Publisher Health

Blue light kills both dried cells and biofilms of the pathogen Listeria monocytogenes, a frequent contaminant of food processing facilities. Demise of L. monocytogenes occurred quickest when cells or biofilms were placed on polystyrene, a widely used, transparent form of plastic. The research is published in Applied and Environmental Microbiology, a journal of the American Society for Microbiology.
“These results contribute to advancing our understanding of the potential of blue light to treat inert surfaces contaminated with L. monocytogenes,” said corresponding author Francisco Diez-Gonzalez, Ph.D., Director and Professor, Center for Food Safety, University of Georgia. Although biofilms of pathogens are generally powerfully resistant to being exterminated, the results suggest that blue light could effectively destroy L. monocytogenes.
In the study, the investigators deposited liquid suspensions of mixtures of 5 strains of L. monocytogenes on small, sterile rectangular plates made of 6 different materials, including polystyrene, stainless steel and silicone rubber, which were then allowed to dry. The investigators also used similar plates to grow biofilms, which they also allowed to dry.
Then, they shined blue light onto the biofilms and onto the dried suspensions of cells on the plates to determine the most effective combinations of doses and wavelengths, as well as the most effective surfaces on which to extirpate the pathogens.
“The application of blue light for controlling microbial contamination has the potential to offer an additional technology that could complement existing methods for disinfecting surfaces in contact with foods,” said Diez-Gonzalez, noting that blue light has been used for disinfection in hospitals. As compared to ultraviolet light, blue light offers reduced risk for the user, he said.
A post-doc in Diez-Gonzalez’ laboratory, Fereidoun Forghani, Ph.D., kick-started the investigation when — searching for new ideas — he came across the use of blue light as a potential antimicrobial intervention to sanitize surfaces. Forghani built some blue light prototypes and produced the first preliminary results treating pure cultures of Listeria.

Schizophrenia, a neurodevelopmental disorder that features psychosis among its symptoms, is thought to arise from disorganization in brain connectivity and functional integration. Now, a new study in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, published by Elsevier, finds differences in functional brain connectivity in people with and without psychosis and schizophrenia that could help researchers understand the neural underpinnings of this disease.
The brain’s cortex is organized in a hierarchical fashion, anchored by the sensorimotor cortex at one end and by multimodal association areas at the other, with the task of integrating incoming sensory information with internal and external sensory signals. The loss of executive control in schizophrenia may stem from disruption of this hierarchical signaling.
Alexander Holmes, a PhD candidate at Monash University who led the study, said, “We used brain imaging and novel mathematical techniques to investigate the hierarchical organization of the brains of individuals with early psychosis and established schizophrenia. This organization is important for brain health, as it regulates how we can effectively respond to and process stimuli from the external world.”
The researchers used resting-state functional magnetic resonance imaging (fMRI) to measure gradients, an estimate of inter-regional functional coupling. Previous work had suggested that the primary sensory-fugal gradient was disrupted with schizophrenia, but the current study showed instead that secondary processing of the sensorimotor-visual gradient was affected in people with the disease.
Holmes added, “We found that the organizational pattern that differentiates visual and sensorimotor pathways is significantly impaired in individuals with schizophrenia but not in individuals with early psychosis. We then found that this impairment explains behavioral and clinical symptoms of schizophrenia. Our results highlight that changes in brain organization provide valuable insights into the mechanisms of schizophrenia, helping us better understand the disease and how it progresses.”
Cameron Carter, MD, Editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, said of the work, “These new approaches to test mathematical models of the organization of circuits in the human brain are beginning to reveal the nature of the disruption of neural integration that underlies psychotic symptoms in people with schizophrenia. Targeting these changes offers a new approach to how we think about developing treatments for this often difficult to treat illness.”

