Category: Neuroscience Page 1 of 15

How Changes in Lemur Brains Made Some Mean Girls Nice

On April 21, 2025

If there was a contest for biggest female bullies of the animal world, lemurs would be near the top of the list. In these distant primate cousins, it’s the ladies who call the shots, relying on physical aggression to get their way and keep males in line.

*Male and female blue-eyed black lemurs at the Duke Lemur Center. In these distant primate cousins, females get their way most of the time. Photo: David Haring.*

Not all lemur societies are built about female rule, however. In one branch of the lemur family tree, some species have evolved, within the last million years, to have a more harmonious relationship between the sexes.

Now, new findings suggest that this amiable shift in lemurs was at least partly driven by changes in the action of the “love hormone” oxytocin inside their brains. The research could shed light on how hormones influence behavior in humans and other animals.

In a study published in the journal Biology Letters, Duke University researchers studied seven closely related lemur species in the genus Eulemur, noting which ones had domineering females and which were more egalitarian.

Take blue-eyed black lemurs, for example. Females get first dibs on food and prime resting spots; smacking, biting and chasing the males to get their way.

Their behavior isn’t the fierce protectiveness of a mother defending her babies, said senior author Christine Drea, a professor of evolutionary anthropology at Duke. Aggression in these females can be entirely unprovoked, simply to remind others who’s in charge.

“Males let females have priority access to whatever they want,” Drea said.

Others species, like the collared lemurs, are more peaceful and egalitarian, with males and females sharing equal status. “It’s more of an even playing field,” said first author Allie Schrock, who earned her Ph.D. in the Drea lab.

*Collared lemurs huddle at the Duke Lemur Center. Photo: David Haring*

The lemurs in the study died of natural causes some time ago, but their tissues live on, thanks to a bank of tissues from these endangered primates kept frozen at the Duke Lemur Center. Using an imaging technique called autoradiography, the researchers mapped brain binding sites for oxytocin, a hormone involved in social behaviors like trust and bonding.

The results revealed a striking pattern.

The researchers found that the more recently evolved egalitarian species had more oxytocin receptors than the others, essentially giving them more targets for oxytocin to act on.

The key difference was in the amygdala, a region of the brain typically associated with emotions such as fear, anxiety and anger.

The pattern held up for both sexes, suggesting that egalitarian species achieved gender parity by becoming less aggressive towards others overall, rather than males ramping up their aggression to match their female counterparts, Drea said.

*In these cross-sectional images of two lemur brains, arrows show oxytocin binding in the amygdala in domineering and egalitarian species. Courtesy: Allie Schrock, Duke University*

The potential implications go beyond lemurs, the researchers said. Problems with oxytocin signaling in the brain have been linked to aggression, personality disorders and autism in humans, rodents and other animals.

Next, the researchers plan to examine links between hormone receptors and additional aspects of social behavior in lemurs, such as whether they are solitary or social.

“There’s a lot more that we can learn from lemurs about how the brain regulates behavior,” Schrock said.

CITATION: “Neuropeptide Receptor Distributions in Male and Female Eulemur Vary Between Female-Dominant and Egalitarian Species,” Allie E. Schrock, Mia R. Grossman, Nicholas M. Grebe, Annika Sharma, Sara M. Freeman, Michelle C. Palumbo, Karen L. Bales, Heather B. Patisaul and Christine M. Drea. Biology Letters, March 19, 2025. DOI:10.1098/rsbl.2024.0647

By Robin Smith, Duke Marketing and Communications

The Imperfect Ways of a Perfectionist

By Sarah Pusser

On March 18, 2025

In Behavior/Psychology, Faculty, Field Research, Neuroscience

Perfectionism, although a way to control our surroundings, can often control us. As a student in the stressful and competitive environment of college, I’ve seen the pursuit of perfection overwhelm me and those around me. These incidents caught the attention of Duke psychiatry and behavioral science professors Nancy Zucker and Rachel Alison Adcock. The two decided to do an in-depth study of perfectionism, and how perfectionists can better handle their stress and be more productive.

Photo credits: *Halyna Dorozhynska* via Canva

When first trying to measure perfectionism, Zucker and Adcock found that “…the core essence of perfectionism was the sphere of failure,” meaning that out of everyone they studied, the majority of participants tended to be pushed to perfectionism because of a fear of failing. Given this, Zucker and Adcock were able to show a correlation between one’s concern over mistakes and their anxiety, social anxiety, and depressive symptoms.

