Publisher Health

Older adults who are socially isolated are more likely to have missing teeth — and to lose their teeth more quickly over time — than those with more social interaction, according to a new study of Chinese older adults led by researchers at NYU Rory Meyers College of Nursing. The findings are published in Community Dentistry and Oral Epidemiology.
“Our study suggests that maintaining and improving social connections may benefit the oral health of older adults,” said Xiang Qi, a PhD student at NYU Meyers and the study’s first author. “The findings align with previous studies demonstrating that structural indicators of social disconnection can have powerful effects on indicators of health and well-being.”
Social isolation and loneliness in older adults are major public health concerns around the world and are risk factors for heart disease, mental health disorders, cognitive decline, and premature death. In some countries, including the United States and China, up to one in three older adults are lonely, according to the World Health Organization. The COVID-19 pandemic has exacerbated these issues among older adults, as many in-person interactions have been interrupted to protect older adults from infection.
Social isolation and loneliness are related but different. Social isolation is an objective measure defined as having few social relationships or infrequent social contact with others, while loneliness is the feeling created by a lack of social connection.
“While social isolation and loneliness often go hand in hand, it’s possible to live alone and be socially isolated but to not feel lonely, or to be surrounded by people but still feel lonely,” said Bei Wu, Dean’s Professor in Global Health at NYU Meyers and the study’s senior author.
Older adults are also at risk for another health concern: losing teeth. In China, older adults aged 65 to 74 have fewer than 23 teeth on average (adults typically have 32 teeth, or 28 if wisdom teeth have been removed) and 4.5% of this age group has lost all of their teeth. Gum disease, smoking, lack of access to dental care, and chronic illnesses like diabetes and heart disease increase the risks of tooth loss. Missing teeth can have a significant impact on one’s quality of life, affecting nutrition, speech, and self-esteem.

An investigational cancer drug that starves tumors of their energy supply also shows evidence of improving whole body metabolism, leading to improved weight control, according to a new study in mice from researchers at Washington University School of Medicine in St. Louis.
The findings are published in the journal Cell Reports Medicine.
In a group of mice genetically prone to obesity and in a separate group of mice that became obese due to a high-fat, high-sugar diet, treatment with the drug ADI-PEG 20 increased insulin sensitivity, improved cholesterol levels, reduced fat buildup in the liver and lowered inflammation. For the mice genetically prone to obesity from birth, treatment with the drug protected them from their typical weight gain. And for the mice that became obese on a high-fat, high-sugar diet, treatment with the drug caused the mice to lose weight.
The drug is being investigated for potential use as a treatment for a number of cancers, including sarcoma, breast and pancreatic cancers. The drug breaks down the amino acid arginine in the blood, which deprives cancer cells of a key source of fuel. The researchers became interested in studying the drug after finding that genes responsible for breaking down arginine are dialed up tremendously when the body is in a fasting state. They wondered if the drug could mimic this effect of fasting.
Indeed, the researchers found that the drug triggers cells to undergo a process called autophagy, or self-eating, a cellular-level housecleaning process. Cells undergoing autophagy burn their own cellular waste products for fuel. During fasting, when no new fuel is coming from the outside, cells shift to autophagy, turning inward for their fuel supply.
“Giving this drug seems to mimic some of the metabolic and therapeutic effects of fasting,” said senior author Brian DeBosch, MD, PhD, an associate professor of pediatrics. “I was surprised by how large the effect was. In the mice prone to weight gain, the group that received the drug ended up weighing about 25% less than the mice that didn’t get the drug. And in the mice on the high-fat, high-sugar diet, we saw similar weight loss from the drug. Also, we don’t think that the preponderance of the drug’s metabolic benefits are from changes in body weight. In fact, for several outcome measures, the metabolic changes preceded significant changes in weight.”
The drug has been tested in clinical trials investigating its safety and efficacy in treating several tumor types, including breast, prostate, pancreatic and liver cancers. In general, metabolic therapies tend to have fewer side effects and are safer than chemotherapy, radiation and even newer immunotherapies used to treat cancer.
