New insights into dopamine in focal cortical dysplasia: For the first time, a research team in Bonn is systematically investigating the role of the dopamine system in a common form of therapy-resistant epilepsy. Their research, published in Brain, has found major changes in the signalling pathway in a brain malformation linked to treatment-resistant epilepsy.
Focal cortical dysplasia (FCD) type 2 is a congenital malformation of the cerebral cortex associated with hard-to-treat epilepsy. In the affected areas, nerve cells and their layer structures are arranged abnormally, impeding drug therapy. A research team from the University Hospital Bonn (UKB) and the University of Bonn, in collaboration with the German Center for Neurodegenerative Diseases (DZNE), has now found evidence of profound changes in the dopamine system in FCD type 2.
Dopamine is a central neurotransmitter that regulates attention, learning and the excitability of neuronal networks, among other things. Whether and how this system is affected by FCD has so far remained largely unclear. The current study shows that the dopaminergic supply in the affected brain areas is altered. In addition, an increased expression of certain dopamine receptors was observed – both in human tissue and in a corresponding mouse model.
Evidence of disturbed modulation in the developing cortex
“Our data suggest a disrupted dopaminergic system in FCD type 2,” explains Norisa Meli, a doctoral student at the University of Bonn at the Institute for Reconstructive Neurobiology at the UKB and first author of the study. ”Particularly striking was the significantly increased expression of dopaminergic receptors in the neurons that are central role to the disease process.”
These changes could play a role in the development of epileptic seizures – and possibly also explain why many sufferers also experience concentration problems or mood swings.
“Dopamine modulates the excitability of neuronal networks and their formation in the developing cortex,” emphasizes Prof. Sandra Blaess, Professor of Neurodevelopment at UKB and member of the TRA ‘Life & Health’ at the University of Bonn. ”Our results show that this modulation may be disturbed in FCD type 2 – an aspect that has hardly been investigated to date.”
Prof. Albert Becker, Head of Department at the Institute for Cellular Neuroscience II at the UKB and also a member of the TRA “Life & Health” at the University of Bonn, adds: “These findings broaden our understanding of the complex neuropathology of dysplasias. They provide important clues for new potential therapeutic approaches that could go beyond the mere control of seizures.”
The study combines comprehensive molecular analyses of human tissue samples with a preclinical mouse model that replicates the genetic changes in FCD type 2. The researchers hope that these results will contribute to more targeted and effective treatment strategies in the long term.
In sports, the connection between head injuries and neurodegenerative diseases such as chronic traumatic encephalopathy, Alzheimer’s disease, and Parkinson’s disease is now well recognised.
Researchers at Tufts University and Oxford University have now uncovered mechanisms that may connect the dots between trauma events and the emergence of disease. They point to latent viruses lurking in most of our brains that may be activated by the jolt, leading to inflammation and accumulating damage that can occur over the ensuing months and years.
The results suggest the use of antiviral drugs as potential early preventive treatments post-head injury. The findings are published in a study in Science Signaling.
The microbiome aids in digestion, immune system development, and protection against harmful pathogens.
But the microbiome also includes dozens of viruses that swarm within our bodies at any given time. Some of these can be potentially harmful, but simply lie dormant within our cells. Herpes simplex virus 1 (HSV-1), found in over 80% of people, and varicella-zoster virus, found in 95% of people, are known to make their way into the brain and sleep within our neurons and glial cells.
Dana Cairns, GBS12, research associate in the Department of Biomedical Engineering and lead author of the study, had found evidence in earlier studies suggesting that activation of HSV-1 from its dormant state triggers the signature symptoms of Alzheimer’s disease in lab models of brain tissue: amyloid plaques, neuronal loss, inflammations, and diminished neural network functionality.
“In that study, another virus – varicella – created the inflammatory conditions that activated HSV-1,” said Cairns. “We thought, what would happen if we subjected the brain tissue model to a physical disruption, something akin to a concussion? Would HSV-1 wake up and start the process of neurodegeneration?”
