Researchers Affirm Long-held Belief that Viruses Can Trigger Parkinson’s Disease

A new study shows that a common virus can induce Parkinson’s-like brain damage and movement problems

Source: CC0

Scientists usually use animal models when studying Parkinson’s disease because these models mimic the disease well. They are limited, however, because they require either gene modifications or the injection of toxicants, which may not accurately represent how the disease occurs in humans.

But now, researchers at Texas A&M University have developed a model that uses a nontoxic way to generate the symptoms of Parkinson’s: infection with a virus called Theiler’s murine encephalomyelitis virus (TMEV), a natural pathogen in mice.

Their study is a game changer because it proves that a simple viral infection can trigger the exact brain damage and physical disabilities in animal models that are seen in people with Parkinson’s disease – and it sets the stage for additional studies.

“The toxic-exposure models are useful for studying Parkinson’s, but not all people who are exposed to chemicals go on to develop Parkinson’s, so these models cannot show all the ways a disease as complex as Parkinson’s actually begins or develops over time in people,” said Candice Brinkmeyer-Langford, a neurogenerative disease expert with the Texas A&M University School of Public Health at Texas A&M Health.

Parkinson’s affects more than 10 million people worldwide, making it second only to dementia among brain disorders. It destroys the cells that produce dopamine, a chemical essential for smooth body movement, leading to problems with balance and walking, tremors in the hands or fingers and overall stiffness, as well as mental or emotional distress.

Its origins are unknown, but for decades, experts have believed that the disease could be triggered by the brain inflammation caused by viruses – even those contracted decades earlier – as well as by a combination of a person’s genetics and environmental factors. This idea recently was affirmed by Brinkmeyer-Langford and others at Texas A&M in the case of another devastating motor neuron disease, amyotrophic lateral sclerosis (ALS).

“Viruses are known to cause entirely different diseases based on a person’s genetics,” she said. “For example, the Epstein-Barr virus causes mononucleosis, but may also contribute to cancer or multiple sclerosis, and SARS-CoV-2 can attack the heart and brain as well as the lungs.”

For this pilot study to test the validity of TMEV in studying Parkinson’s, the researchers conducted experiments to measure the following:

  • Brain cell infection and damage. One week after infection, the researchers confirmed that the virus had infected the dopamine-producing brain cells. At one month after infection, the dopamine-producing cells were destroyed in the site of viral infection. Dopamine-induced behaviours were compared between 13 infected animal models and 14 healthy control animal models after administering a dopamine-mimicking drug which produced a distinct movement pattern confirming dopamine neuron loss. This test confirmed that the virus caused a significant loss of these crucial dopamine brain cells over time.
  • Speed and coordination. They compared 13 infected animal models against 14 healthy control animal models to track and measure their motor skills with a standard assessment called the pole test to determine if losing dopamine-producing cells causes the physical movement problems typically seen in Parkinson’s patients. Animal models infected with TMEV had slower times to complete the test compared to the healthy control models, and this still was the case at week 20, when the study ended.
  • Gait abnormalities. They used a specialised treadmill, which evaluated over 100 factors involved in walking, motor function and balance, to analyse how quickly and efficiently the animal models walked. The test confirmed that the virus caused physical weakness following the loss of dopamine producing cells due to viral infection, proving that the virus damaged the brain in a similar way as seen in Parkinson’s patients.

Now that this innovative model has been proven, Brinkmeyer-Langford said future studies will include testing the TMEV model directly against standard, older animal models used in Parkinson’s research, looking for early warning signs and biological markers for Parkinson’s and analyzing how the body’s immune response to a virus changes the brain.

“The clock is ticking, since the rapidly aging global population means the number of people with Parkinson’s is expected to jump significantly,” she said.

By Ann Kellett

Source: Texas A&M University

A Sleepless Night Increases Synaptic Connections

An increase in a marker for connections was associated with deeper sleep during later naps

Photo by Andrea Piacquadio

A night without sleep produced increased markers of connections between brain cells, showing that sleep in humans may be important for restoring cellular balance in the brain, according to a study published June 23rd in the open access journal PLOS Biology by David Elmenhorst from the Forschungszentrum Jülich Institute of Neuroscience and Medicine in North Rhine-Westphalia, Germany, and colleagues.

Scientists have long wondered why exactly humans and other animals need to sleep. One potential mechanism is that sleep is required to restore synaptic connections and homeostasis in the brain. Synapses – the connections between brain cells – become stronger during wakefulness. This increases the amount of energy the brain needs and leads to buildup of proteins in the brain. Sleep is thought to reset these levels, reducing synaptic connections and restoring homeostasis, but evidence has thus far been limited to animal models. To determine whether the synaptic homeostasis hypothesis is supported in humans, the authors of this study used positron emission tomography (PET) to look for markers of synaptic vesicle glycoprotein 2A (SV2A), a marker of brain synapses in 40 participants, half of whom had gone one night without sleep.

