Processed diets, which are low in fiber, may initially reduce the incidence of foodborne infectious diseases such as E. coli infections, but might also increase the incidence of diseases characterized by low-grade chronic infection and inflammation such as diabetes, according to researchers in the Institute for Biomedical Sciences at Georgia State University.
This study used mice to investigate how changing from a grain-based diet to a highly processed, high-fat Western style diet impacts infection with the pathogen Citrobacter rodentium, which resembles Escherichia coli (E. coli) infections in humans. The findings are published in the journal PLOS Pathogens.
Gut microbiota, the microorganisms living in the intestine, provide a number of benefits, such as protecting a host from infection by bacterial pathogens. These microorganisms are influenced by a variety of environmental factors, especially diet, and rely heavily on complex carbohydrates such as fiber.
The Western-style diet, which contains high amounts of processed foods, red meat, high-fat dairy products, high-sugar foods and pre-packaged foods, lacks fiber, which is needed to support gut microbiota. Changes in dietary habits, especially a lack of fiber, are believed to have contributed to increased prevalence of chronic inflammatory diseases such as inflammatory bowel disease, metabolic syndrome and cancer.
In this study, the researchers found switching mice from a standard grain-based rodent chow to a high-fat, low-fiber Western-style diet resulted in a rapid reduction in the number of gut bacteria. Mice fed the Western-style diet were frequently unable to clear the pathogen Citrobacter rodentium from the colon. They were also prone to developing chronic infection when re-challenged by this pathogen.
The researchers conclude the Western-style diet reduces the numbers of gut bacteria and promotes encroachment of microbiota into the intestine, potentially influencing immune system readiness and the body’s defense against pathogenic bacteria.
“We observed that feeding mice a Western-style diet, rather than standard rodent grain-based chow, altered the dynamics of Citrobacter infection, reducing initial colonization and inflammation, which was surprising. However, mice consuming the Western-style diet frequently developed persistent infection that was associated with low-grade inflammation and insulin resistance,” said Dr. Andrew Gewirtz, senior co-author of the study and professor in the Institute for Biomedical Sciences. “These studies demonstrate potential of altering microbiota and their metabolites by diet to impact the course and consequence of infection following exposure to a gut pathogen.”
“We speculate that reshaping gut microbiota by nutrients that promote beneficial bacteria that out-compete pathogens may be a means of broadly promoting health,” said Dr. Jun Zou, senior co-author of the study and assistant professor in the Institute for Biomedical Sciences at Georgia State.
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Researchers at the University of Bath investigating how virtual reality (VR) can help improve balance believe this technology could be a valuable tool in the prevention of falls.
As people grow older, losing balance and falling becomes more common, which increases the risk of injury and affects the person’s independence.
Falls are the leading cause of non-fatal injuries in over 65-yearolds and account for over 4 million bed days per year in England alone, at an estimated cost of £2 billion.
Humans use three ways of keeping their balance: vision, proprioceptive (physical feedback from muscles and joints) and vestibular system (feedback from semi-circular canals in the ear). Of these, vision is the most important.
Traditional ways of assessing balance include patient surveys and physical tests such as using a treadmill or testing agility when performing specific movements or exercises.
However, the accuracy of these tests can be affected by age, sex and motivation, and the movements measured aren’t necessarily reflective of real-life scenarios.

It’s well established that infectious disease is the greatest threat to the endangered chimpanzees made famous by the field studies of Jane Goodall at Gombe National Park in Tanzania. Now, new research led by scientists at Emory University shows that nearly half of the fecal samples from wild chimpanzees contain bacteria that is resistant to a major class of antibiotics commonly used by people in the vicinity of the park.
The journal Pathogens published the findings.
“Our results suggest that antibiotic-resistant bacteria is actually spreading from people to non-human primates by making its way into the local watershed,” says Thomas Gillespie, senior author of the study and associate professor in Emory’s Department of Environmental Sciences and Rollins School of Public Health. “People are bathing and washing in the streams, contaminating the water with drug-resistant bacteria where wild chimpanzees and baboons drink.”