DeBosch, a pediatric gastroenterologist who treats patients at St. Louis Children’s Hospital, said the research team would like to conduct a clinical trial of the drug to see if it triggers similar metabolic benefits and weight loss in people who are overweight or obese. One question that remains is whether the drug is safe to take long term. It’s not a small molecule, like a statin, that can be taken for decades. The drug is a protein, so there is a possibility that patients could develop an immune response to it over time. However, DeBosch still sees a potential role for such a treatment over a matter of weeks to months.
“Many patients with obesity who are considering bariatric surgery must first lose some weight to make the procedure safer,” DeBosch said. “It can be difficult for such patients to lose up to 10% of their body weight before the surgery. This type of therapy could potentially serve as a bridge to help patients lose weight before bariatric surgery, to reduce the risk of complications during and after the procedure.”
This work was supported by the National Institutes of Health (NIH), grant numbers 1R01DK126622-01A1, 1R01HL147968-01A1, 1R21AT010520-01, UL1TR002345 and R56 DK115764; a Pilot Research Award from the American Association for the Study of Liver Disease; an AGA-Gilead Sciences Research Scholar Award in Liver Disease; the AGA-Allergan Foundation Pilot Research Award in Non-Alcoholic Fatty Liver Disease; the Washington University Digestive Disease Research Core Center, grant number P30DK52574; the Washington University Diabetes Research Center, grant number P30DK020579; the Nutrition & Obesity Research Center, grant number P30DK056341; the Association for Aging Research Junior Faculty Award; the Robert Wood Johnson Foundation; the Washington University Center for Autophagy Therapeutics Research; the Longer Life Foundation; and a Washington University School of Medicine Pediatric Gastroenterology Research Training Grant, number T32DK077653.

For more than a century, scientists have known that while the commands that initiate movement come from the brain, the neurons that control locomotion once movement is underway reside within the spinal cord. In a study published January 20 in the journal Cell, researchers report that, in mice, they have identified one particular type of neuron that is both necessary and sufficient for regulating this type of movement. These neurons are called ventral spinocerebellar tract neurons (VSCTs).
“We hope that our findings will open up new avenues toward understanding how complex behaviors like locomotion come about and give us new insight into the mechanisms and biological principles that control this essential behavior,” says the paper’s senior author George Mentis, associate professor of pathology and cell biology in the Department of Neurology at Columbia University. “It’s also possible that our findings will lead to new ideas for therapeutic avenues, whether they involve treatments for spinal cord injury or neurodegenerative diseases that affect movement and motor control.”
VSCTs were discovered in the 1940s, but researchers have long believed that their main function was to relay messages about neuronal activity from the spinal cord to the cerebellum. The new study reports that instead they control locomotor behavior both during development and in adulthood.
“These findings were a huge surprise,” Mentis says. “One of the key discoveries in our study was that apart from their connection to the cerebellum, these neurons make connections with other spinal neurons that are also involved in locomotor behavior via their axon collaterals.”
The research involved several novel experimental approaches. One part of the research used optogenetics, employing LED light to regulate certain proteins that were expressed selectively in VSCTs to either activate or suppress the neuronal activity. Another set of experiments used chemogenetics, a process by which a chemical compound is used to activate or suppress synthetic ligands expressed artificially in these neurons, controlling their activity.
Leveraging the ability of intact spinal cords from newborn mice to function in a dish, the researchers showed that activation of VSCTs by light induced locomotor behavior. When VSCT activity was suppressed by light or by drugs, ongoing locomotor behavior was halted. During adulthood, freely moving mice stopped moving when the activity of VSCT was suppressed by injecting an inhibitory drug. Locomotor behavior was also tested by the ability of mice to swim. Mice were unable to swim and simply floated in the water when VSCTs were silenced. In all of these models and experiments, the researchers demonstrated that VSCTs alone were both necessary and sufficient for controlling locomotor activity — activating them was enough to induce activity while suppressing them was enough to stop it.
Mentis acknowledges that there are limitations to conducting this type of research in mice, including the fact that while humans are bipedal, mice are quadrupedal; thus, their locomotion could be regulated in a different way. But he notes that other research on neurodegenerative diseases and processes in mice has led to clinical trials in human patients, suggesting that these findings are also likely to be applicable.
For their next steps, the team plans to identify and map precisely the neuronal circuits that VSCTs make with motor neurons and other spinal neurons. They also would like to identify select genetic markers and uncover potential subpopulations of VSCTs and explore their role in different modes of locomotion. Finally, they plan to explore how the function of VSCTs is altered in the context of pathology and neurodegenerative diseases.