Rachel Alison Adcock, M.D., Ph.D., and Nancy Zucker, Ph.D. *Credit: Duke*

Even with these correlations being present, “If given the choice between being a perfectionist and not being a perfectionist, 62.5% [of perfectionists] would choose to stay.” This means that in order to better support perfectionists in their everyday lives, Zucker and Adcock had to find ways to support perfectionists without trying to change them–in other words, you can’t just tell perfectionists to not be perfectionists anymore. So together, they created four different solutions to help minimize the harm of perfectionism:

Solution 1: Increase resource

Zucker and Adcock note that this is usually advice given for better mental health; “Go do something fun. Hang out with your friends. Go do yoga…” While these tips can be helpful, Zucker and Adcock were more interested in the opposite side of the issue–how instead perfectionists can work on optimizing their demands

Solution 2: Defining demands

Again, Zucker and Adcock mention some limitations to this argument. It is not expected that perfectionists will reduce their standards–for example, “Duke. A slightly less than exceptional education, Duke Health. Slightly less than exceptional care.” Therefore this solution of defining demands relies on both the perfectionist and those in the position to assign work to the perfectionist. An example of this is a professor reevaluating the importance of the work they are assigning–does the work really need to be completed by this date? By ensuring the work assigned and completed “respect[s] our own resources, prioritize[s] stamina and [is] orient[ed] to growth and progress,” the standards of work become more realistic and achievable.

Solution 3: Change the reward value (and distress) of making mistakes via self-regulation

Through testing how individuals responded to high confidence versus low confidence errors (or in other words, individuals who confidently answer a question that is incorrect are more likely to remember the correct solution after being told than those who answer a question with low confidence and are incorrect), Zucker and Adcock found that “high perfectionism individuals are less sensitive to error than low perfectionism individuals” and “high perfectionism individuals are only sensitive to error after negative or positive framing.” This means that changing how perfectionists are made aware of their mistakes (showing them how mistakes are learning opportunities) can “increase perfectionists’ sensitivity to surprising feedback in updating beliefs,” and thus help those individuals learn from their mistakes better–so as to show how mistakes are crucial for learning.

Solution 4: Change reward value and distress of mistakes via social contingencies and milieu

Similar to solution three, solution four’s goal is to change the perception of mistakes, however, this solution proposes a change through group support instead of self-regulation. This could look like peer support groups for perfectionist individuals. Zucker and Adcock emphasize the importance of the message, “We are more than a single moment in time,” which can be beneficial for a perfectionist individual to hear from their trusted peers.

The importance of mistakes was a theme that continued to pop up throughout Zucker and Adcock’s presentation. And while that can seem cliche, it’s something that we as students, professors, and people, should listen to more (thanks to Zucker and Adcock, we’ve also seen how making mistakes is scientifically proven to teach us the correct answer).

As the researchers wrapped up their talk, they left us with one more quote that stuck with me. “We are in the pursuit of the unknown. Hope is medicine. Imperatives are not hope.”

In a place like college, where just one failure can feel like the end of the world, Zucker and Adcock’s research encourages us to grow comfortable with the unknown so that our mistakes too can be something to be proud of.

Sarah Pusser Class of 2028

Nature On the Brain: Green Space, Cities and Depression

By Crystal Han

On March 1, 2025

In Behavior/Psychology, Engineering, Environment/Sustainability, Lecture, Neuroscience

Though I’ve yet to explore all of Duke’s nooks and crannies, I feel confident that my favorite corner of campus will always be the Sarah P. Duke Gardens. Nature, and green space generally, is good for us as humans. Most of us understand this on an intuitive level, but what’s the underlying reason? How might it be built into our brains?

Psychology professor Marc G. Berman looks for the answers. At the University of Chicago, Berman directs the Environmental Neuroscience Lab, in which he investigates interactions between our brains and our physical surroundings. In a recent virtual Grand Rounds lecture in Duke’s Department of Psychiatry & Behavioral Sciences, Berman spoke about the broad scope of his research and its implications for a better society.

Attention Restoration Theory

Researchers have proposed various theories for why we love nature. For example, the biophilia hypothesis states that humans have an innate attraction to nature on a genetic and evolutionary basis. However, Berman is focused primarily on the Attention Restoration Theory, a concept he’s contributed to significantly. Under this theory, attention is split into two types: directed and involuntary.

The first type is finite––think about the amount of energy it takes you to deliberately concentrate on something. “The first five minutes of lecture, everybody’s very focused on me,” Berman said, using the example of his own classes. Forty-five minutes later, and people inevitably begin to nod off.