The NewsA team of scientists is proposing a new explanation for some cases of long Covid, based on their findings that serotonin levels were lower in people with the complex condition.In their study, published on Monday in the journal Cell, researchers at the University of Pennsylvania suggest that serotonin reduction is triggered by remnants of the virus lingering in the gut. Depleted serotonin could especially explain memory problems and some neurological and cognitive symptoms of long Covid, they say.A colored transmission electron micrograph showing an intestinal endocrine cell, with granules containing serotonin in green.Steve Gschmeissner/Science SourceWhy It Matters: New ways to diagnose and treat long Covid.This is one of several new studies documenting distinct biological changes in the bodies of people with long Covid — offering important discoveries for a condition that takes many forms and often does not register on standard diagnostic tools like X-rays.The research could point the way toward possible treatments, including medications that boost serotonin. And the authors said the biological pathway that their research outlines could unite many of the major theories of what causes long Covid: lingering remnants of the virus, inflammation, increased blood clotting and dysfunction of the autonomic nervous system.“All these different hypotheses might be connected through the serotonin pathway,” said Christoph Thaiss, a lead author of the study and an assistant professor of microbiology at the Perelman School of Medicine at the University of Pennsylvania.“Second of all, even if not everybody experiences difficulties in the serotonin pathway, at least a subset might respond to therapies that activate this pathway,” he said.“This is an excellent study that identifies lower levels of circulating serotonin as a mechanism for long Covid,” said Akiko Iwasaki, an immunologist at Yale University. Her team and colleagues at the Icahn School of Medicine at Mount Sinai recently published a study that identified other biological changes linked to some cases of long Covid, including levels of the hormone cortisol. These studies could point to specific subtypes of long Covid or different biological indicators at different points in the condition.The Back Story: A series of disruptions set off by bits of virus in the gut.Researchers analyzed the blood of 58 patients who had been experiencing long Covid for between three months and 22 months since their infection. Those results were compared to blood analysis of 30 people with no post-Covid symptoms and 60 patients who were in the early, acute stage of coronavirus infection.Maayan Levy, a lead author and assistant professor of microbiology at the Perelman School of Medicine, said levels of serotonin and other metabolites were altered right after a coronavirus infection, something that also happens immediately after other viral infections.But in people with long Covid, serotonin was the only significant molecule that did not recover to pre-infection levels, she said.The team analyzed stool samples from some of the long Covid patients and found that they contained remaining viral particles. Putting the findings in patients together with research on mice and miniature models of the human gut, where most serotonin is produced, the team identified a pathway that could underlie some cases of long Covid.Here’s the idea: Viral remnants prompt the immune system to produce infection-fighting proteins called interferons. Interferons cause inflammation that reduces the body’s ability to absorb tryptophan, an amino acid that helps produce serotonin in the gut. Blood clots that can form after a coronavirus infection may impair the body’s ability to circulate serotonin.Depleted serotonin disrupts the vagus nerve system, which transmits signals between the body and the brain, the researchers said. Serotonin plays a role in short-term memory, and the researchers proposed that depleted serotonin could lead to memory problems and other cognitive issues that many people with long Covid experience.“They showed that one-two-three punch to the serotonin pathway then leads to vagal nerve dysfunction and memory impairment,” Dr. Iwasaki said.There are caveats. The study was not large, so the findings need to be confirmed with other research. Participants in some other long Covid studies, in which some patients had milder symptoms, did not always show depleted serotonin, a result that Dr. Levy said might indicate that depletion happened only in people whose long Covid involves multiple serious symptoms.What’s Next: A clinical trial of Prozac.Scientists want to find biomarkers for long Covid — biological changes that can be measured to help diagnose the condition. Dr. Thaiss said the new study suggested three: the presence of viral remnants in stool, low serotonin and high levels of interferons.Most experts believe that there will not be a single biomarker for the condition, but that several indicators will emerge and might vary, based on the type of symptoms and other factors.There is tremendous need for effective ways to treat long Covid, and clinical trials of several treatments are underway. Dr. Levy and Dr. Thaiss said they would be starting a clinical trial to test fluoxetine, a selective serotonin reuptake inhibitor often marketed as Prozac, and possibly also tryptophan.“If we supplement serotonin or prevent the degradation of serotonin, maybe we can restore some of the vagal signals and improve memory and cognition and so on,” Dr. Levy said.