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Destroying senescent cells in the aging stem cell niche enhances hippocampal neurogenesis and cognitive function in mice, researchers report January 20 in the journal Stem Cell Reports.
“Our results provide further support for the notion that excessive senescence is a driving factor behind aging, and even late-life reduction of these cells can rejuvenate and restore the function of the stem cell niche,” says senior author David Kaplan of The Hospital for Sick Children (SickKids) in Toronto, Canada. “Moreover, they identify stem cells as a key cellular target, potentially explaining the widespread effects of senescent cells on tissue decline.”
Senescent cells, which are permanently arrested because of chronic stress, are partly responsible for tissue decline during aging. Several studies indicate that senescent cells also play a negative role in age-related neurodegenerative disorders. But the cellular mechanisms responsible for tissue failure during aging are still not entirely clear.
Some research has pointed to stem cells as targets for aging and senescence-associated functional decline. The adult mammalian brain contains stem cells that continuously generate new neurons that are important for cognition. The generation of new neurons in the hippocampus declines rapidly with age, and this decline is associated with reduced stem cell activity. This raises the possibility that age-dependent senescent cell accumulation may deregulate neural stem cells and thereby negatively impact brain function.
“Stem cells last throughout life and, like us, are subjected to the ravages of aging, environmental stressors, and deterioration of the machinery that enables them to function optimally,” Kaplan explains. “To survive, many stem cells revert to a dormant, unresponsive, and inactive state. Our goal was to wake up these dormant cells and, in doing so, enable them to carry out their biological functions that facilitate learning, memory, and brain repair.”
In the new study, Kaplan teamed up with Freda Miller and Paul Frankland (@Franklandlab) of SickKids to test the idea that increased senescence within the neural stem cell niche negatively impacts adult neurogenesis, focusing on the middle-aged mouse brain. They observed an aging-dependent accumulation of senescent cells, largely senescent stem cells, within the hippocampal stem cell niche coincident with declining adult neurogenesis. Pharmacological ablation of the senescent cells via a drug called ABT-263 caused a rapid increase in normal stem cell proliferation and neurogenesis, and genetic ablation of senescent cells similarly activated hippocampal stem cells.

Results of a large study led by UCLA Jonsson Comprehensive Cancer Center researchers could help guide treatment planning for patients with high-risk prostate cancer.
An international effort consisting of a consortium of 16 research centers in collaboration with two international cooperative trial groups found that patients receiving high-dose external beam radiation therapy alone may benefit from androgen deprivation therapy (ADT) lasting longer than 18 months, while those with external beam radiation therapy and a brachytherapy boost — the implantation of radioactive seeds to deliver a higher total dose to the prostate — may be optimally managed with 18 months of ADT or possibly less. Results are published in the Jan. 20 issue of JAMA Oncology.
“Adding androgen deprivation therapy to radiation therapy has been consistently shown to improve survival when treating men with high-risk prostate cancer. However, lowering testosterone levels is associated with a number of side effects, including not only a decrement in quality of life, but possibly more serious adverse events when longer durations are used. While it has long been hypothesized that by delivering extremely high doses of radiation, one might be able to shorten the required duration of ADT, this has never been proven,” said lead author Amar Kishan, MD, associate professor and vice chair of clinical and translational research in the Department of Radiation Oncology at UCLA and a researcher at the UCLA Jonsson Comprehensive Cancer Center.
The researchers analyzed individual patient data from three cohorts of patients: a retrospective cohort of patients from 16 cancer treatment referral centers between 2000 and 2014 who received either high-dose external beam radiotherapy or external beam radiotherapy with a brachytherapy boost; a cohort of patients enrolled in a randomized phase 3 trial that included patients from 23 treatment centers in Australia and New Zealand; and a cohort of patients enrolled in a randomized phase 3 trial conducted across 10 treatment centers in Spain. This is the only analysis to include both retrospective and prospective data in evaluating optimal ADT duration in high-risk prostate patients receiving these two forms of radiation therapy.