*Mingo Falls, North Carolina. Author photo*

On the other hand, involuntary attention is not really under our control and isn’t as susceptible to becoming drained. Within stimuli that capture our involuntary attention, some are softer or harsher than others, like a stream compared to flashing lights (the stream being a softer attention capture, which we call soft fascination).

The cornerstone of Attention Restoration Theory is that nature provides an ideal environment for the restoration of directed attention; full of “softly fascinating” features, it stimulates involuntary attention without placing demands on directed attention.

A Walk in the Park

Roughly 20 years ago while Berman was a researcher at the University of Michigan, he and his colleagues wanted to test out the Attention Restoration Theory. So, after asking study participants to perform a backwards digit span task (a test for memory that would require directed attention), they told them to take a walk. Participants were directed to either a route through downtown Ann Arbor, or through the Nichols Arboretum. Then another digit span test. A week later, they repeated the whole procedure, this time walking in the other environment. Interestingly, walking through the arboretum proved more beneficial for memory. “We see about a 20% improvement in this task after people go on this brief 50-minute walk in nature versus walking in the urban environment. So that’s pretty impressive,” Berman said.

Many of us wouldn’t be surprised by this–certainly, I know a walk in the Gardens on a pleasant day recharges my ability to focus. Time in green space and warm weather often lifts our moods, but they discovered that this cognitive benefit occurs regardless of how you feel afterwards. Walkers turned cranky from the winter cold demonstrated improvements on par with those who gladly embraced sunny weather in June.

Berman saw even more of a positive effect for the park-goers when repeating the study with participants diagnosed with depression, contrary to a concern that walks alone might induce rumination on negative thoughts.

Cities: Better Than You Think They Are

In the Environmental Neuroscience Lab, Berman and doctoral students look at everything from brief interactions with nature to the long-term effects of living in large cities. Given everything thus far, it would seem logical that the latter would be far worse for our brains than other environments. Yet, Berman found just the opposite.

As it turns out, cities are beneficial for our social connectivity. Since people tend to encounter each other more often in urban areas, an individual will likely develop more social connections on average. Prior neuroscience studies have connected a greater number of social relationships to protection against depression.

*Chicago is the third largest city in the United States, both in terms of population and metropolitan area*.

Based on this, the risk of depression might be aptly represented by an inverse model of the number of people in one’s social network. In other words, the more people you maintain contact with, the lower your risk. To test it, Berman and collaborators enlisted four different data sets regarding depression–including in-person interviews, phone interviews with personal demographics, and over 15 million tweets (converted via machine learning algorithms into a PH-Q depression inventory score). The results confirmed it. “What we see across all of these different data sets is that as cities get larger, you get less depression per capita,” he said.

“Many of us have this impression that in bigger cities like New York, like Chicago, like Los Angeles, people are not as friendly…but these results suggest the opposite,” Berman said. “It must be on average that those social interactions are positive in cities and that more is better.”

Designing Environments for Our Brains

Regarding the main conversation surrounding mental health, Berman said, “We often think about [depression] in terms of this individual scale…your genetic makeup, brain activity patterns, individual psychological patterns. Maybe things about your family. We don’t really think about your neighborhood and your city.”

Knowing what we do about nature and large social networks can ultimately help us improve mental health outcomes on a broad scale. These two factors might seem to work against each other, but they don’t have to. Ultimately, we need more green space everywhere, including in large cities. The benefits are undeniable–urban areas with more greenery consistently see less aggression and crime, even when adjusting for race, ethnicity and income.

In addition, cities tend to have a lot of harsh stimuli, but that doesn’t mean some features of urban environments can’t be potentially restorative. “We believe that certain environmental features can be designed to improve human performance and well-being, like incorporating more natural features or natural patterns in the environment, trying to figure out ways to increase social interactions,” Berman said. By mimicking aspects of nature like curved lines, we might be able to create “soft fascination” closer to home and reduce the different demands pulling on our attention.

Crystal Han, Class of 2028

Making Sure Drugs Work Where They’re Needed in the Brain

By Guest Post

On February 21, 2025

In Engineering, Medicine, Neuroscience

Treating Parkinson’s and other neurological conditions has been challenging due to a lack of tools capable of navigating the complexity of neural circuits. New precision tools like DART.2 help make those therapeutic aspirations a reality, one tethered drug at a time.