The authors found that after 28 hours of continuous wakefulness, the sleep deprivation group had higher measures of SV2A in several brain regions, including the hippocampus (an area important for memory), and the thalamus, an important information relay in the brain. When the sleep-deprived participants were allowed a two-hour nap, higher levels of SV2A were associated with more slow wave activity during sleep, a marker of deep sleep and sleep pressure. While SV2A is only a proxy for brain cell connections and the elevations were relatively small, the results support the synaptic homeostasis model of sleep, and suggest a biological connection between the need for sleep and the buildup of cell connections. 

The authors add, “During sleep deprivation, the brain remains awake longer and continues to process stimuli and information. Our study shows that after approximately 28.5 hours of wakefulness, a marker for synaptic density increases in several brain regions. This suggests that sleep deprivation not only causes fatigue but is also accompanied by measurable changes in neural connections.”

Provided by PLOS

Higher Vitamin A Levels Linked to Better Lung Function in Asthmatic Kids and Adults

Vitamin D shows similar benefits in adults with asthma, including slower biological ageing

Photo by cottonbro studio from Pexels

Higher levels of circulating vitamin A are linked to better lung function in children and adults with asthma, while vitamin D shows similar benefits in adults, including slower biological ageing, finds the first study of its kind, published online in the respiratory journal Thorax.

Poor lung function is a key predictor of death, irrespective of whether or not a person has lung disease. And making sure that the lungs keep working well is essential for staving off long term respiratory conditions, explain the researchers.

Previously published research suggests that vitamins A and D both protect against and worsen asthma, as well as influencing lung development, depending on the dose and context, they add.

To clarify the role of these vitamins, the researchers drew on two groups of participants with asthma: 1165 children in the GACRS (Genetic Epidemiology of Asthma in Costa Rica Study); and 1041 adults in the ODOLLFA (Omic Determinants of Longitudinal Lung Function in Asthma).

Small molecules that fine-tune the activity of genes (serum microRNAs or miRNAs for short) and those that mark genes as either active or inactive (DNA methylation), plus levels of vitamins A and D, were measured in all the participants.

Lung capacity/health was assessed through measures of forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and the FEV:FVC ratio.

In adults, further analysis assessed whether methylation status and miRNAs influenced the association between the vitamins and lung function or epigenetic ageing – the response of genes to external biological and environmental factors which then promotes cellular ageing.

The findings showed that children and adults with asthma and higher vitamin A levels had better lung function (FEV1 and FVC) than those with lower levels.

And among adults with asthma, those with higher vitamin D levels of at least 30 ng/ml had better lung function than those with lower levels. They also had less evidence of epigenetic ageing, suggesting that vitamin D may help slow biological ageing, particularly in people with asthma, say the researchers.

“These findings emphasise the value of adequate vitamin D, not only for lung health but also in slowing age-related processes,” they write.

In people with asthma, vitamin D deficiency is more common and is associated with more severe disease, worse asthma control, higher inhaled steroid need and more frequent  sudden worsening of asthma symptoms, they explain.

The researchers identified MiRNAs that regulate 248 genes commonly associated with vitamins A and D in both age groups, which, further analysis suggests, are involved in controlling inflammation and lung function.

This secondary analysis also revealed that changes in the expression of specific miRNAs strongly influence the effects of vitamins A and vitamin D on lung function and epigenetic ageing.

“To our knowledge, this is the first study to integrate vitamin A and D levels with lung function and epigenetic markers – miRNA expression and DNA methylation – in both children and adults with asthma,” write the researchers.

Lung function was inversely correlated with all age acceleration measures, reinforcing the link between respiratory health and ageing,” they add.

They conclude: “Our findings emphasise that epigenetic mechanisms play a key role in mediating the effects of vitamins on lung function in individuals with asthma, pointing to potential targets for personalised nutrition and therapeutic strategies in asthma care.”

In a linked editorial, Drs Sze Man Tse and Genevieve Mailhot of the CHU Sainte-Justine Research Center, Montreal, and the University of Montreal, caution: “While these findings open a novel line of investigation linking vitamin D, biological ageing and lung health, there is a need for further studies to clarify causality.”

But they add: “By examining the underlying biological mechanisms, [the researchers have] revealed a nuanced interplay between vitamins A and D, lung function, and their epigenetic mediators.

“Their findings highlight age-dependent and age-independent mechanisms, underscoring complex interactions between vitamin levels and lung physiology.”

And they conclude: “Overall, advancing our understanding of how nutritional exposures impact gene regulation may open new avenues for managing asthma across the lifespan.”

Source: The BMJ Group

Cortisol from Adrenal Tumours Progressively Raises Cardiovascular Risk

Landmark international study finds persistent mild cortisol excess drives hypertension progression, challenging the standard diagnostic test.