The link between HSV-1 and Alzheimer’s disease was first suggested by co-author Ruth Itzhaki, visiting professorial fellow at Oxford University, who more than 30 years ago identified the virus in a high proportion of brains from the elderly population. Her subsequent studies suggested that the virus can be reactivated in the brain from a latent state by events such as stress or immunosuppression, ultimately leading to neuronal damage.
Blows to Brain-like Tissue
In the current study, the researchers used a lab model that reconstructs the environment of the brain to better understand how concussions may set off the first stages of virus reactivation and neurodegeneration.
The brain tissue model consists of a 6mm-wide donut-shaped sponge-like material made of silk protein and collagen suffused with neural stem cells, which are then coaxed into mature neurons, growing axons and dendrite extensions and forming a network. Glial cells also emerge from the stem cells to help mimic the brain environment and nurture the neurons.
The neurons communicate with each other through their extensions similarly to how they would communicate in a brain. And just like cells in the brain, they can carry within them the DNA of dormant HSV-1 virus.
After enclosing the brain-like tissue in a cylinder and giving it a sudden jolt atop a piston, mimicking a concussion, Cairns examined the tissue under the microscope over time. Some of the tissue models had neurons with HSV-1, and some were virus-free.
Following the controlled blows, she observed that the infected cells showed re-activation of the virus, and shortly after that the signature markers of Alzheimer’s disease, including amyloid plaques, p-tau (a protein that creates fiber-like “tangles” in the brain), inflammation, dying neurons, and a proliferation of glial cells called gliosis.
More strikes with the pistons on the tissue models mimicking repetitive head injuries led to the same reactions, which were even more severe. Meanwhile, the cells without HSV-1 showed some gliosis, but none of the other markers of Alzheimer’s disease.
The results were a strong indicator that athletes suffering concussions could be triggering reactivation of latent infections in the brain that can lead to Alzheimer’s disease. Epidemiological studies have shown that multiple blows to the head can lead to doubling or even greater chances of having a neurodegenerative condition months or years down the line.
“This opens the question as to whether antiviral drugs or anti-inflammatory agents might be useful as early preventive treatments after head trauma to stop HSV-1 activation in its tracks, and lower the risk of Alzheimer’s disease,” said Cairns.
The problem goes far beyond the concerns for athletes. Traumatic brain injury is one of the most common causes of disability and death in adults, affecting about 69 million people worldwide each year, at an economic cost estimated at $400 billion annually.
“The brain tissue model takes us to another level in investigating these connections between injury, infection, and Alzheimer’s disease,” said David Kaplan, Stern Family Endowed Professor of Engineering at Tufts.
“We can re-create normal tissue environments that look like the inside of a brain, track viruses, plaques, proteins, genetic activity, inflammation and even measure the level of signalling between neurons,” he said. “There is a lot of epidemiological evidence about environmental and other links to the risk of Alzheimer’s. The tissue model will help us put that information on a mechanistic footing and provide a starting point for testing new drugs.”
According to a study published by Nature Metabolism, marathon runners experience reversible changes in their brain myelin. These findings indicate that myelin exhibits previously unknown behaviour, which contributes towards the brain’s energy metabolism when other sources of energy are running low. Understanding how myelin in the runners recovers quickly may provide clues for developing treatments for demyelinating diseases such as multiple sclerosis.
Exercise for a long period of time forces the human body to resort to its energy reserves. When running a marathon, for example, the body mainly consumes carbohydrates, such as glycogen, as a source of energy, but it resorts to fats when the glycogen in the muscles is used up. Myelin, which surrounds neurons in the brain and acts as an electrical insulator, mainly comprises lipids, and previous research in rodents suggests that these lipids can act as an energy reserve in extreme metabolic conditions.
A study conducted by researchers from the UPV/EHU, CIC biomaGUNE and IIS Biobizkaia shows that people who run a marathon experience a decrease in the amount of myelin in certain regions of the brain. According to the study, this effect is completely reversed two months after the marathon.