A cheap and widely available prescription drug can improve symptoms of irritable bowel syndrome in patients seen in GP surgeries, new research presented today at UEG Week 2023 has found.
Amitriptyline, which is commonly used at low doses for a range of health concerns, has been found to improve irritable bowel syndrome (IBS) symptoms too, according to the results of the ATLANTIS trial.
Led by researchers at the Universities of Leeds, Southampton, and Bristol and funded by the National Institute for Health and Care Research (NIHR), the study was conducted in primary care. GPs prescribed the drug and patients managed their own dose based on the severity of their symptoms, using an adjustment document designed for the trial. Most people with IBS are seen and managed in primary care by their GP, which means that the results of this trial are likely to be applicable to many people with the condition.
The results, published today in The Lancet, showed that patients taking amitriptyline were almost twice as likely to report an overall improvement in symptoms as those taking a placebo.
Now the trial team is recommending that GPs support their patients with IBS to use amitriptyline to manage their symptoms — and has made the dose adjustment document available for clinicians and patients.
Co-chief Investigator Alexander Ford, Professor of Gastroenterology in the University of Leeds’s School of Medicine, said: “Amitriptyline is an effective treatment for IBS and is safe and well tolerated. This new rigorously conducted research indicates that general practitioners should support patients in primary care to try low-dose amitriptyline if their IBS symptoms haven’t improved with recommended first-line treatments.”
IBS, which affects around 1 in 20 people worldwide, causes abdominal pain and changes to bowel movements. The long-term condition, which has no known cure, fluctuates in severity over time. It can have a substantial impact on quality of life and ability to work and socialise. Most treatments only have a modest effect and people often have ongoing troublesome symptoms.

The legendary Alexander Fleming, who famously discovered penicillin, once said “never to neglect an extraordinary appearance or happening.” And the path of science often leads to just that. New UNLV research is turning the page in our understanding of harmful bacteria and how they turn on certain genes, causing disease in our bodies.
A team of interdisciplinary scientists, led by professor and microbiologist Helen Wing, focuses on Shigella — a lethal bacterial pathogen that causes abdominal cramping, fever, and diarrhea. The Centers for Disease Control and Prevention estimates that Shigella cases lead to 600,000 deaths globally each year.
Shigella contains a major ‘switch’ protein (VirB), which triggers the bacterium to cause disease in humans. VirB does this by binding to Shigella’s DNA, activating the disease. The researchers showed that it is possible that interfering with VirB’s binding process can prevent Shigella from making us sick.
The study  was published Sept. 20 in the microbiology journal mBIO.
“When molecular substitutions are made in VirB, this protein loses the ability to turn on virulence genes in Shigella, therefore making Shigella non-infectious,” said Taylor Gerson, a fourth-year Ph.D. student at UNLV and the study’s first author.
Traditionally, proteins that control how harmful a disease is, such as VirB, have been underappreciated. The goal of the team’s microbiology lab is to better understand these ‘switch’ proteins, which turn an otherwise harmless bacteria into an aggressive pathogen.
“I think our research has a broader impact,” said Monika Karney, a UNLV lab technician and study co-author. “What we’re seeing with this one protein in this one bacterium — there’s room for it to be applied to other proteins in other clinically relevant bacteria.”
The implications this research has for other pathogens remain to be seen, but the hope is that it is a major stepping stone toward putting a big red “X” through some of the diseases plaguing many parts of the world.
“We study these molecules to understand how they function in disease, so that other labs may look into finding drugs that kill these pathogens,” said Wing. “Understanding these proteins and what they interact with is critical.”
Integral to the research is CPT, or cytidine triphosphate, and its role in the binding process. The molecule is traditionally used as a building block for making DNA and RNA, and is needed by VirB for this process. Interfering with that binding process is what ultimately opens the door for future treatment strategies and potentially minimizes the impacts of harmful bacteria, such as Shigella.

