Latest news with #RockefellerUniversity
New York Times
5 days ago
- Health
- New York Times
Gene Editing: The Lessons of a Medical Breakthrough
To the Editor: Re 'Custom Gene-Editing Treatment Helps Baby in World's First Case' (front page, May 16): Your article highlighting the remarkable work of Dr. Rebecca Ahrens-Nicklas in developing a bespoke gene-editing therapy for KJ, a child with a rare disorder, is a powerful testament to translational research that bridges the clinic and the lab. It is no coincidence that Dr. Ahrens-Nicklas is a physician-scientist trained in both medicine and research through a program funded by the National Institutes of Health. Dr. Ahrens-Nicklas and I were classmates in the Tri-Institutional M.D.-Ph.D. Program, run jointly by Weill Cornell Medicine, Rockefeller University and Memorial Sloan Kettering Cancer Center. Our peers from this program are advancing our understanding of cancer, H.I.V.-AIDS and other illnesses, each drawing on the unique ability to connect patient care with scientific discovery. These dual-degree programs exist to train precisely the kind of visionary thinkers who can identify unmet clinical needs and then return to the lab to devise novel solutions. This is possible only when scientists understand disease at both the molecular and human level. Recent and proposed cuts to the National Institutes of Health threaten the pipeline that makes such breakthroughs possible. Without strong federal support, we risk losing a generation of physician-scientists — and with them, the kinds of lifesaving advances described in this incredible story.
Economic Times
24-05-2025
- Health
- Economic Times
Why do mosquitoes bite you more than your friends? Science reveals the surprising skin chemistry behind it
iStock Some people attract mosquitoes far more than others, and a 2022 study by Rockefeller University explains why. Individuals who emit higher levels of carboxylic acids through their skin are significantly more appealing to Aedes aegypti mosquitoes. Ever wondered why, during a summer evening outdoors, you're being relentlessly attacked by mosquitoes while your friends sip their drinks in peace? If you've blamed your blood type or bad luck, science has a more intriguing answer. A groundbreaking study has revealed that your body scent—specifically, the acids your skin emits—might be what's turning you into a mosquito's favourite meal. In a 2022 study conducted by researchers at The Rockefeller University and published in the prestigious journal Cell , scientists uncovered that certain individuals produce significantly higher levels of carboxylic acids on their skin. These acids, a component of natural body odor, seem to act as a siren song to Aedes aegypti , the mosquito species infamous for spreading diseases like dengue, Zika, chikungunya, and yellow fever. The research involved an unusual but telling experiment. Volunteers wore nylon stockings on their arms to collect their body scent. These were then cut into small pieces and placed in chambers with mosquitoes. What followed was a surprising and consistent pattern: the insects flocked to certain samples again and again, completely ignoring others. One particular participant, known only as 'Subject 33,' was an irresistible hit. 'They won a hundred games,' said lead researcher Leslie Vosshall. 'They were totally undefeated.' In every round, the mosquitoes were drawn to this subject's scent more than anyone else's. The secret? An unusually high presence of carboxylic acids on their skin. This isn't just a fluke. These scent-based preferences remained stable over time, suggesting that mosquito attraction isn't just about what you eat or what you wear—it's rooted in your body chemistry. Although the study doesn't confirm why mosquitoes are obsessed with carboxylic acids, it strongly suggests that an individual's unique 'skin climate'—the natural cocktail of chemicals we exude—is what seals the deal for mosquitoes. And while the researchers couldn't strip these acids from the high-attraction subjects to prove their exact role, they did note that human skin odor is a complex blend of many compounds. This study, however, focused exclusively on those with carboxylic acid groups, providing a promising lead in the quest to understand mosquito preferences. This isn't just about annoyance. Mosquitoes aren't merely buzzing pests—they are deadly vectors that contribute to over 700 million infections globally each year. Understanding why some people are more prone to bites could change the game in mosquito control and repellent design. Future repellents might target the specific chemical signatures mosquitoes crave, offering more personalized protection—especially crucial for vulnerable populations in disease-prone regions. If you've ever joked that you're a 'mosquito magnet,' it might be more scientific than you think. Your skin may be giving off signals that these insects find impossible to ignore. Until science finds a way to mask or neutralize those signals, your best defense might still be the classic combo of repellents, covered clothing, and clever timing. But at least now, you can say: it's not you. It's your chemistry.