Carlos Matute, Professor of Anatomy and Human Embriology at the UPV/EHU and a researcher at IIS Biobizkaia, and Pedro Ramos-Cabrer, Ikerbasque Research Professor at CIC biomaGUNE, together with Alberto Cabrera-Zubizarreta, radiologist at HT Médica, used magnetic resonance imaging to obtain images of the brains of ten marathon runners (eight men and two women) before and 48 hours after the 42-kilometre race. Likewise, the researchers took images of the brains of two of the runners two weeks after the race, and of six runners two months after the race as a follow-up.
By measuring the fraction of myelin water in the brain – an indirect indicator of the amount of myelin – the authors discovered “a reduction in the myelin content in 12 areas of white matter in the brain, which are related to motor coordination and sensory and emotional integration”, explained Carlos Matute. Two weeks later, “the myelin concentrations had increased substantially, but had not yet reached pre-race levels”, added Pedro Ramos. The authors saw that the myelin content had recovered fully two months after the marathon.
Myelin, the brain’s fuel
The researchers concluded that “myelin seems to act as an energy source when other brain nutrients are depleted during endurance exercise, and that further research is needed to establish how extreme exercise is related to the amount of myelin in the brain. Trials in a larger cohort are needed”, said Ramos-Cabrer.
This study reveals that “brain energy metabolism is more complex than previously thought. The use of myelin as brain fuel opens up new insights into the brain’s energy requirements”, explained Matute. Furthermore, according to the authors, more studies are needed to assess whether these changes exert any effect on the neurophysiological and cognitive functions associated with these regions, but they point out that most of the myelin in the brain is not affected.
The results of this work break new ground in the energy role of healthy, aging and diseased myelin in the brain. “Understanding how the myelin in the runners recovers quickly may provide clues for developing treatments for demyelinating diseases, such as multiple sclerosis, in which the disappearance of myelin and, therefore, of its energy contribution, facilitates structural damage and degeneration,” said Matute. At the same time, the researchers are keen to stress that running marathons is not harmful for the brain; “on the contrary, the use and replacement of myelin as an energy reserve is beneficial because this exercises the brain’s metabolic machinery”.
Researchers at Nagoya University Graduate School of Medicine has discovered that using “a unique sound stimulation technology” – a device that stimulates the inner ear with a specific wavelength of sound – reduces motion sickness. Even a single minute of stimulation reduced the staggering and discomfort felt by people that read in a moving vehicle. The results, published in Environmental Health and Preventive Medicine, suggest a simple and effective way to treat this common disorder.
“Our study demonstrated that short-term stimulation using a unique sound called ‘sound spice®’ alleviates symptoms of motion sickness, such as nausea and dizziness,” said study leader Takumi Kagawa. “The effective sound level falls within the range of everyday environmental noise exposure, suggesting that the sound technology is both effective and safe.”
The discovery is an important expansion of recent findings about sound and its effect on the inner ear. Increasing evidence has suggested that stimulating the part of the inner ear associated with balance using a unique sound can potentially improve balance. Using a mouse model and humans, the researchers identified a unique sound at 100Hz as being the optimal frequency.
“Vibrations at the unique sound stimulate the otolithic organs in the inner ear, which detect linear acceleration and gravity,” study leader Masashi Kato explained. “This suggests that a unique sound stimulation can broadly activate the vestibular system, which is responsible for maintaining balance and spatial orientation.”
To test the effectiveness of the devices, they recruited voluntary participants who were exposed to the unique sound. Following the stimulation, motion sickness was induced by a swing, a driving simulator, or riding in a car. The researchers used postural control, ECG readings, and Motion Sickness Assessment Questionnaire results to assess the effectiveness of the stimulation.
Exposure to the unique sound before being exposed to the driving simulator enhanced sympathetic nerve activation. The researchers found symptoms such as “lightheadedness” and “nausea,” which are often seen with motion sickness, were alleviated.
“These results suggest that activation of sympathetic nerves, which are often dysregulated in motion sickness, was objectively improved by the unique sound exposure,” Kato said.
“The health risk of short-term exposure to our unique sound is minimal,” Kagawa said. “Given that the stimulus level is well below workplace noise safety standards, this stimulation is expected to be safe when used properly.”