A new study by Australian researchers has shown that fluctuating blood pressure can increase the risk of dementia and vascular problems in older people.
Short blood pressure (BP) fluctuations within 24 hours as well as over several days or weeks are linked with impaired cognition, say University of South Australia (UniSA) researchers who led the study.
Higher systolic BP variations (the top number that measures the pressure in arteries when a heart beats) are also linked with stiffening of the arteries, associated with heart disease.
The findings have been published in the journal Cerebral Circulation — Cognition and Behaviour.
Lead author Daria Gutteridge, a PhD candidate based in UniSA’s Cognitive Ageing and Impairment Neuroscience Laboratory (CAIN), says it’s well known that high blood pressure is a risk factor for dementia, but little attention is paid to fluctuating blood pressure.
“Clinical treatments focus on hypertension, while ignoring the variability of blood pressure,” Gutteridge says.
“Blood pressure can fluctuate across different time frames — short and long — and this appears to heighten the risk of dementia and blood vessel health.”
To help explore the mechanisms that link BP fluctuations with dementia, UniSA researchers recruited 70 healthy older adults aged 60-80 years, with no signs of dementia or cognitive impairment.

Clinicians who show more empathy promote better psychological health among breast cancer patients, according to a Rutgers study examining how oncology doctors facilitate psychological well-being.
“Our findings suggest that provider communication is a key component to reducing uncertainty, and thus providers play a key role in helping to facilitate psychological well-being,” said Liesl Broadbridge, a doctoral degree candidate at the Rutgers School of Communication and Information (SC&I) and the lead author of the studypublished in Patient Education and Counseling.
Researcher findings suggest that discussing uncertainties with patients and being empathetic to their concerns is critical to their healing and recovery.
“Our findings are directly applicable as targets for communication training modules for health care providers, because by continuing to advance skills in empathic communication, clinicians can enhance the health care experiences of their patients,” Broadbridge said.
In addition to Broadbridge, the authors of the study include SC&I Professor of Communication Kathryn Greene; SC&I Associate Professor of Communication Maria Venetis; SC&I doctoral degree student Lauren Lee; SC&I alumna Smita C. Banerjee, an associate attending behavioral scientist at Memorial Sloan Kettering Cancer Center; Biren Saraiya, an associate professor of medicine at Rutgers Robert Wood Johnson Medical School (RWJMS) and medical oncologist at Rutgers Cancer Institute of New Jersey; and Katie A. Devine, an associate professor of pediatrics at RWJMS and chief of pediatric population science, outcomes, and disparities research at Rutgers Cancer Institute.
According to research, patients with breast cancer are at significant risk for developing symptoms of anxiety and depression related to their cancer diagnosis.
“As health communication researchers, we are interested in how health care providers can communicate in ways that help their patients cope with/manage their illness and support their psychological health,” said Broadbridge.