“Because of androgen deprivation therapy’s unpleasant side effects, it is often underutilized, with men receiving considerably shorter durations of ADT than might be recommended. To discern the ADT duration thresholds that provide the greatest metastasis-free survival benefit for these patients, we analyzed a multi-institutional database of patients, developed hypotheses, and then evaluated our findings by analyzing individual patient data from randomized trials,” said Kishan.
“The consistency of our results across multiple different patient cohorts greatly strengthens our findings,” said Tahmineh Romero, senior statistician in the UCLA Department of Medicine Statistics Core and the senior author of the article.
In the retrospective cohort — looking at ADT durations of less than six months, six to 18 months, and greater than 18 months — a significant interaction was seen between treatment type and ADT duration. A duration of 18 months or more was associated with improved outcomes, relative to shorter durations, for patients receiving high-dose external beam radiation therapy without a brachytherapy boost. In contrast, among patients receiving radiation therapy and brachytherapy, an ADT duration of at least six months but less than 18 months was associated with improved metastasis-free survival and overall survival, compared to receipt of less than six months of ADT. But there appeared to be no improvement in metastasis-free survival for those receiving both forms of radiation therapy and more than 18 months of ADT.
With further analysis, the researchers determined that for patients receiving radiation therapy without brachytherapy, the optimal ADT duration was 26.3 months; for those treated with radiation therapy and a brachytherapy boost, the minimum threshold was 12 months. Their hypotheses drawn from the retrospective study appeared to be supported by effects observed in the randomized clinical trials.
“Contrary to findings in a previous study, our results suggest that optimal duration of ADT for patients receiving high-dose radiation therapy may be more than 18 months. This is implied by findings from all the cohorts we analyzed. A secondary conclusion, based on the retrospective dataset, is that ADT duration shorter than 18 months may be sufficient for patients undergoing both radiation therapy and brachytherapy. Although current and future studies will continue to offer clarification, individual patient meta-analyses incorporating data from various trials may provide the best current guidance for doctors and patients. We have additional studies underway to explore this concept further,” said Kishan.

An oral supplement intended to stimulate a natural body process appears to promote muscle endurance and mitochondrial health in humans. New research suggests that the supplement, urolithin A, may help improve or prolong muscle activity in people who are aging or who have diseases that make exercise difficult.
The paper was published in JAMA Network Open.
“This is relevant both to people with chronic diseases and people who want to be more active later in life,” said the lead author, David Marcinek, a professor of radiology at the University of Washington School of Medicine. His research has focused on the role of mitochondria in aging and chronic disease.
Urolithin A is a byproduct of a person’s gut bacteria and a diet comprising polyphenols found in pomegranates, berries and nuts. Because diet, age, genetics and disease affect the makeup of the gut microbiome, people produce urolithin A at variable rates. The compound also is produced and sold by dietary supplement companies.
Supplemental urolithin A has been shown in animal tests and molecular studies of humans to stimulate mitophagy, a process that Marcinek explained as “mitochondrial quality control.”
“Mitochondria are like batteries that power the cells in your body,” he said. “But over time they break down. The process of mitophagy recognizes this failure and proactively tears down the mitochondria, reducing it to elemental components that a cell can reuse. But with aging, mitophagy becomes less efficient and your body accumulates this pool of failing mitochondria. It’s one way that muscles become less functional as we age.”
The researchers studied a small cohort of people over age 65 who were randomized to receive a placebo or a daily supplement of 1,000 mg urolithin A for four months. Each of the 66 subjects was confirmed at the outset to have average or subpar capacity to produce adenosine triphosphate (ATP), which mitochondria produce to help cells perform myriad functions.

A team of researchers from Charité — Universitätsmedizin Berlin has identified a neural network which is responsible for generating tic disorders. Targeting of this network via deep brain stimulation delivered by a pacemaker-like device has resulted in the alleviation of symptoms in people with Tourette syndrome. The researchers’ findings, which have been published in Brain, could serve as a basis for improving the treatment of people with severe tic disorders.
Tics usually manifest as fast movements or sounds which occur suddenly, in quick succession, and without any obvious contextual embedment. Motor tics include rapid eye blinking or head jerking; vocal tics include throat clearing and whistling. Tic disorders are often associated with additional behavioral symptoms such as anxiety, obsessive-compulsive disorders, ADHD and depression, and can therefore often lead to social isolation. One of the most widely known tic disorders is Tourette syndrome, which describes individuals who have both motor and vocal tics. Tics usually first appear during childhood. Estimates suggest that up to four percent of children are affected by tics and that approximately one percent of children meet the diagnostic criteria for Tourette syndrome. In many (but not all) cases, symptoms become milder as children reach adulthood.
