Michigan State graduate student Heath Baldwin won the decathlon at the U.S. Track and Field trials on Saturday night at Historic Hayward Field in Eugene, Oregon, to secure a spot at the 2024 Paris Olympic Games. He is the first Spartan to qualify for the Olympic decathlon since Paul Terek in 2004.
Baldwin, who opted out of the 2024 NCAA Outdoor Championships earlier this month to prepare for the trials, totaled a personal-best 8,625 points to finish first in the 19-athlete field. His score is the sixth-best in the world this year and third all-time on the all-dates collegiate list.
He is joined on the Olympic team by 2020 Olympian Zach Ziemek in second place with 8,516 points and Harrison Williams in third place with 8,384 points.
Baldwin kicked off decathlon action Friday morning and ended the first day of competition at the top of the leaderboard with 4,508 points. He set personal bests in the 400m with 48.58 and shot put with 16.52m, while adding a season-best 2.13m clearance in the high jump, securing the top spot in the field in both the shot put and high jump.
A 13.77-second performance in the 110 meters hurdles for 1,004 points helped Baldwin hold the top spot in the field to start the second day of competition. He set his third personal best of the meet in the following event, the discus throw with 49.87 meters, to maintain a 34-point lead over second-place Ziemek. Ziemek, who held the lead after the first four events on day one, retook the lead after eight events with a 5.35 meters clearance in the pole vault, while Baldwin moved to second with a 4.85 meters jump in the event.
The national title came down to the final event after Baldwin’s 66.69 meters effort in the javelin throw. His throw, good for 839 points, was 16 feet better than the second-place finisher in the event. Baldwin wrapped his historic weekend with a time of 4:41.87 in the 1500 meters to top Ziemek’s 4:53.65 and secure the gold.
MSU teammate Ryan Talbot competed alongside Baldwin in the decathlon, earning four top-five finishes en route to a season-best 7,872 points. Former Spartan standout Tori Franklin finished third in the triple jump with a 13.72m leap and will await USA Track & Field’s Olympic team announcement for the event. In 2022, she earned bronze at the World Championships to become the first American woman to medal in the triple jump at a World Championship. No American has finished better than fourth at the Olympics in the event.
Track and field action at the Paris Olympics begins Aug. 1 and concludes Aug. 11.
This story originally appeared on msuspartans.com.
Researchers say that how objects feel can influence the ways in which people proceed to interpret them
Psychologists report in the journal Science that interpersonal interactions can be shaped, profoundly yet unconsciously, by the physical attributes of incidental objects: Resumes reviewed on a heavy clipboard are judged to be more substantive, while a negotiator seated in a soft chair is less likely to drive a hard bargain.
The research was conducted by psychologists at Harvard University, the Massachusetts Institute of Technology, and Yale University. The authors say the work suggests that physical touch — the first of our senses to develop — may continue to operate throughout life like a scaffold upon which people build their social judgments and decisions.
“Touch remains perhaps the most underappreciated sense in behavioral research,” said co-author Christopher C. Nocera, a graduate student in Harvard’s Department of Psychology. “Our work suggests that greetings involving touch, such as handshakes and cheek kisses, may in fact have critical influences on our social interactions, in an unconscious fashion.”
Nocera conducted the research with Joshua M. Ackerman, assistant professor of marketing at MIT’s Sloan School of Management, and John A. Bargh, professor of psychology at Yale.
“First impressions are liable to be influenced by the tactile environment, and control over this environment may be especially important for negotiators, pollsters, job seekers, and others interested in interpersonal communication,” the authors wrote in the latest issue of Science. “The use of ‘tactile tactics’ may represent a new frontier in social influence and communication.”
The researchers conducted a series of experiments probing how objects’ weight, texture, and hardness can unconsciously influence judgments about unrelated events and situations:
— To test the effects of weight, metaphorically associated with seriousness and importance, subjects used either light or heavy clipboards while evaluating resumes. They judged candidates whose resumes were seen on a heavy clipboard as better qualified and more serious about the position, and rated their own accuracy at the task as more important.
— An experiment testing texture’s effects had participants arrange rough or smooth puzzle pieces before hearing a story about a social interaction. Those who worked with the rough puzzle were likelier to describe the interaction in the story as uncoordinated and harsh.
