcomes,” according to Bradt and her co-authors.

When comparing music therapy to music medicine, the team saw a moderate increase in patients’ quality of life when music therapy was applied. There was not a similar effect in the case of music medicine interventions.

“Both music medicine and music therapy interventions play an important role in cancer care but we didn’t quite know yet which interventions may be best suited for which type of outcome,” Bradt said.

In light of the benefits to cancer patients’ quality of life, and specifically their levels of anxiety, pain and fatigue, the researchers hope music interventions will become more widespread.

“We hope that the findings of this review will encourage health care providers in medical settings to seriously consider the use of music therapy in the psychosocial care of people with cancer,” Bradt said.

{Research into the bacterial interactions in our nasal microbiome suggest novel approaches for preventing Staphylococcus aureus infections without antibiotic use}

Staphylococcus aureus is a common colonizer of the human body. Although, one quarter of the US population live with the bacteria and never get sick, having S. aureus present in the nostrils is a risk for infections that range in severity from mild skin to life- threatening MRSA infections. Research is providing insight into how harmless Corynebacterium species, bacterial members of the nasal and skin microbiome, help protect humans from disease.

A recent study by senior-author Katherine P. Lemon MD, PhD and first-author Matthew M. Ramsey PhD, along with Dr. Marcelo Freire at the Forsyth Institute, and with Rebecca Gabrilska and Dr. Kendra Rumbaugh from Texas Tech University, shows that when the two bacteria interact, Corynebacterium inhibits the virulence of S. aureus. Further understanding of these interactions is likely to help researchers to develop new treatments for preventing S. aureus infections. In addition, further research on the interactions between benign members of the human microbiome and bacteria, like S. aureus, that exhibit similar dual characteristics of living in harmony with and causing infections of humans, so-called pathobionts, could lead to the development of novel treatments for other diseases.

“Our research helps set the stage for the development of small molecules and, potentially, probiotic therapies for promoting health by actively managing nasal microbiome composition,” says Lemon. “This research identifies a role for Corynebacterium species in suppressing S. aureus virulence, and is an exciting early stage in our exploration of the molecular mechanisms that sculpt the composition of the nasal microbiome and influence colonization by pathobionts. We look forward to an increase in research on commensal-pathobiont interactions within the human microbiome and an ever-increasing understanding of the significance of our beneficial bacteria partners.”

In recent years, the emergence of an antibiotic resistant form of S. aureus infection (methicillin-resistance S. aureus or MRSA) has been a vexing problem. According to the Centers for Disease Control and Prevention, MRSA caused over 80,000 cases of invasive disease and over 10,000 deaths annually from 2005 through 2011. As more and more species of bacteria become antibiotic resistant, a deeper understanding of the interactions between potentially helpful and harmful bacteria in our microbiomes offers new approaches for treating diseases by harnessing the functions of already-present “beneficial” bacteria. Because pathobiont colonization is a prerequisite for infection and transmission, a possible approach to prevent infections by bacteria such as S. aureus is to limit or decrease their abundance or to shift them towards harmless behavior using either compounds derived from benign/beneficial members of the microbiome or by using these beneficial bacteria themselves as probiotics.

{Computer models supporting spectroscopy unlock behavior of actinium-225.}

{A new study greatly improves scientists’ understanding of the element actinium.The insights could support innovation in creating new classes of anticancer drugs.}

A new study at Los Alamos National Laboratory and in collaboration with Stanford Synchrotron Radiation Lightsource greatly improves scientists’ understanding of the element actinium. The insights could support innovation in creating new classes of anticancer drugs.

“The short half-life of actinium-225 offers opportunity for new alpha-emitting drugs to treat cancer, although very little has been known about actinium because all of its isotopes are radioactive and have short half-lives,” said Maryline Ferrier, a Seaborg post-doctoral researcher on the Los Alamos team. “This makes it hard to handle large enough quantities of actinium to characterize its chemistry and bonding, which is critical for designing chelators.”