The researchers tested for genes conferring resistance to sulfonamides — drugs often used by people in the region to treat diarrheal diseases — in fecal samples from humans, domestic animals, chimpanzees and baboons in and around Gombe National Park. They also tested stream water used by these groups.
Sulfonamide resistance appeared in 74 percent of the human samples overall, 48 percent of chimpanzee samples, 34 percent of baboon samples, and 17 percent of the domestic animal samples. Sulfonamide also showed up in 19 percent of the samples taken from streams shared by people, domestic animals and wildlife.
The researchers also tested all the groups in the study for genes conferring resistance to tetracycline — another class of antibiotics that is used much less frequently by people in the vicinity, likely due to its greater expense and the fact that it is less available in the area. As expected, very few of the fecal samples from any of the groups, and none of the water samples from the streams, showed evidence of tetracycline resistance.

Psychedelic drugs have shown promise for treating neuropsychiatric disorders such as depression and posttraumatic stress disorder. However, due to their hallucinatory side effects, some researchers are trying to identify drugs that could offer the benefits of psychedelics without causing hallucinations. In the journal Cell on April 28, researchers report they have identified one such drug through the development of a genetically encoded fluorescent sensor — called psychLight — that can screen for hallucinogenic potential by indicating when a compound activates the serotonin 2A receptor.
“Serotonin reuptake inhibitors have long been used for treating depression, but we don’t know much about their mechanism. It’s like a black box,” says senior author Lin Tian (@LinTianLab), an associate professor in the Department of Biochemistry and Molecular Medicine in the School of Medicine at the University of California, Davis. “This sensor allows us to image serotonin dynamics in real time when animals learn or are stressed and visualize the interaction between the compound of interest and the receptor in real time.”
Tian’s lab joined forces with the lab of David E. Olson, an assistant professor in the Department of Chemistry at UC Davis, whose lab is focused on drug discovery. “This paper was an exceptionally collaborative effort,” says Olson, a co-author on the study. “My lab is really interested in the serotonin 2A receptor, which is the target of both psychedelic drugs and classic antipsychotics. Lin’s lab is a leader in developing sensors for neuromodulators like serotonin. It just made perfect sense for us to tackle this problem together.”
Experts believe that one of the benefits of using psychedelic drugs over existing drugs is that they appear to promote neural plasticity — essentially allowing the brain to rewire itself. If proven effective, this approach could lead to a drug that works in a single dose or a small number of doses, rather than having to be taken indefinitely. But one thing that researchers don’t know is whether patients would be able to gain the full benefit of neural plasticity without undergoing the “psychedelic trip” part of the treatment.
In the paper, the investigators report that they used psychLight to identify a compound called AAZ-A-154, a previously unstudied molecule that has the potential to act on beneficial pathways in the brain without hallucinogenic effects. “One of the problems with psychedelic therapies is that they require close guidance and supervision from a medical team,” Olson says. “A drug that doesn’t cause hallucinations could be taken at home.”
The serotonin 2A receptor, also known as 5-HT2AR, belongs to a class of receptors called G protein-coupled receptors (GPCRs). “More than one-third of all FDA-approved drugs target GPCRs, so this sensor technology has broad implications for drug development,” Tian says. “The special funding mechanisms of BRAIN Initiative from the National Institutes of Health allowed us to take a risky and radical approach to developing this technology, which could open the door to discovering better drugs without side effects and studying neurochemical signaling in the brain.”
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A multidecade study of young adults living in the United Kingdom has found higher rates of mental illness symptoms among those exposed to higher levels of traffic-related air pollutants, particularly nitrogen oxides, during childhood and adolescence.
Previous studies have identified a link between air pollution and the risk of specific mental disorders, including depression and anxiety, but this study looked at changes in mental health that span all forms of disorder and psychological distress associated with exposure to traffic-related air pollutants.