Little is known about the way in which tics are generated inside the brain. “Over the past few years, neuroscientists have identified a number of different areas in the brain which are involved in tic generation,” says last author Dr. Andreas Horn, who leads an Emmy Noether Junior Research Group dedicated to the study of network-based brain stimulation. This Group is located at the Department of Neurology with Experimental Neurology on Campus Charité Mitte, with additional sites at Massachusetts General Hospital and Brigham and Women’s Hospital, two hospitals associated with Harvard Medical School. He explains: “Despite these recent breakthroughs, however, some important questions have remained unanswered. Which of these brain regions are responsible for generating tics? Which of them become active in order to compensate for faulty processes? We have now been able to show that it is not a single brain region which is responsible for generating tics. Rather, tics are caused by a network comprising different areas of the brain.”
The team of researchers started by consulting published case reports on patients with an extremely rare cause of tic disorder: brain injury following conditions such as stroke or trauma. In these individuals, the tics observed are the direct result of lesions within a specific area of the brain. Having identified at total of 22 such cases in the literature, the researchers then produced a detailed map of the brain areas containing the lesions and any other areas of the brain normally connected to them via nerve fibers. For this ‘connectivity analysis’, the researchers used a map describing the connectivity patterns found within the average human brain. This map was the result of years of development work conducted by the Department of Neurology with Experimental Neurology in collaboration with Harvard Medical School and was based on the brain scans of more than 1,000 healthy individuals.
The researchers were able to show that nearly all of the patients’ brain lesions — irrespective of their precise location within the brain — formed part of a common neural network comprising a wide range of areas, including the insular cortex, cingulate gyrus, striatum, globus pallidus internus, thalamus, and cerebellum. One of the study’s first authors, Bassam Al-Fatly of the Department of Neurology with Experimental Neurology, explains: “These structures are distributed almost across the entire brain and have a wide range of functions, from motor control to the processing of emotions. They have all been discussed as potential causes for tics in the past but, until now, we had no clear evidence available and no knowledge of a direct link between these structures. We now know that these brain regions form a network and that they may in fact cause tic disorders.”
The fact that this newly identified neural network is also of relevance to the treatment of ‘classic’ tics was demonstrated by analyzing data on 30 patients with Tourette syndrome, each of whom had received pacemaker-like devices whose electrodes had been placed in different areas of the brain. This type of deep brain stimulation (DBS) is currently only used in particularly severe cases, where behavioral interventions and medication have failed to achieve adequate results. For each of the 30 Tourette patients, the Berlin-based team of researchers determined the precise locations of the DBS device’s electrodes within the brain and whether they had been stimulating the tic-inducing neural network. Symptom improvement was found to be most pronounced in individuals whose electrodes produced the greatest degree of stimulation of the tic-inducing network.
“The benefit for people with severe tic disorders appears to be greatest when deep brain stimulation targets the tic-inducing network,” says the study’s first author, PD Dr. Christos Ganos, senior physician in charge of the Tic Disorders Outpatient Unit at the Department of Neurology with Experimental Neurology. Emphasizing the significance of the research, PD Dr. Ganos, who holds a Freigeist Fellowship from the Volkswagen Foundation, says: “By taking the tic-inducing network into account when placing brain-stimulating devices, we will ensure that these findings inform the ways in which we treat our patients. We hope that this will enable us to better alleviate the burden of those affected, enabling them to lead largely independent and socially active lives.”

Faulty DNA damage repair can lead to many types of cancer, neurodegenerative diseases, and other serious disorders. Investigators have developed high-throughput microscopy and machine learning systems that can identify and classify DNA repair factors. The investigators have identified nine previously unknown factors involved in the process of cellular DNA repair.
The DNA that lies tightly coiled in nearly every human cell is subjected to thousands of insults and injuries from within and without daily, which is why the human body has evolved multiple highly effective mechanisms for repairing DNA damage.