— In a test of hardness, subjects handled either a soft blanket or a hard wooden block before being told an ambiguous story about a workplace interaction between a supervisor and an employee. Those who touched the block judged the employee as more rigid and strict.
— A second hardness experiment showed that even passive touch can shape interactions. Subjects seated in hard or soft chairs engaged in mock haggling over the price of a new car. Subjects in hard chairs were less
flexible, showing less movement between successive offers. They also judged their adversaries in the negotiations as more stable and less emotional.
Nocera and his colleagues say these experiments suggest that information acquired through touch exerts broad, if generally imperceptible, influence over cognition. They propose that encounters with objects can elicit a “haptic mindset,” triggering application of associated concepts even to unrelated people and situations.
“People often assume that exploration of new things occurs primarily through the eyes,” Nocera said. “While the informative power of vision is irrefutable, this is not the whole story. For example, the typical reaction to an unknown object is usually as follows: With an outstretched arm and an open hand, we ask, ‘Can I see that?’ This
response suggests the investigation is not limited to vision, but rather the integrative sum of seeing, feeling, touching, and manipulating the unfamiliar object.”
Nocera said that because touch appears to be the first sense that people use to experience the world ╤ for example, by equating the warm and gentle touch of a mother with comfort and safety ╤ it may provide part of
the basis by which metaphorical abstraction allows for the development of a more complex understanding of comfort and safety. This physical-to-mental abstraction is reflected in metaphors and shared linguistic descriptors, such as the multiple meanings of words like “hard,” “rough,” and “heavy.”
Novel approach to treating tactile hypersensitivity in patients with autism-spectrum disorders
Harvard University and Deerfield Management announced today the selection of a first project for funding under the Lab1636 R&D alliance that aims to advance promising innovations from labs across the University toward the clinical development of novel therapeutics. The project arises from the lab of David Ginty, the Edward R. and Anne G. Lefler Professor of Neurobiology in the Blavatnik Institute at Harvard Medical School (HMS) and a Howard Hughes Medical Institute investigator. Lauren Orefice is a former postdoctoral researcher in the Ginty Lab and now assistant professor of genetics at HMS and Massachusetts General Hospital. In a question-and-answer session, Ginty and Orefice discuss their recent progress toward identifying possible treatments for the touch hypersensitivity that often occurs in people with autism spectrum disorders (ASD), and their hope for further innovation in neuroscience.
Q&A
David Ginty and Lauren Orefice
OTD: How do people experience touch hypersensitivity?
GINTY: Well, the truth is we don’t really know how they experience it. We do know that in certain disorders, including autism, light touch can be highly aversive. In fact, there are several examples of disorders where we see touch overreactivity; a person will react abnormally to what you and I would consider innocuous touch stimuli. For a large number of people with autism, light touch can be aversive, and normal, developmental nurturing touch may also be aversive. We refer to this phenomenon with terms like “tactile avoidance” and “tactile defensiveness.”
OREFICE: People with ASD often describe that certain types of clothing can be itchy or difficult to wear. Haircuts can even be really difficult for people to deal with, and there are certain barbers or hairstylists that they’ll go to. Things like inclement weather, heavy rain, can be really overwhelming or frightening for some people. For most of us, we are not typically aware of the fact that we are sitting in a chair, wearing a sweater, and the air conditioning is on, etcetera. But for some people with autism, some of these tactile aspects of their environment feel more present, or more profound, as though the volume is turned up.
GINTY: Interestingly, we don’t only see this tactile sensitivity in ASD. In other disorders such as neuropathic pain, which can be caused by chemotherapy, diabetes, or damage affecting the somatosensory system, light touch can also be aversive. It can be painful.
“We think there’s a critical need for normal tactile input during an early period in development. We’d like to be able to identify that critical window, to treat tactile overreactivity in young children.”Lauren Orefice
OTD: For people who are born with this, developmentally, how does it play out over the long term?
OREFICE: This is, I think, a really important aspect of what David and I do in our labs, and what we continue to ask questions about. We’re trying to understand how an abnormal sense of touch impacts the brain and ultimately complex social behaviors.
GINTY: We think that touch is the first sense to develop. The first social exchange between a baby and her parents occurs through the sense of touch. You might say that touch is where social development begins. It’s fascinating that a number of studies in humans, nonhuman primates, and other animals have suggested that normal touch is required for the development of normal cognitive processes.