Their results suggest a safe and effective way to improve motion sickness, potentially offering help to millions of sufferers. The researchers plan to further develop the technology with the aim of practical application for a variety of travel situations including air and sea travel.
Heavy drinkers who have eight or more alcoholic drinks per week have an increased risk of brain lesions called hyaline arteriolosclerosis, signs of brain injury that are associated with memory and thinking problems, according to a study published on April 9, 2025, online in Neurology®, the medical journal of the American Academy of Neurology (AAN).
Hyaline arteriolosclerosis is a condition that causes the small blood vessels to narrow, becoming thick and stiff. This makes it harder for blood to flow, which can damage the brain over time. It appears as lesions, areas of damaged tissue in the brain.
“Heavy alcohol consumption is a major global health concern linked to increased health problems and death,” said study author Alberto Fernando Oliveira Justo, PhD, of University of Sao Paulo Medical School in Brazil. “We looked at how alcohol affects the brain as people get older. Our research shows that heavy alcohol consumption is damaging to the brain, which can lead to memory and thinking problems.”
The study included 1781 people who had an average age of 75 at death. All had brain autopsies. Researchers examined brain tissue to look for signs of brain injury including tau tangles and hyaline arteriolosclerosis. They also measured brain weight and the height of each participant. Family members answered questions about participants’ alcohol consumption. Researchers then divided the participants into four groups: 965 people who never drank, 319 moderate drinkers who had seven or fewer drinks per week; 129 heavy drinkers who had eight or more drinks per week; and 368 former heavy drinkers.
Researchers defined one drink as having 14 grams of alcohol, which is about 350mL of beer, 150mL of wine or 45mL of distilled spirits. Of those who never drank, 40% had vascular brain lesions. Of the moderate drinkers, 45% had vascular brain lesions. Of the heavy drinkers, 44% had vascular brain lesions. Of the former heavy drinkers, 50% had vascular brain lesions.
After adjusting for factors that could affect brain health such as age at death, smoking and physical activity, heavy drinkers had 133% higher odds of having vascular brain lesions compared to those who never drank, former heavy drinkers had 89% higher odds and moderate drinkers, 60%.
Researchers also found heavy and former heavy drinkers had higher odds of developing tau tangles, a biomarker associated with Alzheimer’s disease, with 41% and 31% higher odds, respectively. Former heavy drinking was associated with a lower brain mass ratio, a smaller proportion of brain mass compared to body mass, and worse cognitive abilities.
No link was found between moderate or heavy drinking and brain mass ratio or cognitive abilities. Justo noted that, in addition to brain injuries, impaired cognitive abilities were observed only in former drinkers. Researchers also found that heavy drinkers died an average of 13 years earlier than those who never drank.
“We found heavy drinking is directly linked to signs of injury in the brain, and this can cause long-term effects on brain health, which may impact memory and thinking abilities,” said Justo. “Understanding these effects is crucial for public health awareness and continuing to implement preventive measures to reduce heavy drinking.”
A limitation of the study was that it did not look at participants before death and did not have information on the duration of alcohol consumption and cognitive abilities.
New research shows that the adult brain can generate new neurons that integrate into key motor circuits. The findings demonstrate that stimulating natural brain processes may help repair damaged neural networks in Huntington’s and other diseases.
“Our research shows that we can encourage the brain’s own cells to grow new neurons that join in naturally with the circuits controlling movement,” said Abdellatif Benraiss, PhD, a senior author of the study, which appears in the journal Cell Reports. “This discovery offers a potential new way to restore brain function and slow the progression of these diseases.” Benraiss is a research associate professor in the University of Rochester Medical Center (URMC) lab of Steve Goldman, MD, PhD, in the Center for Translational Neuromedicine.
Is neuron regeneration in the adult brain possible?
It is now understood that niches in the brain contain reservoirs of progenitor cells capable of producing new neurons. While these cells actively produce neurons during early development, they switch to producing support cells called glia shortly after birth. One of the areas of the brain where these cells congregate is the ventricular zone, which is adjacent to the striatum, a region of the brain devastated by Huntington’s disease.