A graphic of a human skeleton, also showing the kidneys with the adrenal glands on top, highlighted in red.
The adrenal glands produce the steroid hormone cortisol, a master regulator of metabolism, blood pressure and immune function.

A major new study, led by the University of Birmingham and published in The Lancet Diabetes & Endocrinology, has shown that cortisol levels in patients with adrenal tumours are far less stable than previously assumed.

The study also identified that those in whom cortisol remains persistently elevated carry a significantly greater risk of worsening high blood pressure and a heavier overall cardiometabolic burden.

Cortisol, often referred to as the “stress hormone”, is a steroid hormone produced by the adrenal glands that acts as a master regulator of metabolism, blood pressure, and immune function. When benign tumours form on the adrenal glands (found incidentally in 3-7% of adults) they can cause the body to produce cortisol independently of normal regulatory controls, a condition known as mild autonomous cortisol secretion (MACS). Until now, it was unclear how cortisol levels in these patients change over time, and what that means for their long-term health.

The study of over 2500 patients is the largest study of its kind to examine how cortisol patterns evolve over time in patients with benign adrenal tumours and what this means for cardiovascular outcomes.

These findings should prompt us to think more carefully about which patients need closer follow-up, and whether active treatment to reduce cortisol excess – including surgery in selected cases – could protect their long-term cardiovascular health.

Alessandro Prete, Clinical Associate Professor in Endocrinology and Diabetes

The study followed 2525 patients with benign adrenal tumours for an average of nearly 7 years. Each patient underwent repeated hormonal testing using the 1mg overnight dexamethasone suppression test, the standard clinical test used to assess whether the adrenal gland is overproducing cortisol autonomously. Patients were classified based on whether their cortisol levels remained normal, remained elevated (persistent MACS), or changed between categories over time.

The researchers found that cortisol secretion status changed in 22% of patients, far more frequently than previously recognised, with most changes occurring within the first three years after diagnosis. These findings challenge the assumption that a single hormonal test is sufficient to characterise a patient’s long-term cortisol profile.

Patients with persistent MACS had the greatest overall cardiovascular burden and faced a 34% higher rate of worsening high blood pressure than those with persistently normal cortisol. Over 10 years, patients with persistent MACS lost an average of 2 years of well-controlled hypertension-free time compared with those whose cortisol remained normal – a clinically meaningful difference in long-term blood pressure control.

Cardiometabolic burden refers to the combined impact of interrelated metabolic and cardiovascular risk factors (including obesity, high blood pressure, type 2 diabetes, and high cholesterol) on overall health, predisposing serious, chronic diseases such as heart failure, heart attack, and stroke.

The study identified patients with persistently abnormal cortisol levels (persistent MACS) as a clinically important, higher-risk group who may benefit from closer monitoring and more proactive management of modifiable risk factors – including blood pressure, cholesterol, weight, and smoking. The results are also consistent with recent randomised trial data, also published in The Lancet Diabetes & Endocrinology, showing that surgery to remove the adrenal tumour can improve blood pressure control in MACS.

Professor Alessandro Prete, Clinical Associate Professor of Endocrinology in the Department of Metabolism and Systems Science at the University of Birmingham, Co-lead for the National Institute for Health and Care Research (NIHR) Biomedical Research Centre: Birmingham’s Women’s Metabolic Health theme, through which the study was delivered, and corresponding author and senior investigator of the study, said: “For many years, the assumption has been that a single hormone test at adrenal tumour diagnosis tells us everything we need to know about a patient’s cortisol status.

“This study shows that it is simply not the case – cortisol levels change over time in a substantial proportion of patients, and those in whom they remain persistently elevated are at a meaningfully higher risk of developing uncontrolled blood pressure.”

The study also provides important new evidence to inform the ongoing debate around whether, and how often, cortisol testing should be repeated in patients with benign adrenal tumours. Current guidelines recommend repeating the test only in specific clinical circumstances; the authors of the study are calling for prospective studies to determine whether repeated hormonal assessment contributes meaningfully to risk stratification beyond established cardiovascular risk factors. 

Source: University of Birmingham

Uncovering Sex-specific Immune Differences in Glioblastoma

Photo by Anna Shvets

Men and women experience many diseases very differently. Certain diseases present more commonly in one sex than in another. Some conditions like heart attacks may cause different symptoms in men and women. Some treatments work better or not at all for one sex over the other.

Cancer is no exception. There are major differences in male and female immune systems, a system critical for cancer’s growth and for successfully becoming cancer-free. For example, some immunotherapies work better in men than in women and vice versa.

Glioblastoma, the most common and fatal form of brain cancer, is more common and more deadly in men than in women. The reasons behind this difference and how the cancer’s biology differs between men and women remain largely unclear.

Now, a study has identified a cellular mechanism that differs between male and female laboratory models with glioblastoma. The study was published in the journal Nature Cancer and led by Defne Bayik, PhD, assistant professor of molecular and cellular pharmacology at the University of Miami Miller School of Medicine, and Asmita Pathak, PhD, a former postdoctoral fellow in the Bayik Lab.