In our own mouse studies, we found that if a genetic lesion that causes tactile overreactivity is introduced developmentally in the peripheral nervous system, the animals also exhibit behavioral alterations — a fairly profound anxiety-like behavior, for example, and some aberrant social-interaction behaviors. On the other hand, if the very same genetic lesions are introduced in young adult mice, the animals still exhibit the tactile overreactivity, but they don’t exhibit anxiety-like behavior. So there’s a profound link between developmental touch and tactile reactivity and the acquisition of normal behavior.
OTD: So the hope and the hypothesis is presumably that if you can address what’s happening in the peripheral nerves at the right developmental window, you may be able to prevent these kinds of things from appearing down the road.
OREFICE:Exactly. We think there’s a critical need for normal tactile input during an early period in development. We’d like to be able to identify that critical window, to treat tactile overreactivity in young children.
GINTY: Our thinking is that, even in adulthood, preventing touch overreactivity and thus tactile avoidance and defensiveness would be highly beneficial. But we hypothesize that if we could treat it developmentally, then it might also have a long-term consequence of improving anxiety and possibly even social-interaction behaviors later in life.
Some parts of the body—our hands and lips, for example—are more sensitive than others, making them essential tools in our ability to discern the most intricate details of the world around us.
This ability is key to our survival, enabling us to safely navigate our surroundings and quickly understand and respond to new situations.
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It is perhaps unsurprising that the brain devotes considerable space to these sensitive skin surfaces that are specialized for fine, discriminative touch and which are continually gathering detailed information via the sensory neurons that innervate them.
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But how does the connection between sensory neurons and the brain result in such exquisitely sensitive skin?
A new study led by researchers at Harvard Medical School has unveiled a mechanism that may underlie the greater sensitivity of certain skin regions. The research, conducted in mice and published Oct. 11 in Cell, shows that the overrepresentation of sensitive skin surfaces in the brain develops in early adolescence and can be pinpointed to the brain stem.
Moreover, the sensory neurons that populate the more sensitive parts of the skin and relay information to the brain stem form more connections and stronger ones than neurons in less sensitive parts of the body.
Sensitive skin regions
“This study provides a mechanistic understanding of why more brain real estate is devoted to surfaces of the skin with high touch acuity,” said senior author David Ginty, the Edward R. and Anne G. Lefler Professor of Neurobiology at Harvard Medical School. “Basically, it’s a mechanism that helps explain why one has greater sensory acuity in the parts of the body that require it.”
While the study was done in mice, the overrepresentation of sensitive skin regions in the brain is seen across mammals—suggesting that the mechanism may be generalizable to other species.
From an evolutionary perspective, mammals have dramatically varied body forms, which translates into sensitivity in different skin surfaces. For example, humans have highly sensitive hands and lips, while pigs explore the world using highly sensitive snouts. Thus, Ginty said this mechanism could provide the developmental flexibility for different species to develop sensitivity in different areas.
Moreover, the findings, while fundamental, could someday help illuminate the touch abnormalities seen in certain neurodevelopmental disorders in humans.
Scientists have long known that certain body parts are overrepresented in the brain—as depicted by the brain’s sensory map, called the somatosensory homunculus, a schematic of human body parts and the corresponding areas in the brain where signals from these body parts are processed. The striking illustration includes cartoonishly oversized hands and lips.
Previously, it was thought that the overrepresentation of sensitive skin regions in the brain could be attributed to a higher density of neurons innervating those skin areas. However, earlier work by the Ginty lab revealed that while sensitive skin does contain more neurons, these extra neurons are not sufficient to account for the additional brain space.
“We noticed that there was a rather meager number of neurons that were innervating the sensitive skin compared to what we’d expect,” said co-first author Brendan Lehnert, a research fellow in neurobiology, who led the study with Celine Santiago, also a research fellow in the Ginty lab.
“It just wasn’t adding up,” Ginty added.
To investigate this contradiction, the researchers conducted a series of experiments in mice that involved imaging the brain and neurons as neurons were stimulated in different ways.
First, they examined how different skin regions were represented in the brain throughout development. Early in development, the sensitive, hairless skin on a mouse’s paw was represented in proportion to the density of sensory neurons.
However, between adolescence and adulthood, this sensitive skin became increasingly overrepresented in the brain, even though the density of neurons remained stable—a shift that was not seen in less sensitive, hairy paw skin.