The brain is one of our most complex organs, full of neurons that are constantly communicating with one another at places called synapses. Synapses both release molecules called ligands and express cell surface receptors that the ligands bind to, prompting the cells to undergo various processes within. The kinds of ligands and receptors that are important to disease are often released by and found on a variety of cell types. It is crucial, therefore that when we use a drug that targets a certain receptor, we also make sure that they only interact with receptors on the desired cell type.

To achieve this, in 2018 a team led by Duke professor Mike Tadross introduced “Drugs Acutely Restricted to Tethering” or “DART,” a drug delivery system that allows researchers to administer drugs to specific neuronal cell types. In June of this year, the Tadross lab unveiled DART.2. Pairing the cell-type specificity provided by DART.2 with the cellular receptor-specificity already provided by a given drug is essential to treating diseases like Parkinson’s without severe off-target effects, something researchers have been unable to do until tools like DART entered the scene.

Think of it like cutting the water supply to an apartment that has had a pipe burst. You don’t want to cut the water to the entire building, just the flooding apartment, because the other tenants still need water. This newest version of DART increases the ability of researchers to flip the right switches.

With increased cell type specificity optimized for drugs targeting two different receptor types, enabling broader dosing techniques and opening the door for discoveries of unknown roles of well-known receptors, researchers have made DART.2 into an “even more subtle, refined, yet transformative drug delivery system, a marked improvement from more rudimentary options that operate more like sledgehammers,” said Brenda Shields, one of the lead scientists on the DART.2 project.

The HaloTag protein (HTP) helps recruit drugs tethered to the HaloTag ligand (RXDART) to the desired cell types. Courtesy of Erin Fykes.

This is, in part, owing to the use of natural, or endogenous, receptor machinery in its design. Organisms are infected with a virus that prompts only certain cell types to express HaloTag, a protein that sits on the surface of the cells of choice. A HaloTag ligand, or small molecule that binds specifically to the HaloTag surface protein, is tethered to a drug of choice. This allows the tethered drug to be selectively recruited to the cells that have the HaloTag protein, bringing the drug into closer proximity to its intended cellular receptor, discouraging it from binding to unintended receptors, and reducing the amount of drug needed for efficacy.

DART.2 is not changing receptors that are already present, nor is it affecting the signaling cascades activated by engagement with the receptors. Cell-specificity of drug delivery was improved in DART.2 by decreasing the time and drug concentration needed to achieve intended effects – it is 100 times more precise than the previous system, with desired effects achieved in just 15 minutes.

Using the previous version of DART, researchers tried delivering a tethered version of the drug gabazine to GABA receptors (neural receptors associated with inhibitory neurotransmission) on a select group of neurons – gabazine blocks GABA from binding to GABA receptors and subsequently increases neural activity. Unfortunately, DART did not achieve high enough cell-specificity and gabazine bound to enough off-target receptors to trigger epileptic responses in mouse models. DART.2, however, is capable of delivering gabazine without these effects. The original version of DART was only optimized to work with drugs targeting excitatory (AMPA receptors) neurotransmission. The ability of the current version to work with inhibitory (GABA) and excitatory (AMPA) neurotransmission makes this system useful for “bi-directional” modifications, greatly increasing its utility.

Interestingly, while testing the effects of the drug gabazine on GABA receptors in ventral tegmental area dopamine neurons, they found that GABA receptors on these cells actually suppress locomotion, opposite to findings in other studies that more broadly focused on GABA receptors in multiple cell types. This highlights the need for tools like DART.2 that allow us to understand diverse receptor/ligand dynamics on a cell-by-cell basis to gain more nuanced approaches to understanding and treating disease.

To visualize dispersion and binding of tethered drugs to HaloTag proteins versus off-target receptors, Tadross’s team developed a way of seeing where the tethered drugs accumulated by introducing a small percentage of HaloTag ligands bound to a fluorescent reporter rather than a drug into the pool of tethered drugs. This visualization further confirmed a significant increase in cell-type specificity and a decrease in off-target effects of DART.2.

With previous levels of cell specificity, local delivery of the tethered drugs via cannula insertion at the brain region of interest was necessary to ensure drugs made it to the right targets. With increased specificity and a new visualization method for seeing where DART.2 drugs bind, researchers were able to assess whether brain wide dosing would be possible, decreasing deleterious effects of pumping high concentrations of drug into a certain area. Excitingly, they found that broad administration of tethered drugs across large areas of the brain did not significantly increase binding at receptors on cells not expressing the HaloTag protein. Drug delivery in the brain is notoriously difficult, so having the flexibility to administer a drug from an easier delivery point without reducing binding at target sites translates to a greater chance of therapeutic success.