The findings, which will appear April 28 in JAMA Network Open, reveal that the greater an individual’s exposure to nitrogen oxides across childhood and adolescence, the more likely they are to show any signs of mental illness at the transition to adulthood, at age 18, when most symptoms of mental illness have emerged or begin to emerge.
The link between air pollution exposure and young adult mental illness symptoms is modest, according to the study’s first-author Aaron Reuben, a graduate student in clinical psychology at Duke University. But “because harmful exposures are so widespread around the world, outdoor air pollutants could be a significant contributor to the global burden of psychiatric disease,” he said.
The World Health Organization (WHO) currently estimates that 9 out of 10 people worldwide are exposed to high levels of outdoor air pollutants, which are emitted during fossil fuel combustion in cars, trucks, and powerplants, and by many manufacturing, waste-disposal, and industrial processes.
In this study, air pollution, a neurotoxicant, was found to be a weaker risk factor for mental illness than other better-known risks, such as family history of mental illness, but was of equal strength to other neurotoxicants known to harm mental health, particularly childhood exposure to lead.

Experimental Alzheimer’s drugs have shown little success in slowing declines in memory and thinking, leaving scientists searching for explanations. But new research in mice has shown that some investigational Alzheimer’s therapies are more effective when paired with a treatment geared toward improving drainage of fluid — and debris — from the brain, according to a study led by researchers at Washington University School of Medicine in St. Louis.
The findings, published April 28 in the journal Nature, suggest that the brain’s drainage system — known as the meningeal lymphatics — plays a pivotal but underappreciated role in neurodegenerative disease, and that repairing faulty drains could be a key to unlocking the potential of certain Alzheimer’s therapies.
“The lymphatics are a sink,” said co-senior author Jonathan Kipnis, PhD, the Alan A. and Edith L. Wolff Distinguished Professor of Pathology & Immunology and a BJC Investigator. “Alzheimer’s and other neurodegenerative diseases such as Parkinson’s and frontotemporal dementia are characterized by protein aggregation in the brain. If you break up these aggregates but you have no way to get rid of the debris because your sink is clogged, you didn’t accomplish much. You have to unclog the sink to really solve the problem.”
Sticky plaques of the protein amyloid start forming in the brains of people with Alzheimer’s two decades or more before symptoms such as forgetfulness and confusion arise. For years, scientists have tried to treat Alzheimer’s by developing therapies that clear away such plaques but have had very limited success. One of the most promising candidates, aducanumab, recently proved effective at slowing cognitive decline in one clinical trial but failed in another, leaving scientists baffled.
Kipnis, who is also a professor of neurosurgery, of neurology and of neuroscience, identified meningeal lymphatics as the brain’s drainage system in 2015. A few years later, in 2018, he demonstrated that damage to the system increases amyloid buildup in mice. He suspects that the mixed and often disappointing performance of anti-amyloid drugs can be explained by differences in lymphatic function among Alzheimer’s patients. But proving this hunch has been challenging, as there are no tools to measure the health of a person’s meningeal lymphatics directly.
In this study, Kipnis and colleagues took an indirect approach to checking the drainage system in the brains of Alzheimer’s patients. The study was undertaken in collaboration with biotherapeutics company PureTech Health.

It is not every day that scientists come across a phenomenon so fundamental that it is observed across fruit flies, rodents and humans.
In a paper published today in Aging Cell, neuroscientists from the University of Pittsburgh Schools of the Health Sciences discovered that a single protein — a glutamate transporter on the membrane of vesicles that carry dopamine in neurons — is key to regulating sex differences in the brain’s vulnerability to age-related neuron loss.
The protein — named VGLUT — was more abundant in dopamine neurons of female fruit flies, rodents and human beings than in males, correlating with females’ greater resilience to age-related neuron loss and mobility deficiencies, the researchers found. Excitingly, genetically reducing VGLUT levels in female flies diminished their protection from neurodegeneration associated with aging, suggesting that VGLUT could be a new target for prolonging dopamine neuron resilience and delaying the onset of symptoms of aging in the brain.