“This immediately told us that there’s something more going on than just the density of innervation of nerve cells in the skin to account for this overrepresentation in the brain,” Ginty said.
“It was really unexpected to see changes over these postnatal developmental timepoints,” Lehnert added. “This might be just one of many changes over postnatal development that are important for allowing us to represent the tactile world around us, and helping us gain the ability to manipulate objects in the world through the sensory motor loop that touch is such a special part of.”
Sensory and brain stem neurons
Next, the team determined that the brain stem—the region at the base of the brain that relays information from sensory neurons to more sophisticated, higher-order brain regions—is the location where the enlarged representation of sensitive skin surfaces occurs.
This finding led the researchers to a realization: The overrepresentation of sensitive skin must emerge from the connections between sensory neurons and brain stem neurons.
To probe even further, the scientists compared the connections between sensory neurons and brain stem neurons for different types of paw skin. They found that these connections between neurons were stronger and more numerous for sensitive, hairless skin than for less sensitive, hairy skin. Thus, the team concluded, the strength and number of connections between neurons play a key role in driving overrepresentation of sensitive skin in the brain.
Finally, even when sensory neurons in sensitive skin weren’t stimulated, mice still developed expanded representation in the brain—suggesting that skin type, rather than stimulation by touch over time, causes these brain changes.
“We think we’ve uncovered a component of this magnification that accounts for the disproportionate central representation of sensory space.” Ginty said. “This is a new way of thinking about how this magnification comes about.”
Next, the researchers want to investigate how different skin regions tell the neurons that innervate them to take on different properties, such as forming more and stronger connections when they innervate sensitive skin.
“What are the signals?” Ginty asked. “That’s a big, big mechanistic question.”
And while Lehnert described the study as purely curiosity-driven, he noted that there is a prevalent class of neurodevelopmental disorders in humans called developmental coordination disorders that affect the connection between touch receptors and the brain—and thus might benefit from elucidating further the interplay between the two.
“This is one of what I hope will be many studies that explore on a mechanistic level changes in how the body is represented over development,” Lehnert said. “Celine and I both think this might lead, at some point in the future, to a better understanding of certain neurodevelopmental disorders.”
Co-investigators included Erica Huey, Alan Emanuel, Sophia Renauld, Nusrat Africawala, Ilayda Alkislar, Yang Zheng, Ling Bai, Charalampia Koutsioumpa, Jennifer Hong, Alexandra Magee, and Christopher Harvey of Harvard Medical School.
In the new study, led by Joseph DeGutis, HMS associate professor of psychiatry at VA Boston, the researchers found that face blindness lies on a spectrum — one that can range in severity and presentation — rather than representing a discrete group. The authors also provide diagnostic suggestions for identifying mild and major forms of prosopagnosia based on guidelines for major and mild neurocognitive disorders in the DSM5, the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders.
The study results are based on a web-based questionnaire and tests administered to 3,341 individuals. First, the researchers asked participants whether they experience difficulties recognizing faces in their everyday lives. Then they administered two objective tests to determine whether they had difficulties learning new faces or recognizing highly familiar, famous faces.
The results showed that 31 individuals out of the 3,341 had major prosopagnosia, while 72 of the 3,341 had a milder form. The researchers also observed that there were no neatly divided discrete groups of people with poor or good ability to recognize faces. Rather, the ability to recognize faces appeared to lie on a continuum, they said.
Finally, the researchers compared face-matching scores among people with prosopagnosia diagnosed using different criteria and found that using stricter diagnostic cutoffs did not correspond with lower face-matching scores.
Harvard Medicine News spoke with DeGutis, the study’s senior author, about the implications of the findings.
Harvard Medicine News: Let’s start with the basics. What causes face blindness?
DeGutis: Prosopagnosia, or face blindness, can be caused by a brain injury to occipital or temporal regions, referred to as acquired prosopagnosia, which affects one in 30,000 people in the United States. Prosopagnosia can also be a lifelong condition caused by genetic or developmental abnormalities, referred to as developmental prosopagnosia, affecting one in 33 people.
HMNews: This is a fascinating condition, but some might say that it’s not a serious health disorder so
DeGutis: First, face blindness can be a socially debilitating disorder that can limit employment opportunities. For example, networking is extremely difficult for people with prosopagnosia and can cause social distress and embarrassment. Recognizing someone is a social signal, indicating that “you are important to me.”