“We have a growing appreciation that cancer doesn’t act the same way in men and women. There are differences in incidence rates. There are differences in treatment responses. There are differences in outcomes,” Dr Bayik said. “But we don’t really have a good, fundamental understanding of the mechanisms underlying these observational studies.”

Delving Into Immune Differences

To uncover that mechanism for glioblastoma, Dr Bayik and her colleagues focused on a certain class of immune cells in the brain known as myeloid-derived suppressor cells, or MDSCs. As their name suggests, these cells suppress other cells’ immune activity, especially that of T cells. In healthy contexts, their activity is important for regulating the immune system and keeping inflammation under control. But in the context of cancer, these cells are often recruited by tumours to suppress surrounding T cells and other immune cells, protecting cancerous cells from the rest of the immune system and allowing them to grow unchecked.

In previous work, Dr Bayik found sex-specific differences in the immune landscape of glioblastoma, with higher levels of monocytic myeloid-derived suppressor cells associated with disease in male laboratory models. Granulocytic MDSCs play a more prominent role in females. In studies of human glioblastoma tumours, she observed a similar pattern. Men tend to have more monocytic MDSCs within their tumours, Granulocytic MDSCs, or proteins associated with these cells, correlate with worse outcomes for women but not for men.

Women still constitute 40% of glioblastoma patients. By identifying these differences, we can better tailor treatments for both men and women.

Dr Defne Bayik

In the new study, Dr Bayik and her colleagues wanted to understand what drives this difference. How do granulocytic MDSCs act to promote cancer growth in female but not male laboratory models? In Dr Bayik’s previous study, she’d found several drug candidates that are predicted to act on granulocytic MDSCs. A few of these candidate drugs target proteins related to GABA, a brain signaling molecule also known as a neurotransmitter.

By exposing different populations of MDSCs to GABA in the lab, the scientists found that the neurotransmitter specifically affects cellular metabolism only in female granulocytic MDSCs. The process is unaffected in male MDSCs. They also found that this reprogramming of the cells’ metabolism by GABA made the granulocytic MDSCs more immunosuppressive. Finally, they found that blocking the GABA receptor in female laboratory models with glioblastoma improved their outcome. This had no effect on male laboratory models with the cancer.

Potential for treatment personalised by sex

Dr Bayik and her colleagues found that many of their lab findings held up in human samples donated by patients with glioblastoma. Tumour biopsies from women had higher levels of GABA and the GABA receptor in granulocytic MDSCs than did those from men. They also found that GABA reprograms granulocytic MDSC metabolism in women as it does in lab models.

These findings point to the potential for a sex-specific treatment for glioblastoma, Dr. Bayik said. She’s currently working to understand the basis for the difference in cellular metabolism in these immune cells between male and female laboratory models. Further uncovering the mechanism of this sex difference will help her and other scientists find new potential drug targets for the disease. MDSCs are involved in many other types of cance. Drugs that target these cells could have broader applications than just glioblastoma.

“Glioblastoma may be more common in men, but women still constitute 40% of patients,” said Dr Bayik. “By identifying these differences, we can better tailor treatments for both men and women.”

By Rachel Tompa, PhD

Source: University of Miami

Autoantibodies and Blood–Brain Barrier Dysfunction in Schizophrenia

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A growing body of research has shown that autoimmunity influences certain psychiatric disorders. A new study by Nemani et al., currently in preprint, has shown that schizophrenia is strongly associated with an elevated level of autoantibodies that target the central nervous system. Using Rapid Extracellular Antigen Profiling (REAP) to screen 352 patients against 971 controls, the researchers found that schizophrenia is marked by an increased autoantibody burden that tracks with disease severity and duration, nearly doubling in the most chronic cases.

These immune responses are present near the start of the illness and tend to increase as the disease progresses, particularly targeting neuronal ion channels and synaptic proteins. Notably, certain autoantibodies appear to compromise the blood–brain barrier, which may further expose the brain to peripheral immune attacks.

The study also discovered that patients with a higher autoantibody burden respond less effectively to standard antipsychotic treatments like risperidone. However, clinical trials showed that these antibody levels significantly declined during successful treatment courses. These findings suggest that humoral autoimmunity is a core component of the disorder, potentially offering new pathways for immune-based therapies.

The article is available on the BioRxiv preprint server.

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Global Trial Shows Safer Antibiotic Option for Staph Blood Infection

Methicillin resistant Staphylococcus aureus (MRSA) – Credit: CDC

A landmark international clinical trial, led in the UK by University College London researchers, has identified the optimal antibiotics for staph blood infection, a breakthrough that is set to reshape treatment for the life-threatening condition.