NDTV
24-05-2025
- Health
- NDTV
Why Mosquitoes Are More Attracted To Some Individuals? Study Explains
Mosquitoes are a nuisance for everyone, but some people seem to attract them more than others. Once these pesky insects find any exposed skin, they use their needle-like proboscises to suck blood. But what is the science behind certain people being more exposed to mosquitoes? It might have something to do with smell. As per a 2022 study by researchers at the Rockefeller University, published in the journal Cell, individuals who have higher levels of certain acids on their skin are 100 times more attractive to the female Aedes aegypti, responsible for the spread of diseases such as dengue, chikungunya, yellow fever and Zika. For the study, researchers collected natural scent from people's skin using nylon stockings on the arms. Afterwards, they were cut into two-inch pieces and placed behind two separate trap doors where mosquitoes were flying. As per Leslie Vosshall, the lead researcher behind the study, mosquitoes were particularly attracted to one sample, described as being from 'subject 33'. "Subject 33 won a hundred games. They were totally undefeated. Nobody beat them," said Ms Vosshall. She added that chemical analysis revealed that 'subject 33' or highly attractive people, produce significantly more carboxylic acids in their skin emissions. "The link between elevated carboxylic acids in "mosquito-magnet" human skin odour and phenotypes of genetic mutations in carboxylic acid receptors suggests that such compounds contribute to differential mosquito attraction," the study highlighted. It remains unclear why mosquitoes are particularly attracted to this chemical, but a person's unique skin climate is believed to play a major role. Limitations and scope The researchers pointed towards the limitations of the study as well, stating that they could not remove carboxylic acids from the skin of highly attractive human subjects to establish necessity. "Human skin odour is a complex blend of several classes of chemical compounds, each of which requires its own specialised analytical detection methods. Our study exclusively focused on compounds with carboxylic acid groups," the study stated. Since mosquito-borne diseases impact about 700 million people per year, the study could provide insights into what skin odorants are most important to the mosquito and subsequently help in developing more effective repellents.
Irish Examiner
23-05-2025
- Health
- Irish Examiner
There may be more to the saying ‘stop to smell the roses' — it may help to keep your brain sharp
Many of us have experienced the sensation of a smell immediately returning us to our childhoods. Freshly-cut grass reminds me of athletics in the back field at school. Enticing aromas from sizzling sausages create mental images of delicious smells wafting up the stairs on Sunday mornings. A turf fire brings me back to summer evenings with cousins in the country. Recent research, led by the National Institute on Aging and published in Neurology (2023), suggests that a declining ability to detect scents as we age could be linked to conditions such as Parkinson's and Alzheimer's. However, the good news is that other studies have found that training our sense of smell may delay cognitive decline and might even help reverse some of its effects. Our olfactory ability works like a muscle — the more we use it, the stronger it gets. It never occurred to me that exercising my sense of smell was important to keeping it in tip-top condition, and I am not the only one who underrates its importance. In 2015, a survey of some 7,000 young people worldwide found that they would 'rather give up their sense of smell than their smartphone'. Human olfaction is less well developed than it is in animals. Dogs are renowned for their tendency to sniff the air, vegetation, other humans, or anything that crosses their path. In the late 19th century, the neuroanatomist Paul Broca defined all mammals as osmatiques, such as dogs, or anosmatiques — animals less guided by their snouts, including dolphins, whales, monkeys, and humans. His categorisation of mammals into two groups was based on variations in the size of the olfactory bulb. A dog's olfactory bulb is about 40 times as big as that of humans. However, more recent evidence suggests that humans' sense of smell is more refined than previously thought. In 2014, research at Rockefeller University in New York used 128 odorous molecules to test participants' ability to notice any change in composition. The researchers found that participants could distinguish subtle changes in scents to a remarkable degree. A further study found that humans can distinguish up to 5,000 odours. Links to mood Brain injury, viral infections, and chronic sinusitis are common causes of anosmia, or a lack of the sense of smell. A study in Nature (2022) investigated just how deeply olfactory dysfunction can affect people. Lead author Thomas Hummel, at the Dresden University of Technology in Germany, tracked 171 people with a damaged sense of smell over 11 months. The researchers found a clear link between patients' ability to smell and their depressive symptoms over this period. Even more interesting, as their olfactory function improved during recovery, so did their mood. There is mounting evidence of a link between olfactory ability and cognitive function. A study published in Alzheimer's Research and Therapy (2019) assessed the sensitivity of 7,000 participants and found a clear correlation between the ability to discern odours and mental abilities. The weaker the sense of smell, the worse participants scored in verbal fluency, attention, memory, and learning. The researchers suggested that