Prosopagnosia can also affect individuals on the autism spectrum and can be a consequence of age-related cognitive decline as well. In a world where social isolation is on the rise, especially in teens and young adults, fostering and maintaining social bonds and good face-to-face interactions are more important than ever.
HMNews: What sparked your interest in this field? What is it about how the brain sees and remembers faces intrigues you the most and why?
DeGutis: Face blindness is fascinating on several levels. Humans are remarkably good at recognizing familiar faces and this is done with very little effort. We know that this face ‘super-power’ relies on several specific perceptual processes: holistic face processing-seeing the face as an integrated whole, for instance; memory processes, readily associating faces with person-related knowledge; and specialized brain mechanisms and regions, too, such as the fusiform face area.
Our knowledge about face recognition in unimpaired individuals provides a very solid framework to understand the ways these processes can break down in prosopagnosia. The processes also provide clues on how to improve face recognition in people with face blindness, which is one of the major goals of our lab. Finally, studying prosopagnosia is fascinating from a phenomenological perspective—what do people with face blindness actually “see” when looking at a face? What comes to mind when they think about a familiar friend’s face?
HMNews: You say that your findings call for an expansion of the diagnostic criteria. Why is that important?
DeGutis: This is important on several levels. First, the majority of researchers have used overly strict diagnostic criteria and many individuals with significant face- recognition problems in daily life have been wrongly told they do not have prosopagnosia. Expanding the diagnosis is important because knowing that you have real objective evidence of prosopagnosia, even a mild form, can help you take steps to reduce its negative impacts on daily life, such as telling consequential coworkers, or seeking treatment.
Recent evidence suggests that people with milder forms of face blindness may benefit more from certain treatments than people with more severe forms of the condition. These treatments might include cognitive training to enhance perceptual abilities or training aimed directly at improving face associations.
Finally, factors such as age-related cognitive decline and social anxiety can further worsen face recognition abilities. Knowing if you have mild prosopagnosia could help you keep an eye out for further situational or age-related declines in face-recognition ability.
HMNews: What do you want clinicians and individuals with the condition to take away from these results?
DeGutis: The take-home message is that prosopagnosia lies on a continuum and stricter vs. looser diagnostic criteria employed in prosopagnosia studies in the past 13 years have identified mechanistically very similar populations, providing justification for expanding the criteria to include those with milder forms of it.
Another take-home message is the importance of using a combination of self-reported daily-life difficulties and validated objective measures when diagnosing prosopagnosia. There are pros and cons to relying just on self-reports because it can be challenging to judge your own abilities or relying solely on objective lab measures that may not reflect everyday life.
When neurobiologist David Corey showed up at a rare disease conference in 2017, he had no idea that he would enter a race against time to develop a treatment for it.
The conference was for Usher syndrome type 1F. Patients with this condition have a gene mutation that causes them to be born deaf and gradually lose their vision as they grow up. Corey, the Bertarelli Professor of Translational Medical Science in the Blavatnik Institute at Harvard Medical School, had devoted decades to studying the defective gene in a different context.
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So when Corey happened upon an announcement for an Usher 1F conference in Boston, he knew he had to attend.
There, he introduced himself to Elliot Chaikof, chief of surgery at Beth Israel Deaconess Medical Center and the Johnson and Johnson professor of surgery at HMS, his wife Melissa, and their adult daughters, Rachel and Jessica, both of whom have Usher 1F. The Chaikofs had organized the conference through the nonprofit research collaborative they founded to find a treatment for the blindness part of the disease.
Meeting the Chaikofs — and especially Rachel and Jessica — stirred in Corey a powerful desire to help.
“We really felt that we know so much about this gene, if we don’t try to do something for the disease, who else is going to,” Corey said.
Six years later, the Corey lab has three candidate gene therapies for Usher 1F blindness. Each takes a different approach to correcting the disease-causing mutation.
The researchers are now testing the therapies in animal models and are confident that at least one will move to clinical trials in humans to become a successful treatment.
Usher 1F is a particularly severe form of Usher syndrome, in which a gene mutation causes cells in the eye and ear to stop producing an essential protein. Rachel and Jessica’s gene mutation is most prevalent in the Ashkenazi Jewish community.