“From flies to rodents to human beings, we found that VGLUT levels distinguish males from females during healthy aging,” said senior author Zachary Freyberg, M.D., Ph.D., assistant professor of psychiatry and cell biology at Pitt. “The fact that this marker of dopamine neuron survival is conserved across the animal kingdom suggests that we are looking at a fundamental piece of biology. Understanding how this mechanism works can help prolong dopamine neuron resilience and delay aging.”
Neurodegenerative disorders such as Parkinson’s disease are more likely to develop as we age. Parkinson’s disease — a slow but relentless loss of dopamine neurons in the brain that impairs one’s ability to move or talk — is known to predominantly affect men. But while biological sex differences, which arise from a combination of hormonal, genetic and environmental influences, seem to explain why females are protected from early stages of Parkinson’s, the driver and regulator of these protections was, until now, unknown.
Using a combination of biochemical and genetic techniques, as well as behavioral studies where flies’ locomotion was monitored for a 24-hour period, researchers found that age-related benefits afforded to females disappeared when the levels of VGLUT gene expression were significantly reduced in dopamine neurons.
“We found that VGLUT expression increases with age, and that flies become more vulnerable to dopamine neuron degeneration when we knock down VGLUT,” said lead author Silas Buck, a Ph.D. candidate at the Pitt Center for Neuroscience. “We also found that VGLUT expression is higher in females than males, suggesting that VGLUT may play a role in regulating sex differences in vulnerability to neurodegeneration in Parkinson’s and other neurological disorders where females are more resilient than males.”
As the rates of Parkinson’s disease are rapidly rising — the number of people affected by the illness worldwide is projected to reach 20 million by 2040 — Pitt scientists hope to further probe the role of VGLUT in neuroprotection in humans.
“We are entering an epidemic of Parkinson’s disease, and we need to understand how to make our neurons more resilient,” said Freyberg. “VGLUT is a tantalizing new target that is key to not only understanding the fundamental biology at the core of dopamine neurons’ survival, but ultimately for developing new therapeutics.”
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For the first time, scientists are able to study changes in the DNA of any human tissue, following the resolution of long-standing technical challenges by scientists at the Wellcome Sanger Institute. The new method, called nanorate sequencing (NanoSeq), makes it possible to study how genetic changes occur in human tissues with unprecedented accuracy.
The study, published today (28 April) in Nature, represents a major advance for research into cancer and ageing. Using NanoSeq to study samples of blood, colon, brain and muscle, the research also challenges the idea that cell division is the main mechanism driving genetic changes. The new method is also expected to allow researchers to study the effect of carcinogens on healthy cells, and to do so more easily and on a much larger scale than has been possible up until now.
The tissues in our body are composed of dividing and non-dividing cells. Stem cells renew themselves throughout our lifetimes and are responsible for supplying non-dividing cells to keep the body running. The vast majority of cells in our bodies are non-dividing or divide only rarely. They include granulocytes in our blood, which are produced in the billions every day and live for a very short time, or neurons in our brain, which live for much longer.
Genetic changes, known as somatic mutations, occur in our cells as we age. This is a natural process, with cells acquiring around 15-40 mutations per year. Most of these mutations will be harmless, but some of them can start a cell on the path to cancer.
Since the advent of genome sequencing in the late twentieth century, cancer researchers have been able to better understand the formation of cancers and how to treat them by studying somatic mutations in tumour DNA. In recent years, new technologies have also enabled scientists to study mutations in stem cells taken from healthy tissue.
But until now, genome sequencing has not been accurate enough to study new mutations in non-dividing cells, meaning that somatic mutation in the vast majority of our cells has been impossible to observe accurately.

Researchers from the Universities of Bristol and Surrey have found that well-fitting, three-layered cloth masks can be as effective at reducing the transmission of COVID-19 as surgical masks.