The idea that the adult brain retains the capacity to produce new neurons, called adult neurogenesis, was first described by Goldman and others in the 1980s while studying neuroplasticity in canaries. Songbirds, like canaries, are unique in the animal kingdom in their ability to lay down new neurons as they learn new songs. The research in songbirds identified proteins—one of which was brain-derived neurotrophic factor (BDNF)—that direct progenitor cells to differentiate and produce neurons.
Further research in Goldman’s lab showed that new neurons were generated when BDNF and another protein, Noggin, were delivered to progenitor cells in the brains of mice. These cells then migrated to a nearby motor control region of the brain—the striatum—where they developed into cells known as medium spiny neurons, the major cells lost in Huntington’s disease. Benraiss and Goldman also demonstrated that the same agents could induce new medium spiny neuron formation in primates.
Rebuilding and reconnecting brain networks
The extent to which newly generated medium spiny neurons integrate into the brain’s networks has remained unclear. The new research, conducted in a mouse model of Huntington’s disease, demonstrates that the newly generated neurons connect with the complex networks in the brain responsible for motor control, replacing the function of the neurons lost in Huntington’s.
The researchers used a genetic tagging method to mark new cells as they were created, which allowed them to follow them over time as they developed new connections. This enabled the researchers to map the connections between the new neurons, their neighbours, and other brain regions. Employing optogenetics techniques, the researchers turned the new cells on and off, confirming their integration into broader brain networks important for motor control.
A new path for Huntington’s disease therapies
The study indicates that a possible treatment for Huntington’s disease would be to encourage the brain to replace lost cells with new, functional ones and restore the brain’s communication pathways. “Taken together with the persistence of these progenitor cells in the adult primate brain, these findings suggest the potential for this regenerative approach as a treatment strategy in Huntington’s and other disorders characterised by the loss of neurons in the striatum,” said Benraiss.
The authors suggest this approach could also be combined with other cell replacement therapies. Research in Goldman’s lab has shown that glial cells called astrocytes also play an important role in Huntington’s disease. These cells do not function properly in the disease and contribute to the impairment of neuronal function. The researchers have found that replacing the diseased glial cells with healthy ones can slow disease progression in a mouse model of Huntington’s. These glial replacement therapies are currently in preclinical development.
Immune molecules called cytokines play important roles in the body’s defence against infection, helping to control inflammation and coordinating the responses of other immune cells. A growing body of evidence suggests that some of these molecules also influence the brain, leading to behavioural changes during illness.
Two new studies from MIT and Harvard Medical School, focused on a cytokine called IL-17, now add to that evidence. The researchers found that IL-17 acts on two distinct brain regions — the amygdala and the somatosensory cortex — to exert two divergent effects. In the amygdala, IL-17 can elicit feelings of anxiety, while in the cortex it promotes sociable behaviour.
These findings suggest that the immune and nervous systems are tightly interconnected, says Gloria Choi, an associate professor of brain and cognitive sciences, a member of MIT’s Picower Institute for Learning and Memory, and one of the senior authors of the studies.
“If you’re sick, there’s so many more things that are happening to your internal states, your mood, and your behavioural states, and that’s not simply you being fatigued physically. It has something to do with the brain,” she says.
Jun Huh, an associate professor of immunology at Harvard Medical School, is also a senior author of both studies, which appear today in Cell. One of the papers was led by research scientists Byeongjun Lee and Jeong-Tae Kwon, and the other was led by postdocs Yunjin Lee and Tomoe Ishikawa.
Behavioral effects
Choi and Huh became interested in IL-17 several years ago, when they found it was involved in a phenomenon known as the fever effect. Large-scale studies of autistic children have found that for many of them, their behavioural symptoms temporarily diminish when they have a fever.
In a 2019 study in mice, Choi and Huh showed that in some cases of infection, IL-17 is released and suppresses a small region of the brain’s cortex known as S1DZ. Overactivation of neurons in this region can lead to autism-like behavioral symptoms in mice, including repetitive behaviours and reduced sociability.
“This molecule became a link that connects immune system activation, manifested as a fever, to changes in brain function and changes in the animals’ behaviour,” Choi says.