People with Usher 1F are usually born deaf and lacking the ability to balance. They develop an eye disease called retinitis pigmentosa, which causes a progressive loss of vision as the retina degenerates. Night vision often disappears first, followed by peripheral vision. For Jessica, this has meant giving up driving and getting a service dog to help her navigate the world around her. Eventually, people become completely blind.
“Everyone with Usher 1F has a unique experience, but one of the biggest challenges for me is slowly losing my independence as I lose my vision,” Jessica said.
Like many people with Usher 1F, Rachel and Jessica have benefited from cochlear implants, which have improved their ability to hear and communicate. However, the Chaikofs learned soon after their daughters were diagnosed that there was almost no research on the condition and virtually no therapies to treat it — so in 2013, they established Usher 1F Collaborative.
“Essentially there were zero research groups working on this particular problem — nothing, nobody,” Elliot said.
A call to action
While the Chaikofs were seeking answers, the Corey lab in the Department of Neurobiology at HMS was studying a protein called protocadherin-15 and its role in deafness.
The researchers figured out that protocadherin-15 in the inner ear helps sensory receptors called hair cells convert mechanical vibrations into electrical signals, which the brain interprets as sound. Without protocadherin-15, the conversion doesn’t happen, and the brain is unable to detect sound.
They also found protocadherin-15 in light-sensing cells, or photoreceptors, in the eye. However, they weren’t sure of its exact function there, nor did they know why people lacking the protein in their eyes lose their sight over time.
In the course of the research, Corey had become aware that in Usher 1F, a mutation in the gene that makes protocadherin-15 causes cells in the ear and eye to stop producing it.
Connecting with the Chaikofs gave Corey a new motivation for his research and reinvigorated the family’s quest for a cure.
“Because David understood the gene so well, he basically leapfrogged ahead of where the research was and hit the ground running,” said Melissa, who is chair of Usher 1F Collaborative.
“For the first time we felt as if we had someone who could truly make a difference on this particular problem,” Elliot added.
For decades, researching dyslexia has been a passion and a fascination for Albert Galaburda, the Emily Fisher Landau Professor of Neurology, Emeritus, at HMS. Ask him why, and he’ll likely say that, for him, it is a quest to untangle a condition shaped by so many facets of who we are.
“It extends from sociology to molecular biology,” he says. “It has to do with how genes regulate themselves, but also with our brains, our schools, our education system, and our cultural attitudes toward reading.”
Prevailing views on dyslexia — which is marked by trouble processing written words — have evolved considerably over Galaburda’s fifty-year career. In the 1970s, Galaburda was among the first researchers to seek evidence of dyslexia in the brain. Along with colleague Norman Geschwind, MD ’51, he developed the Geschwind-Galaburda hypothesis, a foundational theory suggesting that varying patterns of early brain development — such as the asymmetry of brain hemispheres and the ways that neurons migrate — can affect cognitive abilities, including those associated with reading.
Geschwind and Galaburda’s early findings have shaped subsequent research in the field. Their work has shifted the thinking around dyslexia as a problem of laziness, vision, or poor instruction to one with neurobiological roots. It also has pushed scientists to understand how dyslexia can be shaped by both biological and societal forces. This understanding has provoked collaborations between neuroscience, psychology, genetics, and education that have been essential to developing early and effective interventions.
Galaburda spoke with Harvard Medicine about his career. An edited version of that conversation follows.
You spent much of your fifty-year career researching dyslexia. How did you get interested in it?
Originally I didn’t know anything about dyslexia. I was a neurology resident interested in language. During one study, we used a postmortem brain from a person with dyslexia to test one of our ideas: that language areas of the brain related to reading — the biggest task you can give a language system — were small and not well developed in people with dyslexia. But we actually found that those areas were relatively large in the dyslexic brain. And I noticed something else. In areas of the cortex associated with language, clouds of brain cells were found to be out of place: their usual migration paths had not been taken.
We looked at five or six additional postmortem brains from people with dyslexia and basically confirmed these initial findings of abnormal neuronal migration. We decided to try and model this abberant migration in rodents to understand the biology of how the neurons got to be there. Most of my career was spent studying how these changes developed in the brain.
But if written language is a human innovation, what could rodent brains tell us about dyslexia?