For those unfamiliar with the process of drug and therapeutic development, the improvements presented in DART.2 represent a realistic look into the measure of scientific progress. Originally used to treat Parkinson’s mouse models, our conception of DART.2’s therapeutic relevance to other conditions is continually expanding. Shields shared that adaptions for conditions such as anxiety and depression may not be far off, just to name a few. DART.2 also makes it possible to use drugs like opioids in new ways. While helpful for pain management, the addictive potential of opioids sometimes renders them more harmful than helpful. Utilizing DART.2, opioids could be administered more specifically to cells that benefit from the drug, potentially reducing interactions with cell types involved in addiction development. Additionally, researchers are beginning to couple DART.2 with other tools on the market that can enhance its therapeutic promise and applicability (and vice versa). Each improvement of DART brings us closer to the reality of treating conditions we once deemed hopeless.

How the body’s own defense system plays a role in Alzheimer’s disease

By Guest Post

On January 16, 2025

In Guest Post, Immunology, Medicine, Neuroscience, Uncategorized

Carol Colton, a distinguished professor in neurology and pathology and a member of the Duke Institute for Brain Sciences, is renowned for her groundbreaking research on the immune response’s role in the onset and progression of brain diseases, particularly Alzheimer’s disease (AD). She is a firm believer in using animals such as mice for scientific research, saying that progress in understanding and treating diseases like Alizheimer’s would not be possible without them. With a shorter life cycle than humans, mice can be studied throughout their whole life and across multiple generations. They are also biologically similar to humans and susceptible to many of the same health problems, such as Alzheimer’s. Her work has reshaped our understanding of the brain’s immune system, challenging the long-held notion that the brain is “immune privileged.”

Carol Colton, PhD, professor of neurology and pathology at Duke

Central to Colton’s research is the role of “microglia,” the brain’s resident macrophages. Once thought to be passive observers in brain immunity, microglia are now recognized as active defenders, crucial in maintaining brain health. Colton’s early studies revealed that these cells not only eliminate harmful substances but also adapt to chronic conditions like Alzheimer’s. In this disease, microglia’s prolonged immune activity disrupts the brain’s metabolic balance, necessitating adaptations in neurons, astrocytes, and microglia themselves. She likens this adaptation to the brain coexisting with a parasite – functional but at a metabolic cost.

Her research underscores how microglia can initially protect against Alzheimer’s by combating amyloid plaques and phospho-tau proteins but eventually contribute to the disease’s progression as metabolic disruptions intensify.

Colton’s approach integrates physiology and pathology, exploring how changes in normal physiological processes influence disease pathology. Her lab employs a variety of advanced techniques, from cellular microscopy to gene and protein analysis, to map the intricate relationships between brain metabolism and disease. This multidisciplinary approach enables a deeper understanding of how the brain’s unique environment shapes disease progression.

A cornerstone of Colton’s recent work is her discovery of “Radical S-Adenosyl domain 1 (RSAD1),” a mitochondrial protein found at the bottom of the ocean critical to understanding Alzheimer’s. RSAD1 is overexpressed in Alzheimer’s neurons, altering methionine metabolism and mitochondrial function. These disruptions contribute to the disease’s characteristic metabolic imbalance. By developing RSAD1-negative and RSAD1-overexpressing mouse models, her lab provides crucial tools to study the protein’s impact on neuronal and mitochondrial metabolism in the presence of amyloid plaques and phospho-tau.

RSAD1 also appears to be linked to methionine depletion in the brain, which may further exacerbate Alzheimer’s pathology. These findings pave the way for novel therapeutic targets aimed at restoring metabolic equilibrium in the brain.

Colton’s scientific journey is deeply influenced by her family’s academic legacy, particularly her mother, who earned a chemistry degree during an era when women faced significant barriers in science. Inspired by her mother’s determination, Colton is a passionate advocate for women scientists, often emphasizing the importance of diversity and mentorship in STEM fields.

Colton’s work highlights the slow, insidious nature of Alzheimer’s disease, driven by metabolic and immune system changes over decades. By asking fundamental questions, such as whether Alzheimer’s results from the loss of key metabolites or whether microglia contribute to this depletion, her research aims to uncover the mechanisms that underlie the disease and identify strategies for intervention.

In the fight against Alzheimer’s, Colton’s discoveries, particularly those surrounding RSAD1 and microglial activity, are setting the stage for innovative treatments. Her dedication to unraveling the complexities of brain metabolism and immune response solidifies her place as a leader in neurology and pathology, with an enduring impact on the field of Alzheimer’s research.