IL-17 comes in six different forms, and there are five different receptors that can bind to it. In their two new papers, the researchers set out to map which of these receptors are expressed in different parts of the brain. This mapping revealed that a pair of receptors known as IL-17RA and IL-17RB is found in the cortex, including in the S1DZ region that the researchers had previously identified. The receptors are located in a population of neurons that receive proprioceptive input and are involved in controlling behaviour.
When a type of IL-17 known as IL-17E binds to these receptors, the neurons become less excitable, which leads to the behavioural effects seen in the 2019 study.
“IL-17E, which we’ve shown to be necessary for behavioural mitigation, actually does act almost exactly like a neuromodulator in that it will immediately reduce these neurons’ excitability,” Choi says. “So, there is an immune molecule that’s acting as a neuromodulator in the brain, and its main function is to regulate excitability of neurons.”
Choi hypothesises that IL-17 may have originally evolved as a neuromodulator, and later on was appropriated by the immune system to play a role in promoting inflammation. That idea is consistent with previous work showing that in the worm C. elegans, IL-17 has no role in the immune system but instead acts on neurons. Among its effects in worms, IL-17 promotes aggregation, a form of social behaviour. Additionally, in mammals, IL-17E is actually made by neurons in the cortex, including S1DZ.
“There’s a possibility that a couple of forms of IL-17 perhaps evolved first and foremost to act as a neuromodulator in the brain, and maybe later were hijacked by the immune system also to act as immune modulators,” Choi says.
Provoking anxiety
In the other Cell paper, the researchers explored another brain location where they found IL-17 receptors — the amygdala. This almond-shaped structure plays an important role in processing emotions, including fear and anxiety.
That study revealed that in a region known as the basolateral amygdala (BLA), the IL-17RA and IL-17RE receptors, which work as a pair, are expressed in a discrete population of neurons. When these receptors bind to IL-17A and IL-17C, the neurons become more excitable, leading to an increase in anxiety.
The researchers also found that, counterintuitively, if animals are treated with antibodies that block IL-17 receptors, it actually increases the amount of IL-17C circulating in the body. This finding may help to explain unexpected outcomes observed in a clinical trial of a drug targeting the IL-17-RA receptor for psoriasis treatment, particularly regarding its potential adverse effects on mental health.
“We hypothesise that there’s a possibility that the IL-17 ligand that is upregulated in this patient cohort might act on the brain to induce suicide ideation, while in animals there is an anxiogenic phenotype,” Choi says.
During infections, this anxiety may be a beneficial response, keeping the sick individual away from others to whom the infection could spread, Choi hypothesises.
“Other than its main function of fighting pathogens, one of the ways that the immune system works is to control the host behaviour, to protect the host itself and also protect the community the host belongs to,” she says. “One of the ways the immune system is doing that is to use cytokines, secreted factors, to go to the brain as communication tools.”
The researchers found that the same BLA neurons that have receptors for IL-17 also have receptors for IL-10, a cytokine that suppresses inflammation. This molecule counteracts the excitability generated by IL-17, giving the body a way to shut off anxiety once it’s no longer useful.
Distinctive behaviours
Together, the two studies suggest that the immune system, and even a single family of cytokines, can exert a variety of effects in the brain.
“We have now different combinations of IL-17 receptors being expressed in different populations of neurons, in two different brain regions, that regulate very distinct behaviours. One is actually somewhat positive and enhances social behaviours, and another is somewhat negative and induces anxiogenic phenotypes,” Choi says.
Her lab is now working on additional mapping of IL-17 receptor locations, as well as the IL-17 molecules that bind to them, focusing on the S1DZ region. Eventually, a better understanding of these neuro-immune interactions may help researchers develop new treatments for neurological conditions such as autism or depression.
“The fact that these molecules are made by the immune system gives us a novel approach to influence brain function as means of therapeutics,” Choi says. “Instead of thinking about directly going for the brain, can we think about doing something to the immune system?”
Two undergraduate medicine students at University of Galway have led a major study examining how cardioprotective glucose-lowering therapies affect the risk of developing dementia.