The SNAP trial found that a little used antibiotic, cefazolin, is as effective as and safer than the current UK standard therapy, flucloxacillin, for treating life-threatening staph blood infections.  More than half of staph blood infections lead to sepsis and 15% to 25% of those who get these infections die within three months.

The researchers also found that a commonly used antibiotic, penicillin, can be used when the staph is treatable with this in the laboratory. And that similarly this is probably as effective as flucloxacillin, and safer.

The findings from the SNAP trial, published in the New England Journal of Medicine (NEJM) and The Lancet, challenge the long-held assumption that flucloxacillin should remain the default treatment and provide important new evidence to guide treatment strategy.

Staph (Staphylococcus aureus) is a leading cause of deadly blood infection, associated with over 1 million deaths worldwide each year. While effective antibiotic treatments exist, there has been no clear agreement about which antibiotic leads to the best outcomes for patients.

The NEJM results – Comparing cefazolin and flucloxacillin

In the trial published in the NEJM, researchers compared antibiotics used to treat meticillin-susceptible Staphylococcus aureus (MSSA) infections (i.e. blood infections that are not resistant to the meticillin antibiotic). It found cefazolin is at least as good as flucloxacillin for helping people to survive this infection, and associated with fewer side effects and a lower risk of kidney injury. It compared cefazolin and flucloxacillin in 1341 adults with staph blood infections across eight countries taking part in this part of the trial.

In patients who received cefazolin there were fewer cases of changes in how the kidneys are working (as measured by blood tests). Such kidney changes can cause long-term health problems and occurred in fewer of those given cefazolin compared to those given flucloxacillin.

The Lancet results – Comparing benzylpenicillin and flucloxacillin

In the paper published in The Lancet, the trial evaluated whether penicillin could be used to treat penicillin-susceptible Staphylococcus aureus (PSSA) infections where laboratory testing confirmed the susceptibility to penicillin.

This trial compared penicillin and flucloxacillin in 281 adults with staph blood infections. Penicillin was found to be likely to be at least as good for helping people to live with this infection as flucloxacillin.

In patients who received penicillin there were similarly fewer cases of changes in how the kidneys are working (as measured by blood tests). These occurred in 11% of those given penicillin compared to 22% of those given flucloxacillin. Mortality was also 14% in the penicillin group compared with 22% in the flucloxacillin group.

Professor Anna Goodman, UK lead of the SNAP trial at the UCL Innovative Clinical Trials, said: “This trial fills a major research gap. Our results strongly support cefazolin as the new first treatment for most adults with these infections. They also show a role for penicillin in some cases. It’s been helpful to deliver it in collaboration with researchers around the world and patients who have been affected by the condition, who we found via the UK Sepsis Trust.

“The results represent huge progress in the management of this disease with the first change in our approach to antibiotics in decades. Not only are cefazolin and penicillin as effective as flucloxacillin at treating penicillin- and meticillin-susceptible staph blood infection, but they also lead to significantly fewer abnormal blood tests.”

Staph infections are caused by bacteria called Staphylococcus aureus. They most often affect the skin and cause relatively minor problems. However, if the bacteria enter the bloodstream or other parts of the body, they can cause serious infections such as blood poisoning, blood infection or sepsis.

These more serious infections can affect anyone, but individuals at higher risk include people with catheters in their veins (as happens when people receive renal replacement therapy also called haemodialysis) or implanted devices (such as pacemakers), and people with diabetes. Those living with cancer and on immune suppressing medication, those who cannot get out of bed, and those who inject drugs are also more vulnerable to these infections.

The Royal Melbourne Hospital’s Professor Steven Tong, an infectious diseases physician at the Doherty Institute in Australia and global co-lead investigator of the SNAP Trial, said the results provide clear evidence that cefazolin should be considered the first-line option to treat MSSA blood infections.

“In the treatment of MSSA blood infections, there is an 89% probability that cefazolin is associated with lower mortality,” said Professor Tong.

“Patients treated with cefazolin fare better, with fewer deaths within 90 days (15% compared to 17% for those who received flucloxacillin). Cefazolin was also associated with fewer cases of acute kidney injury, at 14%, compared to 20% with flucloxacillin.

“The results are sufficiently compelling that I immediately made the switch in my own clinical practice.”

A shift away from flucloxacillin

Researchers said these results mark a turning point in the treatment of MSSA and PSSA blood infections, signalling a shift in clinical practice.

Penicillin was once widely used to treat Staphylococcus aureus, but antibiotic resistance of staph led clinicians to adopt flucloxacillin as the standard treatment for MSSA and PSSA blood infections. The findings support moving away from flucloxacillin as the default treatment for MSSA and PSSA blood infections, given safer alternatives are available.

The new results mark the first major finding from the ongoing SNAP trial, which aims to improve treatment for Staphylococcus aureus infections around the world. These parts of the trial took place in Australia, Canada, Israel, the Netherlands, New Zealand, Singapore, South Africa and the UK – each supported by regional funders working together to form one global network.