Published16 hours agoShareclose panelShare pageCopy linkAbout sharingImage source, ReutersBy Nadine YousifBBC News, TorontoCanada remains one of the only countries in the world that allows legal and regulated access to recreational marijuana. But five years after the drug’s legalisation, the country’s cannabis industry is struggling for survival. George Smitherman remembers buying his first legal gram of cannabis in October 2018 from a Tweed shop in Newfoundland. The cannabis company had made headlines two years prior for signing a marketing deal with US rapper Snoop Dogg, which was hailed at the time as a sign of a new dawn in the marijuana industry.The shop,Mr Smitherman recalls, was “beautiful”.”I didn’t know if I was in a spa or a jewellery showroom,” he said. He also remembers the juxtaposition of the product he bought versus the striking space he bought it in – all marijuana products in Canada are sold in generic packaging with plain, government-issued labels. Still, it was an exciting time, Mr Smitherman recalls. Canada’s long-anticipated cannabis legalisation had just become a reality. Investment was flowing into a brand new market that many thought would get them rich. Five years later, the industry is dealing with economic struggles far removed from the enthusiasm of those early days. Take Aurora Cannabis, for example. The Alberta-based cannabis manufacturer – one of the largest in Canada – announced in August that it will be diversifying its offerings and start selling orchids.That same month, another company, Canopy Growth, sold the multi-million dollar Ontario headquarters it bought in 2017 back to its original owner, candy manufacturer Hershey Canada. Both companies, along with other cannabis producers, have also given out pink slips to thousands of workers in an effort to cut costs as they continue to generate little to no profit.Inside Thailand’s ‘weed wonderland’ Oklahoma voters say no to recreational cannabisGermany plans to legalise recreational cannabisPart of the problem, experts and industry leaders say, is overregulation of the drug as the country attempts to toe a careful line between public health and building a robust cannabis industry. Others say it’s simply a matter of too many players and too much production that far exceeds demand. And because Canada is one of the only countries in the world that federally allow the manufacturing and consumption of recreational cannabis, the options for domestic producers to make money outside Canada’s borders remain very limited.Image source, Getty ImagesThese challenges were difficult to see early on, said Mr Smitherman, a former Ontario politician who is now the head of the Cannabis Council of Canada. “The thing is, there was no global road map,” he told the BBC, as no other country had attempted to legalise recreational cannabis on such a large scale. When Canada passed its landmark Cannabis Act in 2018, one of its biggest goals was to move marijuana users away from the illicit market towards a legal, regulated market. It was designed to keep the drug away from minors and limit money flowing into the illegal marijuana trade.There was also the economic argument as well – that Canadians and the country’s economy as a whole would stand to benefit.In many ways, that economic equation still holds true: Canada’s domestic recreational market is valued in the billions. In 2022, Deloitte Canada estimated that cannabis added C$43.5bn ($31.91bn; £26.23bn) to the country’s gross domestic product since legalisation. And Canadians can access legal and regulated marijuana just about anywhere in the country. But they have also reportedly lost more than C$131bn investing in cannabis businesses.Michael Armstrong, a cannabis business researcher at Brock University in Ontario, argues that early hiccups paved the way for some of the business challenges seen today. “One way to sum it up would be to say we’ve kind of had a classic boom and bust,” Prof Armstrong said.In the early days, many stores were dealing with chronically empty shelves as production could not keep up with demand. Prof Armstrong said this drove cannabis producers to make too much product, which led to a surplus and an eventual downsizing.It also meant that many still relied on the illicit market to get their marijuana. On the retail side, cannabis stores were initially very profitable. But a clustering of storefronts over time in the same areas meant retailers had to lower their prices and offer other incentives to compete with other stores nearby.As of 2023, there are around 3,600 licensed retail cannabis stores across the country and 970 licensed cannabis producers in Canada.Few of those producers appear to be profitable. Mr Smitherman said a recent survey by the Cannabis Council of Canada found that only 20% are showing some form of positive cashflow. “The attrition, turnover and consolidation is relentless,” he said of the current business landscape. Image source, Toronto Star via Getty ImagesSome also point the finger at what they say is the overregulation of the industry, where cannabis is still a controlled substance. By law, cannabis companies cannot advertise their products or build brand recognition in the way companies in other industries can. Retail locations have tinted windows to conceal what is inside, and the drug is sold in government-approved packaging. They also pay higher regulatory fees than companies selling other controlled substances.It is part of a delicate balance the government has tried to strike between public health and managing a new legal industry, Prof Armstrong said. “The big trade off in legal cannabis is: how do you make the legal market attractive enough to get all the existing users to go with the legal weed, but not so attractive that you get a whole bunch of new users starting up,” he said. Canada also has stringent laws on the types of products that can be sold, as well as their potency. Some argue that this has caused illegal