The new study involved a systematic review and meta-analysis of 26 clinical trials involving more than 160 000 participants.
The researchers found that while most glucose-lowering therapies were not significantly associated with a reduction in dementia risk, one class of drugs – known as GLP-1 receptor agonists (GLP-1Ras) was linked to a significant reduction.
The study was conducted by medical students Allie Seminer and Alfredi Mulihano, alongside researchers from University of Galway, the HRB Clinical Research Facility Galway and University Hospital Galway.
Key Findings:
The research analysed data from 26 randomised controlled trials with a total of 164 531 participants.
While glucose-lowering therapies as a whole did not significantly reduce dementia risk, GLP-1 receptor agonists (GLP-1Ras) were linked to a 45% lower risk of dementia.
The findings provide crucial insights into the potential for diabetes medications to influence long-term brain health.
Dr Catriona Reddin, senior author, researcher at the University of Galway and Registrar in Geriatric Medicine at HSE West North West, said: “This research represents a significant contribution to our understanding of how some diabetes medications may impact brain health. Diabetes is a known risk factor for dementia, but whether glucose-lowering therapies can help prevent cognitive decline has remained unclear. Our findings suggest that GLP-1 receptor agonists, in particular, may have a protective effect on brain health.”
Professor Martin O’Donnell, Dean of the College of Medicine, Nursing and Health Sciences at University of Galway and Consultant Stroke Physician with HSE West North-West said: “Given the increasing prevalence of both diabetes and dementia, findings from this study have important public health implications for prevention of dementia.
“What makes this study particularly exciting for the College of Medicine, Nursing and Health Sciences at University of Galway, is that it was led by two of our undergraduate medicine students. We place a strong emphasis on research as a core component of our undergraduate medicine programme, ensuring that students have opportunities to engage in high-impact studies that shape global healthcare.”
Allie Seminer, a third year student from New York and co-lead author, said: “Being involved in a study of this scale as an undergraduate has been an incredible experience. What stood out for me was the sense of responsibility – knowing that our work could help shape understanding of a global health issue. It was incredibly motivating to be part of a team working at this level, and it has shown me how research is an essential part of becoming a well-rounded doctor. It highlights how research is not just an add-on to our degree but an essential part of how we learn to advance medical knowledge.”
Alfredi Mulihano, a third year student from Dundalk and co-lead author, said: “Being part of this study has completely changed how I see my role as a future doctor. It brought together clinical insight, data analysis, and critical thinking in a way that lectures alone cannot. The experience opened my eyes to the impact we can have beyond the bedside – contributing to knowledge that could change how diseases like dementia are prevented.”
Researchers from the University of Missouri have discovered that kaempferol, a natural antioxidant found in certain fruits and vegetables, such as kale, berries and endives, may support nerve cell health and holds promise as a potential treatment for ALS. Photo: Pixabay CC0
A natural compound found in everyday fruits and vegetables may hold the key to protecting nerve cells — and it’s showing promise as a potential treatment for ALS and dementia, according to new research from the University of Missouri.
“It’s exciting to discover a naturally occurring compound that may help people suffering from ALS or dementia,” Smita Saxena, a professor of physical medicine and rehabilitation at the School of Medicine and lead author of the study, said. “We found this compound had a strong impact in terms of maintaining motor and muscle function and reducing muscle atrophy.”
The study, which appears in Acta Neurologica, discovered that kaempferol, a natural antioxidant found in certain fruits and vegetables, such as kale, berries and endives, may support nerve cell health and holds promise as a potential treatment for ALS.
In lab-grown nerve cells from ALS patients, the compound helped the cells produce more energy and eased stress in the protein-processing center of the cell called the endoplasmic reticulum. Additionally, the compound improved overall cell function and slowed nerve cell damage. Researchers found that kaempferol worked by targeting a crucial pathway that helps control energy production and protein management — two functions that are disrupted in individuals with ALS.
“I believe this is one of the first compounds capable of targeting both the endoplasmic reticulum and mitochondria simultaneously,” Saxena said. “By interacting with both of these components within nerve cells, it has the potential to elicit a powerful neuroprotective effect.”