“We have in place exquisite mechanisms to repair DNA breaks, and when those fail, we end up with disease. We accumulate genomic instability, we accumulate mutations, and many diseases happen because of the inability of cells to repair DNA,” says Raul Mostoslavsky, MD, PhD, scientific co-director of the MGH Cancer Center and the Laurel Schwartz Professor of Oncology (Medicine) at Harvard Medical School.
DNA damage repair is a double-edged sword: When it goes awry, it can lead to diseases such as cancer and degenerative motor disorders, but it can also be exploited to treat many forms of cancer using drugs that interfere with DNA’s ability to fix itself, thereby causing cancerous cells to stop replicating and die.
Previous studies of DNA repair mechanisms were performed using systems developed by biochemists to purify proteins, but these systems have relatively low yields or “throughput,” Mostoslavsky explains.
“We decided to develop a high-throughput assay to try to identify repair factors in a more unbiased way. We ended up developing a unique microscope-based automatic system to generate DNA damage and to collect information on proteins that are recruited to these types of damage,” he says.
With co-investigators at the National Cancer Research Center in Madrid and at other centers in the U.S., Canada and China, Mostoslavsky and colleagues at MGH and Harvard have developed a highly sensitive method for visualizing DNA repair mechanisms at work. Using the technique, they have identified nine new proteins that are involved in DNA repair, a finding that can help researchers develop new cancer drugs, as well as methods for improving the effectiveness of existing therapies.
They describe their technique — a combination of high-throughput microscopy and machine learning — in the journal Cell Reports.
The investigators first developed a high-throughput microscopy test to analyze how proteins are attracted to or excluded from double-strand DNA breaks. With this system they generated a library of 384 mostly unknown factors and were able to identify which of these proteins are called into action when DNA damage occurs.
They then performed a proof-of-principle study, following one specific factor labeled PHF20 that is kept away from the site of DNA damage, and discovered that PHF20 is excluded because it can interfere with recruitment of another critical DNA repair factor labeled 53BP1.
The systems Mostoslavsky and colleagues developed could, for example, help improve the treatment of breast and ovarian cancers caused by mutations in the cancer susceptibility genes BRCA1 and BRCA2. These cancers are treated with a class of drugs known as PARP inhibitors that work by inhibiting a particular DNA repair factor.
The work is supported by MGH, the National Institutes of Health, the Spanish Ministry of Science and Innovation, the Carlos III Institute of Health, the Marie Curie COFUND FP7, European Research Council, and the Natural Sciences and Engineering Research Council of Canada.
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A greater adherence to the Mediterranean diet which had been assessed through an index made with biomarkers during a 20-year scientific monitoring is associated with a lower mortality in adults over 65. This is one of the main conclusions of a study led by Cristina Andrés-Lacueva, head of the Research Group on Biomarkers and Nutritional & Food Metabolomics of the Faculty of Pharmacy and Food Sciences of the University of Barcelona (UB) and the CIBER on Fragility and Healthy Ageing (CIBERFES), also formed by the Food Innovation Network of Catalonia (XIA).
he paper, published in the journal BCM Medicine, has been carried out in collaboration with the National Institute on Ageing (NIA) of the United States. According to the conclusions, the analysis of dietary biomarkers in plasma and urine can contribute to the individualized food assessment for old people. The study is based on the InCHIANTI project, conducted in the region of the Italian Tuscany, a study that has been carried out during twenty years in a total of 642 participants (56% women) aged over 65 or more and which enabled researchers to obtain complete data on food biomarkers.
As stated by the UB Professor Cristina Andrés-Lacueva, head of the research group in CIBERFES, “we develop an index of dietary biomarkers based on food groups that are part of the Mediterranean diet, and we assess their association with mortality.”
In the study, researchers chose the reference levels of the following dietary biomarkers in the urine: total polyphenols and resveratrol metabolites (from grape intake) and presents in plasma, plasma carotenoids, selenium, vitamin B12, fatty acids and their proportion of monounsaturated and saturated fatty acids. Using a predictive model, they assessed the associations of the Mediterranean diet index and the food-frequency questionnaire (FFQ) with mortality.
During the twenty years of monitoring, there were 425 deaths (139 due to cardiovascular diseases and 89 due to cancer-related causes). Once the models were analysed, the score of the Mediterranean diet using the biomarkers was inversely associated with all causes of death.