cannabis in the country to continue to thrive even under legalisation.Consumers of cannabis edibles, for example, are able to go online and find products with a potency higher than the legal amount, Mr Smitherman said. Often, those products are sold at a considerably lower cost than what is being offered in licensed stores.In late 2022, Canada’s Department of Public Safety estimated that 33% of the marijuana market is still controlled by the illicit drug trade. There are also limited options for Canada’s cannabis producers to profit outside of the country’s borders.Canada remains the only country with a legal, federal cannabis framework outside of Uruguay, and the export of recreational products is not allowed. While some states in the US have legalised marijuana, the drug remains illegal at the federal level.Countries in the European Union have toyed with the idea of legalisation, but “they are moving very slowly”, Prof Armstrong said, partly due to stringent EU laws. Industry leaders like Mr Smitherman have long lobbied the government for looser laws that, he argues, will benefit the cannabis industry while not straying away from the country’s public health objectives.”Our argument is: ‘Hey, if we can make some incremental changes here, collectively, we can grow the pie,'” he said. Despite the challenges, many still hail legalisation as somewhat of a success.”From a public policy standpoint, the people of Canada are very satisfied with it,” Mr Smitherman said.”But one of the measures of success is, are we creating a sustainable model here where, in the next five years, we are going to see good cannabis companies bringing innovative products and winning that battle for market share, or are we going to retreat?”Prof Armstrong said that what Canada has is “what no other country in the world has”. “Now, having said that, legalisation is not a roaring success.”More on this storyCanada legalises sale and use of cannabisPublished17 October 2018As it happened: First day of legal Canadian potPublished17 October 2018Why Canada’s cannabis bubble burstPublished29 December 2019

The products, often marketed to Black women, have been linked to an increased risk of uterine cancer.The Food and Drug Administration has proposed banning hair-straightening products that contain or emit formaldehyde, more than a decade after the cosmetic industry’s own experts declared the products unsafe.Frequent use of chemical hair straighteners has been linked to a possible increase in the risk of developing cancer of the uterus, which is also called endometrial cancer. Women who use the products often face more than twice the risk of those who do not.Other studies have linked hair straighteners and dyes to breast and ovarian cancer. The agency’s scientists deemed formaldehyde to be a human carcinogen seven years ago, and its lawyers started drafting a proposed ban then.Workers like embalmers who are exposed to high levels of formaldehyde have higher rates of myeloid leukemia and other rare cancers. The F.D.A. warns that immediate reactions can include irritation of the eyes and throat, coughing, wheezing or chest pain. Chronic or long-term problems include frequent headaches, asthma, skin irritation and allergic reactions.The hair-straightening products are marketed largely to Black women. While rates of uterine cancer have been rising among all women in recent years, the increase has been steepest among women of color, including Asian and Hispanic women.The agency’s proposed rule would ban formaldehyde and other formaldehyde-releasing chemicals from hair-straightening and hair-smoothing products marketed in the United States. The target date for the ban is April 2024.Some treatments, including so-called keratin treatments, claim to be formaldehyde-free but contain a substance called methylene glycol, which converts to formaldehyde gas after coming in contact with air. (Scientists consider methylene glycol simply to be formaldehyde in a solution.)The F.D.A. has always had the authority to ban a specific ingredient like formaldehyde, and it has removed about a dozen ingredients, including mercury compounds, from cosmetics.But the industry went largely unregulated until last year, when Congress gave the F.D.A. oversight authority. The action was not related to the new authority, however, the F.D.A. said.The expanded oversight does not mean that new products will typically undergo agency review before they are marketed to the public. But manufacturers of shampoo, nail polish, makeup and other items are now required to register their manufacturing sites with the F.D.A., and they are required to disclose the ingredients on the packaging.The F.D.A. can also issue a mandatory recall of a cosmetic product if a serious health concern arises or a death occurs.Controversy over formaldehyde in hair straighteners has persisted for years. The Environmental Working Group, an advocacy organization, petitioned the agency in 2011 and again in 2021 to ban hair products with formaldehyde.F.D.A. lawyers started drafting rules for a proposed ban in 2016. But the process halted abruptly a few months later, and no explanation was given.“The F.D.A. has known for decades now that these products are dangerous,’’ said Melanie Benesh, vice president for government affairs at the Environmental Working Group. “There is no reason for them not to have acted sooner.”“This is the first public indication we’ve seen that they are planning to ban it in hair-straightening products,” Ms. Benesh added. The products pose a real risk of harm, she said, both to hair stylists regularly exposed to formaldehyde vapor while providing the treatment, as well as to customers receiving it.The agency currently encourages consumers to read the labels of hair products before purchasing them and to avoid those that contain formaldehyde, formalin or methylene glycol. The agency urges consumers to ask hairdressers what products they are using and to report adverse reactions.