olfactory testing could be a useful screening test for cognitive impairment. A study published in Alzheimer's Research and Therapy (2019) assessed the sensitivity of 7,000 participants and found a clear correlation between the ability to discern odours and mental abilities. Other studies have reached similar conclusions, with some researchers suggesting that lost smell sensitivity could contribute to the brain's deterioration. Brain scans support this theory. A study in Frontiers in Allergy (2023) reported widespread loss of brain grey matter accompanying olfactory dysfunction, with the most pronounced changes seen in the olfactory bulb itself. Research has also linked olfactory dysfunction with impaired immunity. The Karolinska Institute in Sweden found a clear link between participants' ability to distinguish between smells such as rotten eggs, urine, vomit, and fermented fish, and markers of inflammation in their saliva. The fouler the stench, the higher the levels of inflammation. This finding suggests that the foul stench primed the body to produce an inflammatory response to protect against pathogens. Meanwhile, pleasant odours such as eucalyptus, lavender, ginger, citrus, and peppermint have been shown to suppress inflammation. Could a healthy sense of smell help to keep our immune system in check, raising inflammation when it perceives a potential threat to our health and lowering it when we are in a safe environment? Scientists at the Karolinska Institute suggested that olfactory dysfunction may throw this balance out of kilter, leading to chronic inflammation that damages the brain. Smelling trouble Paying more attention to our sense of smell could help improve our olfactory sensitivity and support cognitive function. A study published in Laryngoscope (2009) recruited 56 people with olfactory dysfunction. Forty were assigned to smell training over 12 weeks, during which time they sniffed four odours for at least 10 seconds twice a day and kept a diary of their experiences. The study group demonstrated increased odour sensitivity, compared to no change in the control group. Crucially, the training was shown to boost brain function. A study in Neuropsychology Review (2023) found promising evidence that smell training can slow or even reverse certain signs of cognitive decline. This included some evidence of neurological changes in the brain, in regions such as the hippocampus, that are important for cognitive ability. There may be more to the saying 'stop to smell the roses' than taking the time to enjoy life. It might also be helping to keep your brain sharp as you age. Pure essential oils, such as lemon, clove, eucalyptus, and rose, are available in health shops or online and can help make regular 'smell training' part of your daily routine. Catherine Conlon is a public health doctor Read More What your step count says about your fitness levels
NZ Herald
01-05-2025
- Health
- NZ Herald
What nearly brainless rodents know about weight loss and hunger
To find out, Grill dripped liquid food into their mouths. 'When they reached a stopping point, they allowed the food to drain out of their mouths,' he said. Those studies, initiated decades ago, were a starting point for a body of research that has continually surprised scientists and driven home that how full animals feel has nothing to do with consciousness. The work has gained more relevance as scientists puzzle out how exactly the new drugs that cause weight loss, commonly called GLP-1s and including Ozempic, affect the brain's eating-control systems. The emerging story does not explain why some people get obese and others do not. Instead, it offers clues about what makes us start eating, and when we stop. While most of the studies were in rodents, it defies belief to think that humans are somehow different, said Dr Jeffrey Friedman, an obesity researcher at Rockefeller University in New York. Humans, he said, are subject to billions of years of evolution leading to elaborate neural pathways that control when to eat and when to stop eating. The second this rodent looks at food, its brain starts assessing how many calories it may have. Photo / Josh Norem, The New York Times As they have probed how eating is controlled, researchers learned that the brain is steadily getting signals that hint at how calorically dense a food is. There's a certain amount of calories the body needs, and these signals make sure the body gets them. The process begins before a lab animal takes a single bite. Just the sight of food spurs neurons to anticipate whether a lot of calories will be packed into that food. The neurons respond more strongly to a food like peanut butter – loaded with calories – than to a low-calorie one like mouse chow. The next control point occurs when the animal tastes the food: neurons calculate the caloric density again from signals sent from the mouth to the brainstem. Finally, when the food makes its way to the gut, a new set of signals to the brain lets the neurons again ascertain the caloric content. And it is actually the calorie content that the gut assesses, as Zachary Knight, a neuroscientist at the University of California San Francisco, learned. He saw this when he directly infused three types of food into the stomachs of mice. One infusion was of fatty food, another of carbohydrates and the third of protein. Each infusion had the same number of calories. In each case, the message to the brain was the same: The neurons were signalling the amount of energy, in the form of calories, and not the source of the calories. When the brain determines enough calories were consumed, neurons send a signal to stop eating. Knight said these discoveries surprised him. He'd always thought that