This study highlights the use of dietary biomarkers to improve the nutritional assessment and guide a customized assessment for older people. As noted by the CIBERFES researcher of the UB Tomás Meroño, co-first signatory of the study, the researchers “confirm that an adherence to the Mediterranean diet assessed by a panel of dietary biomarkers is inversely associated with the long-term mortality in older adults, which supports the use of these biomarkers in monitoring evaluations to study the health benefits associated with the Mediterranean diet.”
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The Centers for Disease Control and Prevention estimates that more than 2.8 million Americans experience antibiotic-resistant infections each year; more than 35,000 die from those infections.
To address this critical and worldwide public health issue, a team of researchers led by Hongjun (Henry) Liang, Ph.D., from the Texas Tech University Health Sciences Center (TTUHSC) Department of Cell Physiology and Molecular Biophysics, recently investigated whether or not a series of novel nanoparticles can kill some of the pathogens that lead to human infection without affecting healthy cells.
The study, “Hydrophilic Nanoparticles that Kill Bacteria while Sparing Mammalian Cells Reveal the Antibiotic Role of Nanostructures,” was published Jan. 11 by Nature Communications. Other study members of the Liang team, all from TTUHSC, included Yunjiang Jiang, Ph.D., Wan Zheng, Ph.D., Keith Tran, Elizabeth Kamilar, Jitender Bariwal, Ph.D., and Hairong Ma, Ph.D.
Past research has shown that hydrophobicity (a molecule’s ability to repel water) and hydrophilicity (a molecule’s ability to attract and dissolve in water) affects cells; the more hydrophobic a substance is, the more adverse the reaction it will cause. However, Liang said, there is no quantitative standard for how much hydrophobicity is acceptable.
“Basically, you can kill bacteria when you increase hydrophobicity,” Liang said. “But it will also kill healthy cells, and we don’t want that.”
For their study, the Liang team used novel hydrophilic nanoparticles known as nanoantibiotics that were developed by Liang’s laboratory. Structurally speaking, these novel nanoantibiotics resemble tiny hairy spheres, each composed of many hydrophilic polymer brushes grafted onto silica nanoparticles of different sizes.
These synthetic compounds, which Liang’s lab produces, are designed to kill bacteria via membrane disruptions like antimicrobial peptides do, but through a different mode of membrane remodeling that damages bacterial membranes and not mammalian cells. Antimicrobial peptides are a diverse class of amphipathic molecules (partially hydrophilic-partially hydrophobic), which occur naturally and serve as the first line of defense for all multicellular organisms. The direct use of antimicrobial peptides as antibiotics is limited by their stability and toxicity.
There have been other studies in which researchers grafted amphipathic molecules onto nanoparticles, and they too kill bacteria. However, Liang said the primary issue in using amphipathic molecules is that it becomes very difficult to strike the right balance between their hydrophobicity and hydrophilicity so that the toxicity of these molecules to our own cells is significantly reduced.
“In our case, we remove that uncertainty from the equation because we started with a hydrophilic polymer,” Liang pointed out. “The cytotoxicity of hydrophobic moieties is not a concern anymore. Those hydrophilic polymers by themselves, or the silica nanoparticles alone don’t kill bacteria; they have to be grafted onto the nanostructure to be able to kill bacteria. And so, this is the first important discovery.”
The Liang team also discovered that the degree of antibiotic activity is affected by the size of the hairy spheres, which according to Liang is the second important discovery of this research. Those measuring 50 nanometers and below appear to be much more active than those whose size exceeds 50 nanometers. Liang said those measuring approximately 10 nanometers appear to be the most active. (Using synchrotron small angle x-ray scattering and other methods, the Liang team is able to interpret the molecular mechanism of the size-dependent antibiotic activity.)
These discoveries are important because using nanoantibiotics to kill bacteria evades all known mechanisms of bacterial resistance unless bacteria completely revamp their pathways for making cell membranes, which Liang said is unlikely.
“It is also nearly impossible for bacteria to develop new resistance against the nanoantibiotics,” Liang emphasized. “Furthermore, this discovery illuminates a blueprint to develop new antibiotics that would kill bacteria upon contact, but remain amiable to humans because they are produced using non-toxic and environmentally friendly ingredients via nanoengineering.”