Invincible Insect Pests Don’t Faze This Researcher

By Guest Post

On January 9, 2025

In Animals, Biology, Faculty, Guest Post, Neuroscience

“My passion for what I do saved my life.”

Meet Ke Dong, a biology professor at Duke University. She’s a lover of nature, a great cook, and a Lupus survivor. About 20-25 years ago, she developed Lupus during her research years at Michigan State University. Her time with this autoimmune disease was not kind. “The Lupus brought depression,” she said.

Fortunately, she was surrounded by amazing peers and her passion: research. Dong’s research focuses on ion channels and their reaction to various toxins and stimuli. These ion channels are incredibly important to the physiology of insects because of their impact on neuronal activity.

However, her passion didn’t develop from thin air. Dong grew up on a college campus in southeastern China. With both parents leading careers as professors — her father in history and her mother in biochemistry — she had the amazing opportunity to develop her passions early in childhood.

Growing up, she “had never been afraid of insects” as her mother’s work focused on the development of an increased production rate of silk in silkworms. However, it was the incidents in the area around her that sparked her passion. People in the area were often poisoned from the consumption of insecticides from the rice they were growing. This piqued her interest in toxicology as she was curious about how these insecticides were toxic to the townspeople.

Combining her fearlessness in the face of insects and her interest in toxicology, Dong has found the best of both worlds.

Dong also loves to dabble in the culinary worlds of a diverse range of cultures. As she travels from country to country, she brings with her the memorable flavors of each dish she tastes. Once arriving back home, she immediately purchases cookbooks from those countries to add to her rolodex of culinary skills. As she reads each recipe on her nightstand, she dreams of ways to introduce various flavors and techniques into her dishes. A creative cook, she has no time for following measurements. Her kitchen is her sandbox and allows her to dance with each flavor in her pot, adding less sugar but a little more salt.

Dong has been through ups and downs in her life, but there’s nothing that’s going to stop her from her passion: research.

*Post by Eubey Kang, NCSSM Class of 2025*

Advancing Immunotherapy for Glioblastoma

By Guest Post

On January 8, 2025

In Cancer, Guest Post, Medicine, Neuroscience

Vidyalakshmi Chandramohan, associate professor in neurosurgery and pathology, and member of the Duke Cancer Institute. Credit: Duke Department of Neurosurgery

Duke professor Vidyalakshmi Chandramohan is a pioneering neuro-oncologist whose work is redefining the future of glioblastoma (GBM) treatment. As a researcher in the Department of Neurosurgery at Duke, she is driven by a profound commitment to improving patient outcomes and providing new hope for those battling one of the most aggressive forms of brain cancer.

Her journey into science began with an interest in immunology and oncology, which led her to earn a Ph.D. and conduct postdoctoral research focused on the complex relationship between cancer and immune responses. Her fascination with GBM stemmed from the urgent need to develop innovative treatments for a disease with limited therapeutic options. Today, her groundbreaking research offers new avenues for fighting GBM and improving patient survival.

PET scan showing glioblastoma brain cancer. Credit: Wikimedia Commons.

Chandramohan’s work is centered on immunotherapy, particularly the development of D2C7-IT, a dual-specific immunotoxin currently in Phase I clinical trials for recurrent GBM patients. This precision medicine approach targets tumors with remarkable specificity, minimizing damage to healthy tissue. Her ongoing research aims to enhance the efficacy of D2C7-IT and expand its potential as a viable alternative to traditional treatments.

For Chandramohan, translating her research into tangible solutions is essential. “Developing a therapy is one thing, but making sure it works in the real world is another,” she says. She is exploring ways to combine D2C7-IT with other therapies to improve treatment outcomes and minimize side effects, pushing the boundaries of what is possible in GBM care.

A critical aspect of her research involves identifying biomarkers that predict patient responses to treatment, enabling personalized therapies. “Personalized medicine is the future,” she believes. “Tailoring treatment to each patient’s unique response will improve survival rates and outcomes.”

Collaboration is at the heart of Chandramohan’s work. She fosters an interdisciplinary environment where scientists, clinicians, and engineers work together toward a shared goal. “No one person can do it all,” she emphasizes. “It takes a community of experts to make breakthroughs happen.”

Despite the challenges of translating research into clinical practice, Chandramohan remains unwavering in her determination. “When our work leads to better treatment options, it reminds us why we do this every day,” she says. Her dedication to improving patient care fuels her optimism for the future of GBM treatment.