Previous research has implicated fungi in chronic neurodegenerative conditions such as Alzheimer’s disease, but there is limited understanding of how these common microbes could be involved in the development of these conditions.
Working with animal models, researchers at Baylor College of Medicine and collaborating institutions discovered how the fungus Candida albicans enters the brain, activates two separate mechanisms in brain cells that promote its clearance, and, important for the understanding of Alzheimer’s disease development, generates amyloid beta (Ab)-like peptides, toxic protein fragments from the amyloid precursor protein that are considered to be at the center of the development of Alzheimer’s disease. The study appears in the journal Cell Reports.
“Our lab has years of experience studying fungi, so we embarked on the study of the connection between C. albicans and Alzheimer’s disease in animal models,” said corresponding author Dr. David Corry, Fulbright Endowed Chair in Pathology and professor of pathology and immunology and medicine at Baylor. He also is a member of Baylor’s Dan L Duncan Comprehensive Cancer Center. “In 2019, we reported that C. albicans does get into the brain where it produces changes that are very similar to what is seen in Alzheimer’s disease. The current study extends that work to understand the molecular mechanisms.”
“Our first question was, how does C. albicans enter the brain? We found that C. albicans produces enzymes called secreted aspartic proteases (Saps) that breakdown the blood-brain barrier, giving the fungus access to the brain where it causes damage,” said first author Dr. Yifan Wu, postdoctoral scientist in pediatrics working in the Corry lab.
Next, the researchers asked, how is the fungus effectively cleared from the brain? Corry and his colleagues had previously shown that a C. albicans brain infection is fully resolved in otherwise healthy mice after 10 days. In this study, they reported that this occurred thanks to two mechanisms triggered by the fungus in brain cells called microglia.
“The same Saps that the fungus uses to break the blood-brain barrier also break down the amyloid precursor protein into AB-like peptides,” Wu said. “These peptides activate microglial brain cells via a cell surface receptor called Toll-like receptor 4, which keeps the fungi load low in the brain, but does not clear the infection.”
C. albicans also produces a protein called candidalysin that also binds to microglia via a different receptor, CD11b. “Candidalysin-mediated activation of microglia is essential for clearance of Candida in the brain,” Wu said. “If we take away this pathway, fungi are no longer effectively cleared in the brain.”
“This work potentially contributes an important new piece of the puzzle regarding the development of Alzheimer’s disease,” Corry said. “The current explanation for this condition is that it is mostly the result of the accumulation of toxic Ab-like peptides in the brain that leads to neurodegeneration. The dominant thinking is that these peptides are produced endogenously, our own brain proteases break down the amyloid precursor proteins generating the toxic Ab peptides.”
Here, the researchers show that the Ab-like peptides also can be generated from a different source — C. albicans. This common fungus, which has been detected in the brains of people with Alzheimer’s disease and other chronic neurodegenerative disorders, has its own set of proteases that can generate the same Ab-like peptides the brain can generate endogenously.
“We propose that the brain Ab-peptide aggregates that characterize multiple Candida-associated neurodegenerative conditions including Alzheimer’s disease, Parkinson’s disease and others, may be generated both intrinsically by the brain and by C. albicans,” Corry said. “These findings in animal models support conducting further studies to evaluate the role of C. albicans in the development of Alzheimer’s disease in people, which can potentially lead to innovative therapeutic strategies.”