At the height of the COVID-19 pandemic, 139 countries mandated the use of face coverings in public space such as supermarkets and public transports. The World Health Organization also advises the use of face coverings and offers guidance on their effective features. Face coverings suppress the onward transmission of COVID-19 through exhalation and protect the wearer on inhalation.
In a paper published by the Physics of Fluids journal, the researchers detail how they looked at how liquid droplets are captured and filtered out in cloth masks by reviewing and modelling filtration processes, including inertial impaction.
Inertial impaction does not filter as a sieve or colander does — it works by forcing the air in your breath to twist and turn inside the mask so much that the droplets can’t follow the path of the air. Instead, the droplets crash into fibres inside the mask to prevent inhalation.
The team found that, under ideal conditions and dependent on the fit, three-layered cloth masks can perform similarly to surgical masks for filtering droplets — with both reducing exposure by around 50 to 75 per cent. For example, if an infected person and a healthy individual are both wearing masks, scientists believe this could result in up to 94 per cent less exposure.
Dr Richard Sear, co-author of the study and Leader of the Soft Matter Group at the University of Surrey, said:
“While wearing a simple and relatively inexpensive cloth face mask cannot eliminate the risk of contracting COVID-19, measurements and our theoretical model suggests they are highly effective in reducing transmission. We hope that our work inspires mask designs to be optimised in the future and we hope it helps to remind people of the importance of continuing to wear masks while COVID-19 remains present in the community.”
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Parkinson’s disease (PD) is characterized by slowness of movement and tremors, which often appear asymmetrically in patients. The new model of PD described in this review article published in the Journal of Parkinson’s Disease may explain these perplexing asymmetrical motor symptoms and other known variations such as different degrees of constipation and sleep disorders.
PD is a heterogenous disorder. Symptoms and the speed with which symptoms progress vary greatly among patients. In three-quarters of patients, motor symptoms initially appear in one side of the body. Some patients develop constipation, loss of smell, sleep disorders, and other symptoms several years before diagnosis, but others do not. Although it is possible to define several subtypes of PD characterized by similar constellations of symptoms, the underlying causes of these differences are poorly understood. Aggregation and neuron-to-neuron spread of the protein alpha-synuclein is thought to be involved.
The alpha-synuclein Origin and Connectome (SOC) model presented by Per Borghammer, MD, PhD, DMSc, Department of Nuclear Medicine & PET, Aarhus University Hospital, Aarhus, Denmark, proposes a unifying model, which may explain much of this variation among patients. The SOC model is fundamentally based on two ideas: the location or origin of the first alpha-synuclein aggregates, and the importance played by the neural connectome in transmitting the alpha-synuclein pathology to other parts of the nervous system.
This model was developed by integrating already available evidence from clinical and imaging studies of patients, animal models of PD, and postmortem findings in brain tissue from PD patients. This unifying model seems capable of explaining why PD is often an asymmetric disease in the first place, but also why some patients show more asymmetry than others and some no asymmetry at all. It also explains why certain subtypes of PD seem to exist, including why constipation and sleep disorders emerge prior to diagnosis only in some patients.
“Imaging studies of living PD patients and studies of biopsies and gut and brain tissue from biobanks clearly suggest that PD patients display different profiles of neuronal damage,” explained Dr. Borghammer. “In some patients, the brain is damaged before the peripheral nervous system, and in others the opposite pattern is seen. This new model, which is an extended version of the body-first versus brain-first hypothesis we described in this journal in 2019, proposes a simple explanation for motor asymmetry, while simultaneously offering explanations for several other unexplained phenomena in PD.”
The model postulates that the first instance of pathological alpha-synuclein typically starts in a single location, and then spreads from this origin site using permissible neural connections. The origin site can occur in the enteric nervous system of the gut, leading to a body-first subtype of PD. This type is characterized by early symptoms from gut and other peripheral organs and also sleep symptoms stemming from the lower parts of the brainstem.