Looking ahead, Chandramohan is hopeful that the integration of immunotherapy, precision medicine, and innovative technologies will revolutionize the field of neuro-oncology. “We’re just scratching the surface,” she says, confident in the potential to improve outcomes for GBM patients.

Through her relentless pursuit of excellence, Chandramohan is not only advancing the science of glioblastoma treatment but also inspiring the next generation of researchers to push the boundaries of what is possible in the fight against cancer.

Blog post by Adarsh Magesh, NCSSM Class of 2025

Advancing Care and Research in Traumatic Brain Injury

By Guest Post

On January 6, 2025

In Guest Post, Medicine, Neuroscience

Meet a trailblazer in the realm of neurocritical care and emergency medicine: Dr. Katharine Rose Colton, MD. Balancing roles as a clinician, researcher, and educator, Colton serves as an Assistant Professor of Neurology and Neurosurgery at Duke University. Her dedication to understanding and treating traumatic brain injury (TBI) exemplifies her commitment to improving the lives of patients facing severe neurological challenges.

TBI is a significant public health issue, often resulting from falls, motor vehicle accidents, or sports injuries. It can range from mild concussions to severe brain trauma, leaving patients in comas or with long-term disabilities. While treatments for TBI have evolved, many gaps remain in understanding how to optimize recovery and outcomes. Colton’s work bridges this divide, combining cutting-edge research with compassionate patient care.

Colton’s journey into medicine wasn’t linear. A Canadian native, she initially pursued an eclectic range of interests, including ethnobotany and anthropology, during her undergraduate studies. She pivoted to medicine, taking the MCAT on a whim and earning her M.D. from Duke University School of Medicine.

Her first exposure to TBI occurred during a research year at the University of Maryland’s Shock Trauma Center. A project initially focused on trauma surgery shifted to neurocritical care, igniting her passion for studying brain injuries. “I loved it,” she recalls. “It was a completely different way of looking at medicine.”

Colton’s clinical path led her to a residency in Emergency Medicine at Northwestern University and a fellowship in Neurocritical Care. While she enjoyed the fast-paced decision-making of emergency medicine, she found herself drawn to the intricate details of critical care. “I struggled with letting patients go and handing them off to others,” she says. “I wanted to stay involved and see the whole story unfold.”

Now focused primarily on neurocritical care, Colton dedicates a third of her time to research, primarily on clinical trials targeting severe TBI. She has worked on large-scale, multi-site studies investigating drug therapies and monitoring systems to optimize treatment for comatose patients.

Her approach to research is pragmatic: “I’m a clinician first. I want to know how the things we do today will benefit the patient tomorrow.” For instance, her current trials explore the potential of older, cost-effective drugs previously overlooked by pharmaceutical companies to improve outcomes in TBI patients. These trials adopt adaptive designs, allowing for real-time adjustments based on early results to maximize impact.

Colton is also a strong advocate for personalizing TBI treatment. “TBI is an incredibly heterogeneous condition,” she explains. “We can’t treat a 20-year-old in a car accident the same as a 70-year-old who fell. They have completely different recovery pathways.” Her work aims to identify biomarkers and refine classifications of TBI to develop more targeted interventions.

One of the most memorable cases from Colton’s career underscores her dedication to patient care. A young woman struck by a car in Chicago arrived at the ICU in a deep coma, with little hope of recovery. Months later, to Colton’s astonishment, the patient returned to work and resumed her life. “You just don’t know,” she reflects. “That case taught me the importance of patience and persistence in medicine.”

Colton’s role extends beyond the ICU, often involving interactions with patients’ families during some of their most vulnerable moments. “Families often show incredible grace, even in tragedy,” she says. “It’s humbling to see their resilience and willingness to contribute to research, even when it might not help their loved one directly.”

Despite the challenges of long, emotionally taxing weeks in the ICU, Colton finds fulfillment in both the technical and human aspects of her work. “There’s something beautiful about the physiology — adjusting treatments and seeing how the body responds,” she explains. Yet, she never loses sight of the bigger picture: the patient. “Numbers on a screen don’t matter if we’re not improving their lives.”

Outside of work, Colton enjoys paddleboarding, camping, and spending time with her two young children. Her background in ethnobotany and love for snowboarding reflect her multifaceted personality, blending curiosity, determination, and a deep appreciation for life.

Dr. Katharine Colton is shaping the future of TBI care through her dedication to research, her patients, and the families she serves. Her journey is a testament to the impact of resilience, curiosity, and compassion in medicine.