The challenge
The catch? The body doesn’t absorb kaempferol easily, and it could take a large amount to see real benefits in humans. For instance, an individual with ALS would need to consume at least 4.5kg of kale in a day to obtain a beneficial dose.
“Our bodies don’t absorb kaempferol very well from the vegetables we eat,” Saxena said. “Because of this, only a small amount reaches our tissues, limiting how effective it can be. We need to find ways to increase the dose of kaempferol or modify it so it’s absorbed into the bloodstream more easily.”
Another hurdle is getting the compound into the brain. The blood-brain barrier — a tightly locked layer of cells that blocks harmful substances — also makes it harder for larger molecules like kaempferol to pass through.
What’s next?
Despite its challenges, kaempferol remains a promising candidate for treating ALS, especially since it works even after symptoms start. It also shows potential for other neurodegenerative diseases including Alzheimer’s and Parkinson’s.
To make the compound easier for the body to absorb, Saxena’s team at the Roy Blunt NextGen Precision Health building is exploring ways to boost its uptake by neurons. One promising approach involves packaging lipid-based nanoparticles — tiny spherical particles made of fats that are commonly used in drug delivery.
“The idea is to encapsulate kaempferol within lipid-based nanoparticles that are easily absorbed by the neurons,” Saxena said. “This would target kaempferol to neurons to greatly increase its beneficial effect.”
The team is currently generating the nanoparticles with hopes of testing them by the end of the year.
Mass General Brigham investigators have linked difficult early life experiences with reduced quality and quantity of the white matter communication highways throughout the adolescent brain. This reduced connectivity is also associated with lower performance on cognitive tasks. However, certain social resiliency factors like neighbourhood cohesion and positive parenting may have a protective effect. Results are published in Proceedings of the National Academy of Sciences (PNAS).
White matter are the communication highways that allow the brain networks to carry out the necessary functions for cognition and behaviour. They develop over the course of childhood, and childhood experiences may drive individual differences in how white matter matures. Lead author Sofia Carozza, PhD, and senior author Amar Dhand, MD, PhD, of the Department of Neurology at Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system, wanted to understand what role this process plays in cognition once children reach adolescence.
“The aspects of white matter that show a relationship with our early life environment are much more pervasive throughout the brain than we’d thought. Instead of being just one or two tracts that are important for cognition, the whole brain is related to the adversities that someone might experience early in life,” said Carozza.
The team studied data from 9082 children (about half of them girls, with an average age of 9.5) collected in the Adolescent Brain Cognitive Development (ABCD) study. This study, funded by the National Institutes of Health and conducted at 21 centres across the U.S., gathered information on brain activity and structure, cognitive abilities, environment, mood and mental health. The researchers looked at several categories of early environmental factors, including prenatal risk factors, interpersonal adversity, household economic deprivation, neighbourhood adversity, and social resiliency factors.
Carozza and Dhand used diffusion imaging scanning of the brain to measure fractional anisotropy (FA)—a way of estimating the integrity of the white matter connections—and streamline count, an estimate of their strength. They then used a computational model to compare how these features of white matter were related to both childhood environmental factors and current cognitive abilities such as language skills and mental arithmetic.
Their analysis revealed widespread differences in white matter connections throughout the brain depending on the children’s early-life environments. In particular, the researchers found lower quality of white matter connections in parts of the brain tied to mental arithmetic and receptive language. These white matter differences accounted for some of the relationship between adverse life experiences in early childhood and lower cognitive performance in adolescence.
“We are all embedded in an environment, and features of that environment such as our relationships, home life, neighbourhood, or material circumstances can shape how our brains and bodies grow, which in turn affects what we can do with them,” said Carozza. “We should work to make sure that more people can have those stable, healthy home lives that the brain expects, especially in childhood.”
The researchers note that their study is based on observational data, which means they cannot draw strong causal conclusions. Brain imaging was also only available at a single timepoint, offering a snapshot but not allowing researchers to track changes over time. Prospective studies—following children over time and collecting brain imaging information at multiple time points—would be needed to more definitively connect adversity and cognitive performance.