Global leadership was provided by the University of Melbourne trial team led by Professor Steven Tong and Professor Josh Davis.

So far, over 6000 participants have been enrolled in over 150 sites in those countries stated, and more recently in Germany and Sweden, Germany, Japan, Malaysia, and the United States.  The trial will continue testing new approaches to improve outcomes for patients facing this serious infection.

Translating the findings

Researchers say the next challenge will be translating the findings into routine clinical practice.

While cefazolin availability may need to increase in some countries, researchers say implementation will ultimately depend on hospitals, laboratories and guideline groups incorporating the findings into clinical care. 

Professor Goodman said: “Sepsis and staph blood infections are devastating for those affected and those who care for them. We are grateful to all those who took part and supported these two trials which will change practice.  The platform trial continues as we ask further important questions in this area.”

Links

Source: University College London

How Wits Donald Gordon Medical Centre is Advancing Specialised Reconstructive Surgery in South Africa

Photo by Natanael Melchor on Unsplash

When 12-year-old Eugene underwent a highly specialised facial reanimation procedure earlier this year, the surgery represented something profoundly human, the possibility of smiling for the first time.

Born with Moebius syndrome, a rare neurological condition that affects facial movement and expression, Eugene had spent his life unable to smile, blink properly or express emotion through facial movement. And while his story is emotionally powerful, it also shines a light on a far broader healthcare reality, the growing importance of highly specialised reconstructive surgery in restoring not only appearance but movement, function, dignity and quality of life.

At Wits Donald Gordon Medical Centre (WDGMC), reconstructive microsurgery is helping redefine what is possible for patients facing some of the most complex medical challenges, from congenital conditions and cancer to severe trauma and tissue loss.

Often misunderstood as a field focused primarily on cosmetic procedures, reconstructive microsurgery sits at the intersection of surgical precision, innovation and long-term patient rehabilitation. These procedures frequently involve transplanting tissue, muscle and nerves from one part of the body to another and reconnecting blood vessels, often measuring less than two millimetres in diameter, under microscopic magnification.

Leading this work at WDGMC is Dr Dimitri Liakos, a plastic and reconstructive surgeon with fellowship training in reconstructive microsurgery and super microsurgery.

Dr Dimitri Liakos, a plastic and reconstructive surgeon with fellowship training in reconstructive microsurgery and super microsurgery.

“These procedures are not simply about appearance,” says Dr Liakos. “They are about restoring function, movement and ultimately helping patients regain parts of their lives that were lost or that they were born without.” In Eugene’s case, surgeons transferred functioning muscle together with its blood and nerve supply into the face, reconnecting these delicate structures under a microscope so movement could gradually return over time.

Eugene’s procedure was facilitated through the support of the Smile Foundation, which works to improve access to reconstructive surgery for children requiring specialised care.

“We are deeply grateful to Wits Donald Gordon Medical Centre and Dr Dimitri Liakos for their dedication in supporting Eugene on his journey,” says Tarri Parfitt, CEO of Smile Foundation. “It is truly remarkable to open a world-class facility to this family and provide care at the highest level of expertise. Facial reanimation surgery is profoundly life-changing. For Eugene, it represents the possibility of expression, connection and a future he may never have imagined before. For Smile, it was also an invaluable opportunity for other surgeons to learn from such a rare and complex case, turning one surgery into the potential to help many more children like Eugene. We highly value the opportunity to work alongside Wits Donald Gordon Medical Centre on cases such as this and look forward to helping many more children together.”

While these procedures are performed in highly specialised centres globally, access to this level of care remains limited in South Africa due to the advanced infrastructure, multidisciplinary expertise and years of specialised training required to perform them successfully.

For WDGMC, however, the ability to perform these surgeries forms part of a broader commitment to advancing highly specialised care within South Africa’s healthcare system while simultaneously strengthening academic medicine and specialist training.

As an academic hospital affiliated with the University of the Witwatersrand, WDGMC has become an important training environment for complex reconstructive microsurgery in South Africa. The hospital recently established the country’s first reconstructive microsurgery fellowship programme for qualified plastic surgeons, helping expand the number of specialists capable of performing these highly technical procedures.

“We have a responsibility not only to perform these surgeries, but to transfer the skill,” says Dr Liakos. “If we do not train future microsurgeons, access to this level of specialised care will remain limited.”

According to Dr Liakos, successful reconstructive microsurgery depends not only on surgical expertise but on building the right multidisciplinary environment around patients.

“To do these cases successfully, you need a dedicated team and an environment that functions seamlessly,” he explains. “Microsurgery is never a one-person effort. It is the nursing staff, anaesthetists, theatre teams and systems around you that make these outcomes possible.”

For surgeons working in the field, the impact of reconstructive microsurgery extends far beyond the operating theatre.