The Dukies Cited Most Highly

By Karl Bates

On November 19, 2024

In Behavior/Psychology, Biology, Biomedical Engineering, Cardiology, Engineering, Environment/Sustainability, Faculty, Genetics/Genomics, Medicine, Neuroscience, Physics, Space

The Web of Science ranking of the world’s most highly-cited scientists was released this morning, telling us who makes up the top 1 percent of the world’s scientists. These are the authors of influential papers that other scientists point to when making their arguments.

EDITOR’S NOTE! — Web of Science shared last year’s data! We apologize. List below is now corrected, changes to copy in bold. We’re so sorry.

Twenty-three of the citation laureates are Duke scholars or had a Duke affiliation when the landmark works were created over the last decade.

*A couple of these Duke people disappeared from this year’s list, but we’re still proud of them.*

Two names on the list belong to Duke’s international powerhouse of developmental psychology, the Genes, Environment, Health and Behavior Lab, led by Terrie Moffitt and Avshalom Caspi.

Dan Scolnic of Physics returns as our lone entry in Space Science, which just makes Duke sound cooler all around, don’t you think?

This is a big deal for the named faculty and an impressive line on their CVs. But the selection process weeds out “hyper-authorship, excessive self-citation and anomalous citation patterns,” so don’t even think about gaming it.

Fifty-nine nations are represented by the 6,636 individual researchers on this year’s list. About half of the citation champions are in specific fields and half in ‘cross-field’ — where interdisciplinary Duke typically dominates. The U.S. is still the most-cited nation with 36 percent of the world’s share, but shrinking slightly. Mainland China continues to rise, claiming second place with 20 percent of the cohort, up 2.5 percent from just last year. Then, in order, the UK, Germany and Australia round out the top five.

Tiny Singapore, home of the Duke NUS Graduate Medical School, is the tenth-most-cited with 1.6 percent of the global share.

In fact, five Duke NUS faculty made this year’s list: Antonio Bertoletti, Derek Hausenloy and Jenny Guek-Hong Low for cross-field; Carolyn S. P. Lam for clinical medicine, and the world famous “Bat Man,” Lin-Fa Wang, for microbiology.

Okay, you scrolled this far, let’s go!

Biology and Biochemistry

Charles A. Gersbach

Clinical Medicine

Christopher Bull Granger

Adrian F. Hernandez

Gary Lyman

Cross-Field

Priyamvada Acharya

Chris Beyrer

Stefano Curtarolo

Vance G. Fowler Jr.

Po-Chun Hsu (adjunct, now U. Chicago)

Ru-Rong Ji

William E. Kraus

David B. Mitzi

Christopher B. Newgard

Pratiksha I. Thakore (now with Genentech)

Xiaofei Wang

Mark R. Wiesner

Environment and Ecology

Robert B. Jackson (adjunct, now Stanford U.)

Microbiology

Barton F. Haynes

Neuroscience and Behavior

Quinn T. Ostrom

Plant and Animal Science

Sheng-Yang He

Psychiatry and Psychology

Avshalom Caspi

William E. Copeland

Terrie E. Moffitt

Space Science

Dan Scolnic

Wiring the Brain

By Robin Smith

On June 26, 2024

In Animals, Neuroscience, Students

From tiny flies, Duke researchers are finding new clues to how the brain sets up its circuitry.

In her time at Duke, Khanh Vien figures she’s dissected close to 10,000 fly brains. For her PhD she spent up to eight hours each day peering at baby flies under the microscope, teasing out tiny brains a fraction the size of a poppy seed.

“I find it very meditative,” she said.

Vien acknowledges that, to most people, fruit flies are little more than a kitchen nuisance; something to swat away. But to researchers like her, they hold clues to how animal brains — including our own — are built.

While the human brain has some 86 billion neurons, a baby fruit fly’s brain has a mere 3016 — making it millions of times simpler. Those neurons talk to each other via long wire-like extensions, called axons, that relay electrical and chemical signals from one cell to the next.

Vien and other researchers in Professor Pelin Volkan’s lab at Duke are interested in how that wiring gets established during the fly’s development.

By analyzing a subset of neurons responsible for the fly’s sense of smell, the researchers have identified a protein that helps ensure that new neurons extend their axons to the correct spots in the olfactory area of the young fly’s brain and not elsewhere.

Because the same protein is found across the animal kingdom, including humans, the researchers say the work could ultimately shed light on what goes awry within the brains of people living with schizophrenia and other mental illnesses.

Their findings are published in the journal iScience.