the signal to stop eating would be 'a communication between the gut and the brain,' he said. There would be a sensation of having a full stomach and a deliberate decision to stop eating. Using that reasoning, some dieters try to drink a big glass of water before a meal, or fill up on low-calorie foods, like celery. But those tricks have not worked for most people because they don't account for how the brain controls eating. In fact, Knight found that mice do not even send satiety signals to the brain when all they are getting is water. It is true that people can decide to eat even when they are sated, or can decide not to eat when they are trying to lose weight. And, Grill said, in an intact brain – not just a brainstem – other areas of the brain also exert control. But, Friedman said, in the end the brain's controls typically override a person's conscious decisions about whether they feel a need to eat. He said, by analogy, you can hold your breath – but only for so long. And you can suppress a cough – but only up to a point. Scott Sternson, a neuroscientist with the University of California in San Diego and Howard Hughes Medical Institute, agreed. 'There is a very large proportion of appetite control that is automatic,' said Sternson, a co-founder of a startup company, Penguin Bio, that is developing obesity treatments. People can decide to eat or not at a given moment. But, he added, maintaining that sort of control uses a lot of mental resources. 'Eventually, attention goes to other things and the automatic process will wind up dominating,' he said. As they probed the brain's eating-control systems, researchers were continually surprised. They learned, for example, about the brain's rapid response to just the sight of food. Neuroscientists had found in mice a few thousand neurons in the hypothalamus, deep in the brain, that responded to hunger. But how are they regulated? They knew from previous studies that fasting turned these hunger neurons on and that the neurons were less active when an animal was well fed. Their theory was that the neurons were responding to the body's fat stores. When fat stores were low – as happens when an animal fasts, for example – levels of leptin, a hormone released from fat, also are low. That would turn the hunger neurons on. As an animal eats, its fat stores are replenished, leptin levels go up, and the neurons, it was assumed, would quieten down. The whole system was thought to respond only slowly to the state of energy storage in the body. But then three groups of researchers, independently led by Knight, Sternson and Mark Andermann of Beth Israel Deaconess Medical Center, examined the moment-to-moment activity of the hunger neurons. They began with hungry mice. Their hunger neurons were firing rapidly, a sign the animals needed food. The surprise happened when the investigators showed the animals food. 'Even before the first bite of food, the activity of those neurons shut off,' Knight said. 'The neurons were making a prediction. The mouse looks at food. The mouse predicts how many calories it will eat.' The more calorie-rich the food, the more neurons turn off. 'All three labs were shocked,' said Dr Bradford Lowell, who worked with Andermann at Beth Israel Deaconess. 'It was very unexpected.' Lowell then asked what might happen if he deliberately turned off the hunger neurons even though the mice hadn't had much to eat. Researchers can do this with genetic manipulations that mark neurons so they can turn them on and off with either a drug or with a blue light. These mice would not eat for hours, even with food right in front of them. Lowell and Sternson independently did the opposite experiment, turning the neurons on in mice that had just had a huge meal, the mouse equivalent of a Thanksgiving dinner. The animals were reclining, feeling stuffed. But, said Andermann, who repeated the experiment, when they turned the hunger neurons on, 'The mouse gets up and eats another 10 to 15% of its body weight.' He added, 'The neurons are saying, 'Just focus on food.'' Researchers could switch neurons on and off, and it would affect how much a rodent was willing to eat. Photo / Zachary Knight, Thew New York Times Researchers continue to be amazed by what they are finding – layers of controls in the brain that ensure eating is rigorously regulated. And hints of new ways to develop drugs to control eating. One line of evidence was discovered by Amber Alhadeff, a neuroscientist at the Monell Chemical Senses Center and the University of Pennsylvania. She recently found two separate groups of neurons in the brainstem that respond to the GLP-1 obesity drugs. One group of neurons signalled that the animals have had enough to eat. The other group caused the rodent equivalent of nausea. The current obesity drugs hit both groups of neurons, she reports, which may be a factor in the side effects many feel. She proposes that it might be possible to develop drugs that hit the satiety neurons but not the nausea ones. Alexander Nectow, of Columbia University, has another surprise discovery. He identified a group of neurons in the brainstem that regulate how big a meal is desired, tracking each bite of food. 'We don't know how they do it,' he said. 'I've been studying this brainstem region for a decade and a half,' Nectow said, 'but when we went and used all of our fancy tools, we found this population of neurons we had never studied.' He's now asking if the neurons could be targets for a class of weight loss drugs that could upstage the GLP-1s. 'That would be really amazing,' Nectow said. This article originally appeared in The New York Times. Written by: Gina Kolata Photographs by: Josh Norem, Zachary Knight ©2025 THE NEW YORK TIMES