“These surgeries can take 10 or 12 hours. They are physically and emotionally demanding,” says Dr Liakos. “But when you step back and realise that what you are doing may change the course of a person’s life forever, it gives meaning to every moment spent in theatre.”

As WDGMC continues to build on its reconstructive microsurgery programme and the country’s first fellowship of its kind, the hospital is helping shape a future in which South African patients can access world-class reconstructive care close to home and in which the specialists capable of providing that care are trained locally.

Study Links Oral Contraceptives to Increased Binge Eating

Emotional eating increased when women were taking hormone-containing birth control pills compared to the hormone-free pills taken at the end of each monthly cycle

Photo by Reproductive Health Supplies Coalition on Unsplash

Birth control pills are safe and effective for millions of women, but researchers are still working to understand how the hormones they contain may influence eating behaviour.

A new study in JAMA Network Open followed 422 women who were already using combined oral contraceptives, tracking their eating patterns daily for 49 consecutive days. The goal: to examine whether binge-related eating changes depending on whether women are taking hormone-containing pills or hormone-free pills within the same cycle.

In a typical birth control pack, women take about three weeks of “active” pills that contain hormones, followed by about a week of “inactive” pills that contain no hormones.

“Because we tracked the same women day to day, we could see how eating changed with hormone exposure,” said Dr. Shaunna Clark, a co-author and associate professor of psychiatry and behavioral sciences at Texas A&M University’s Naresh K. Vashisht College of Medicine.

How birth control hormones may increase binge-eating risk

The study used a within-person design, meaning each participant served as her own comparison. Researchers measured emotional eating (overeating in response to negative emotions) while tracking whether each day corresponded to an active or inactive pill.

They found a consistent pattern:

Emotional eating was significantly higher during active pill days than during inactive pill days.

This pattern appeared:

  • across two full pill cycles
  • in the full sample of 422 women
  • and in a subset of women with diagnosed binge eating

Clark says the findings held even after accounting for negative mood, suggesting the change was not fully explained by emotional distress.

“That tells us the hormones themselves may be playing a role, rather than those changes being driven by mood or other factors,” she said.

Why birth control may increase binge-eating risk for some women, but not others

The analysis focused on average changes across the group, but the study emphasizes that not all women experience these shifts in the same way.

“Participants ranged in age from late adolescence to young adulthood and were all using the same type of pill, monophasic combined oral contraceptives, which provide a consistent dose of hormones during active pill days,” said Clark, part of the research team led by Dr Kelly Klump at Michigan State University.

Because the study examined within-person changes, it shows that eating behavior can shift alongside hormone exposure, even if the magnitude of that shift differs between individuals.

“These findings show a pattern at the group level,” she said, “but individual responses can vary.”

Birth control pills linked to binge eating, but not mood or body image

The study does not establish that birth control pills cause binge eating. Instead, it identifies a specific association between hormone exposure and increased emotional eating within individuals.

Importantly, researchers also tested other outcomes:

  • Weight preoccupation did not change across pill type
  • Mood changes in response to pill type were smaller and less consistent than the changes in eating

Clark says that suggests the effect is relatively specific to binge-related eating behaviour, rather than a general shift in mood or body image concerns.

How this study changes what we know about birth control and binge eating

Previous research has shown that binge‑related eating tends to increase after ovulation, when both oestrogen and progesterone are elevated.

This study extends that work by showing that synthetic hormones in birth control pills are linked to similar patterns.

By comparing hormone-containing and hormone-free days within the same individuals, the study provides some of the clearest evidence to date that binge-related eating increases during periods of hormone exposure in the birth control cycle.

“Findings like these can help us better understand how different hormone exposures affect eating behaviour,” Clark said. “Over time, that could help clinicians and patients make more informed decisions about care.”

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By Lesley Henton, Texas A&M University Division of Marketing and Communications

Source: Texas A&M University

AI Mistakes Can Cost Doctors Time when Writing to Patients

Errors and irrelevant details mean physicians may spend more time editing AI-drafted responses than it would take to write them, a large study of an online patient portal shows

Photo by National Cancer Institute on Unsplash

Artificial intelligence is spreading rapidly in health care, with the goal of streamlining critical but onerous clerical tasks such as note-taking and charting so that physicians and nurses can devote more time to patients. But even when AI can free up doctors to correspond with patients, it may fall short in helping them do it by introducing errors and extraneous details into their messages, according to a new Dartmouth study presented at the 2026 Annual Meeting of the Association for Computational Linguistics and published in the conference proceedings

The result is that physicians may spend more time editing responses than it would’ve taken to write them, the researchers report.

“We find that AI can sound like a doctor but not think like one,” says Sarah Preum, an assistant professor of computer science and the study’s co-corresponding author with Parker Seegmiller, a graduate researcher in Preum’s PersistLab at Dartmouth. 