In the later part of my career, people had discovered genes that imparted a risk for developing dyslexia, and we were able to manipulate those genes in mice — to turn them on and off. We produced anomalies in the mouse brains, such as abnormal neuronal migration, that we had seen in the brains of people with dyslexia. This was the first demonstration of risk genes for dyslexia being associated with abnormalities in brain development.
We then gave the animals behavioral tests. We looked at acoustic processing, which was found to be abnormal. The affected animals could not perceive small bits of sound. The innovation of reading spurred this trait to adopt a new biological function without evolutionary modification, a phenomenon that’s called preadaptation.
In order to read, you have to map a bit of sound, called a phoneme, to a bit of text, known as a grapheme, so the ability to distinguish small bits of sound is crucial. The sound of the letter “p,” for example, differs by only 15 milliseconds from the sound of the letter “b.” If the hearing system is slow, the distinction can’t be made, and the letters are confused. This ability to distinguish sounds is particularly important when a person is learning to read; later in life people are able to guess at sounds that they can’t hear well.
We also found that these manipulations of the brain affected male rodents more than females, which was fascinating since dyslexia is more common in boys. We could trace these different responses between males and females all the way back to the brainstem, where sound first comes into the brain; the cochlear nucleus where the brainstem neurons process information from the ear.
In order to read, you have to map a bit of sound, called a phoneme, to a bit of text, known as a grapheme.
All of this led me, by the end of my career, to think that dyslexia was not a language problem initially, but instead a sensory issue related to perceiving sounds, one that leads to the development of abnormal phoneme representation in the brain. Not all sounds, but certain sounds that rapidly move. If you’re not getting the right phonetic representations in the brain because you can’t hear those sounds, you’re not able to map those phonetic representations onto letters or syllables. The cognitive system is intact; it just receives poor quality acoustic information early on, and the phonological disorder follows, This explains why a person with dyslexia can be very, very smart. It doesn’t affect cognitive ability.
One implication of this inability to perceive sounds is that, in principle, you could use some sort of hearing aid to slow down the signal coming into the ears of at-risk babies during the first year of life, when they’re forming those phonological representations. This might help prevent the sound perception problem.
Let’s talk about one idea you mentioned — that people with dyslexia can be very smart. Your colleague Norman Geschwind hypothesized that dyslexia may actually confer some sort of yet-unidentified evolutionary advantage. What do you think of that idea?
It’s estimated that 10 percent of people are dyslexic. It hasn’t disappeared from the population through natural selection, so we know it doesn’t confer something that prevents procreation. Dyslexia need not confer a superiority, and it will not become extinct so long as it doesn’t diminish survival.
Does the presence of something in the brain that is bad for reading cause it to reorganize in such a way that the brain is now good at other things?
The fact that you are dyslexic doesn’t guarantee that you’re going to be better at something else, but it often happens that way. Many people with dyslexia tend to be quite good with visual–spatial tasks. Many of them go into architecture or art or engineering. This brings up really interesting questions. For instance, do the special skills that some people with the condition show appear because they can’t read, so they’re going to spend a lot of time doing something else and get good at it? Or does the presence of something in the brain that is bad for reading cause it to reorganize in such a way that the brain is now good at other things? My guess is that it’s a bit of both. We know that in people who are born blind, parts of the brain dealing with vision now help with hearing and touch. Clearly, the brain can reorganize in dramatic ways.
Picasso was supposedly dyslexic. And so people have said, Hey, don’t muck with this because if you get rid of the dyslexia, you get rid of Picasso. Do we want to do that? And I agree, we have a lot to learn before we do anything like that. Either way, you can see that dyslexia is a human condition that spans a broad range of metaphors about who we are. We’re social beings; we’re molecular beings. It takes a lot of work to figure out what’s going on and how to help it without making things worse.
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Liberal Arts Designed for students who desire to develop a deep appreciation for and understanding of a diverse set of disciplines by studying the arts, humanities and human culture, as well as building effective communication and critical thinking skills.
Sport Communication The sport communication concentration is for students interested in pursuing a career in sport media. By combining courses in communication and media, sports management, and art and design, students will be equipped to work in collegiate sports information offices, media and/or community relations offices of both collegiate and professional sports, and as sport media personnel in either print or electronic media. Students will also be prepared to apply for graduate work in journalism.
Sport Writing Focusing primarily on writing and editing skills as well as management and administrative issues relating to sport information, the sport writing concentration equips students to be highly proficient writers capable of producing articles, marketing or public relations materials for sport organizations.