The insights from this new study could provide the needed chemical information for researchers to develop ways to bind actinium so that it can be safely transported through the body to the tumor cell. “To build an appropriate biological delivery system for actinium, there is a clear need to better establish the chemical fundamentals for actinium,” Ferrier said. “Using only a few micrograms (approximately the weight of one grain of sand) we were able to study actinium-containing compounds at the Stanford Synchrotron Radiation Lightsource and at Los Alamos, and to study actinium in various environments to understand its behavior in solution.”

{{Medical Isotopes at Los Alamos}}

Medical isotopes have long been a product of the Los Alamos specialty facilities, which create strontium-82, germanium-68 and other short-lived isotopes for medical scans. Taking advantage of the unique multidisciplinary capabilities of the Laboratory, researchers use the linear particle accelerator at the Los Alamos Neutron Science Center (LANSCE) to provide rare and important isotopes to the medical community across the United States. The expansion into actinium exploration moves the research forward toward treatment isotopes, as opposed to only diagnostic materials, says Ferrier.

For the actinium work, a spectroscopic analysis called X-ray Absorption Fine Structure (XAFS) was used, a sensitive technique that can determine chemical information such as the number of atoms surrounding actinium, their type (i.e., oxygen or chlorine) and their distances from each other. To help understand actinium’s behavior in solution and interpret the data obtained with XAFS, these experimental results were compared with sophisticated computer model calculations using molecular-dynamics density functional theory (MD-DFT).

The study showed that actinium, in solutions of concentrated hydrochloric acid, is surrounded by three atoms of chlorine and six atoms of water. Americium, another +3 actinide often used as a surrogate for actinium, is surrounded only by one chlorine atom and eight water molecules. It has been assumed in the past that actinium would behave similarly to americium.

“Our study shows that the two are different in a way that could help change how actinium ligands are designed,” Ferrier said. “We’re actively working to gather more fundamental data that will help understand how actinium chemically behaves.”

{{Actinium Useful for Targeted Alpha Therapy}}

Perhaps the most potent impact of these studies will be on the application of the isotope actinium-225, which is used in a novel, attractive cancer treatment technique called targeted alpha therapy (TAT). TAT exploits alpha emissions from radioisotopes to destroy malignant cells while minimizing the damage to healthy surrounding tissue. “Our determination that actinium’s behavior in solution is different than other nearby elements (such as americium) is directly relevant to TAT in a biological environment, which is always a complex solution,” said Ferrier.

Actinium-225 has a relatively short half-life (10 days) and emits four powerful alpha particles as it decays to stable bismuth, which makes it a perfect candidate for TAT. However, TAT with actinium can only become a reliable cancer-treatment if actinium is securely bound to the targeting molecule, as the radioisotope is very toxic to healthy tissue if it is not brought quickly to the site of disease.

{A fall down the stairs, a car crash, a sports injury or an explosive blast can all cause traumatic brain injury (TBI). Patients often recover. But in the days or weeks following the hit, they can develop other serious, chronic conditions, such as depression and thinking and memory problems. Now scientists report a potential way to reduce these effects with a neuron-targeting nanoparticle, using an animal model of TBI.}

When someone suffers from a head injury, the damage doesn’t necessarily stop after the initial blow. The jolt can cause a cascade of after-effects — such as inflammation and ultimately the death of brain cells — and lead to physical and cognitive conditions that can continue for years. One promising approach to treating these after-effects involves delivering short stretches of RNA that can help shut down this chain reaction. But getting the RNA to the damaged part of the brain is a challenge because of the blood-brain barrier, which separates circulating blood from the fluid around brain cells. Sangeeta N. Bhatia and her colleagues at the Massachusetts Institute of Technology’s Institute for Medical Engineering & Science wanted to see if they could rush therapeutic RNA to targeted brain cells soon after an injury while the blood-brain barrier is weakened.

The team, led by postdoctoral researcher Ester Kwon, engineered nanoparticles to target neurons by borrowing a protein from the rabies virus. They also loaded the particles with a strip of RNA designed to inhibit the production of a protein associated with neuronal cell death. When given to mice intravenously within a day of receiving a brain injury, the nanoparticles left the circulation and accumulated in the damaged tissue. Analysis also showed that the levels of the protein that the researchers were trying to reduce dropped by about 80 percent in the injured brain tissue.