The researchers conducted the first large-scale study of an online patient portal that uses AI to draft responses from physicians to patients. The team developed a tool that compares AI-generated replies to a dataset of real responses they developed with health care professionals from Dartmouth Health

They then analysed 146 000 conversations between 10 105 patients and their primary care physicians at the large rural health system, with data anonymised.

The researchers also used their tool to evaluate physician responses drafted by Claude, Gemini, and ChatGPT, as well as the three smaller commercial platforms, Llama, Aloe, and Qwen. 

“We find that AI can sound like a doctor but not think like one.” 

Sarah Preum, corresponding author and assistant professor of computer science

The team reports that AI-generated answers frequently misalign with what clinicians would actually write. This includes automated responses that are too long, don’t ask follow-up questions, and use irrelevant or inaccurate medical details.

“There are smaller studies that say, ‘Oh, AI is amazing,’ but we realised there is a gap in the existing literature of a large-scale evaluation of this technology,” Preum says. “We didn’t just want to measure a platform’s accuracy, but whether it actually helps with the workload, which in this case is measured by how much editing the physician is doing.” 

For example, the portal’s AI suggested telling a 32-year-old woman who is taking an acid reflux drug and was concerned about constant nausea that the medication might take some adjustment in diet. A physician replaced that by asking if there’s any chance she was pregnant. 

Even little changes can add up over hundreds or thousands of messages, Preum says. “You don’t want to integrate large language models into the workflow and just shift the bottleneck so that doctors are devoting their cognitive energy to playing AI janitor and fixing mistakes,” Preum says. “But if we’re not careful, that’s a likely outcome.”

The researchers show, however, that adapting AI to how individual physicians communicate can improve accuracy by 33% and reduce editing by 26%. 

“If message generation is really efficient and high quality, if it asks the right things, then it really has potential to improve efficiency,” says co-author Tim Burdick, an associate professor of community and family medicine in Dartmouth’s Geisel School of Medicine and a family medicine physician at Dartmouth Health. 

“I don’t foresee a time when the portal can respond to a patient without a clinician editing it first. But as we make the models better, we’ll be able to address portal messages much more quickly and with less mental energy,” Burdick says. 

The study shows that there are such things as “good” AI responses and provides a framework for implementing them into patient-physician portals, Preum says. These platforms are increasingly common among large health care systems and often customized, she says.

“That took us a long time to figure out, but if you’re trying to measure how effective this technology is, you need to define what a good response is,” she says. “We can only improve what we can measure and objectively evaluate.” 

The researchers created a technique called TADPOLE (Thematic Agentic Direct Preference Optimization for Learning Enhancement) that trains AI platforms using the hybrid model they constructed from physician- and AI-generated responses.

They plugged TADPOLE into the six commercial LLMs and found that drafted responses better matched physicians’ standards for precision and information quality. “That could save a busy clinician an hour or two of work a day,” Burdick says. 

Doctors and nurses today are inundated with messages from patients and caregivers who can write them online anytime, he says. An ongoing project between Burdick and the Preum Lab called PortalPal aims to streamline patient portals using AI, including by automating some steps in following up with patients to get more information.

“We’re still nowhere near the point of having clinicians removed from the workflow.”

Tim Burdick, co-author and associate professor of community and family medicine

Physicians who Burdick works with say that AI-generated drafts save about 25% of their time on shorter messages. “It’s easier to make small edits to an LLM-generated message than it is to write it from scratch,” he says. But longer drafts can include information that is not correct or accurate. 

“If you have to edit 75% of the message, you may be spending more time and energy on making changes than if you were to just write it from scratch,” Burdick says. “I would guess we need to get to where the physician is editing less than 30% of the content before it has substantial benefit.”

One advantage of AI’s verbosity is that it tends to be more empathetic and thorough than physicians crunched for time, the researchers find. For example, AI is more likely to tell a patient experiencing an upset stomach that it’s sorry to hear they’re feeling nauseated. 

This means AI could be used to help “nudge” doctors to show more understanding and care for the patient’s situation, or answer patient’s questions more effectively so that patients feel more heard, Preum says. The team produced sample responses such as showing empathy by praising patients for following a treatment plan (“You’ve been doing a great job with your tapering.”) or planning for changes in symptoms (“If you’re feeling dizzy, please call triage.”).

The researchers also find that 65% of all the portal messages they studied came from people over 55, with patients over 65 generating 24% of all messages. These figures suggest that patient portals in general should be designed to accommodate older people, Preum says.

Future work will study how much actual time doctors spend editing automated drafts. The team also plans to evaluate their training model TADPOLE from the user perspective, studying if and how it lightens a physician’s workload, and how doctors and patients rate its performance. 

“This is one of the first studies that uses real patient portal messages to establish a generative AI model. In that regard, it’s innovative and shows us that this is not a simple task,” Burdick says. “We’re still nowhere near the point of having clinicians removed from the workflow.”

Source: EurekAlert!