Concentrations for the Bachelor of Science in Interdisciplinary Studies
Biological Mathematics The biological mathematics concentration strives to provide students with an understanding of the connection between and application of mathematics to biology. Students will be prepared for graduate programs integrating the two fields such as mathematical biology, biostatistics and statistics.
Business Mathematics Geared toward the reality that businesses must adapt to dynamic economic environments, this concentration equips students with a combination of math and business skills that are requisite for analyzing and addressing business-related issues from a quantitative perspective.
Business Ministry The business ministry concentration combines a core of ministry preparation courses with a foundational business curriculum to equip students to serve ministries as well as create ministry opportunities within a business framework.
Criminal Justice Administration This concentration is designed to equip students who are preparing to serve or are currently serving in the law enforcement profession to advance into leadership and administrative roles within the criminal justice system. This concentration includes courses from the organizational management major and therefore requires a few online courses.
Criminal Psychology This concentration has been developed to provide an educational program for students who are equally interested in the fields of criminal justice and psychology. The concentration will prepare students for entry into the criminal justice system by providing a solid foundation in human behavior, communication skills, and criminal justice needed to succeed in this dynamic field.
Pre-Forensic Science Students majoring in Pre-Forensic Science will be prepared for entry level laboratory work or graduate programs in forensic science. The major combines a strong core of natural sciences with courses in criminal justice.
Pre-Nursing (Applied Science: Health Care Systems) The Applied Science-Health Care Systems concentration prepares a student to complete a degree at Sterling College as they finish prerequisite courses required for a nursing program.
Wildlife Law Enforcement By combining courses in Criminal Justice and Biology, this concentration provides students with the educational foundation necessary to begin a career as a Natural Resource Officer or other wildlife law enforcement career.
A look at German universities in the 20th century shows that extremism can find space not only in politics and society, but also in science. The turn of the Karlsruhe computer science pioneer Karl Steinbuch to right-wing extremism is an example of this. The Karlsruhe Institute of Technology (KIT) has distanced itself from Steinbuch’s political stance and renamed the information technology center named after him the “Scientific Computing Center”. Against this background, the KIT is organizing a conference on July 17, 2024 on the question “What does ‘never again’ mean here?”.
The public is invited to the evening program of the conference. Register here
“Science is based on openness, tolerance, and diversity. Living and defending these values, as well as the liberal order and fundamental rights, is part of a responsible scientific culture,” says Professor Kora Kristof, Vice President for Digitalization and Sustainability at KIT. “That is why it is important and part of KIT’s culture to look at our own history, to research it scientifically, and to actively engage with it.”
Conference on the prevention of political extremism
The KIT Archive, which is also organizing the conference, is dealing with the historical manifestations of extremism at KIT. The focus is on topics such as current manifestations of extremism in Germany, individual radicalization processes, and fields of action for professional prevention.
“With this event, we want to send the message that KIT is critical of extremism and rejects it,” said Dr. Klaus Nippert, head of the KIT archive and organizer of the event. “Extremism is directed against the free order of our country and against basic rights. It is important to review and further develop our own understanding of institutional responsibility as a scientific organization towards extremism and to gather suggestions for institutional prevention.”
On January 1, 2024, KIT renamed its information technology center “Scientific Computing Center.” Previously, it had been called “Steinbuch Center for Computing” since 2008.
What does ‘Never again’ mean here? Questions and answers on KIT’s approach to political extremism Conference on the occasion of the renaming of the Scientific Computing Center at KIT
Public evening program
Participation only after registration
19:00-19:15 Welcome Professor Oliver Kraft, representing the President of KIT
19:15-20:00 Keynote: The political debate on extremism in Baden-Württemberg. Review, current situation and perspectives Rüdiger Soldt, Frankfurter Allgemeine Zeitung
20:00-21:30 Panel discussion: Political and religious extremism – a topic for scientific organizations? Mathieu Coquelin, Department of Extremism Distancing Stuttgart Dr. Rolf Frankenberger, Institute for Right-Wing Extremism Research at the University of Tübingen Dr. Désirée Schauz, Institute for Technology Futures, Department of History at KIT Rüdiger Soldt, Frankfurter Allgemeine Zeitung Dr. Felix Steinbrenner, State Office for Political Education Baden-Württemberg
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