The Fresh Market Donates More Than $21,000 in Support of the Alzheimer's Association
Throughout the month of June, the premium grocery retailer pledged to donate 10 percent of the sales price of Carla Hall's Sweet Heritage Butter Tarts to the Alzheimer's Association.
Throughout the month of June, the premium grocery retailer pledged to donate 10 percent of the sales price of Carla Hall's Sweet Heritage Butter Tarts to the Alzheimer's Association. The campaign aimed to raise awareness and fund critical research toward a cure. In total, The Fresh Market contributed $21,541.70 to the organization.
'It was our pleasure to partner with Carla Hall to help raise awareness and support for the millions of Americans living with Alzheimer's disease,' said Emily Turner, chief marketing officer at The Fresh Market. 'This cause is close to our hearts at The Fresh Market, and we're incredibly grateful to the Alzheimer's Association, Carla Hall, and—most importantly—our guests for helping us reach our fundraising goals.'
'We're grateful to The Fresh Market and Carla Hall for their commitment to the fight to end Alzheimer's and all other dementia,' said Sarah Fried, vice president, corporate initiatives, Alzheimer's Association. 'Alzheimer's impacts millions of families and partnerships like this help fund critical care and support services and disease research, while spurring important conversation and encouraging others to join us in the fight to end this disease.'
Carla Hall—known for her appearances on Bravo, Food Network, and ABC —is a passionate advocate for individuals living with Alzheimer's disease and a longtime supporter of the Alzheimer's Association. Her advocacy is deeply personal, inspired by her grandmother's experience with the disease.
'A big ol' thank you to everyone who stopped by The Fresh Market and picked up my Sweet Heritage Butter Tarts!' said Carla Hall. 'Y'all didn't just treat yourselves — you helped raise more than $21,000 for the Alzheimer's Association!
'That's a whole lot of goodness doing double duty: satisfying your sweet tooth and supporting critical research to help us get closer to a cure. I'm so proud to be part of this delicious way to give back. Let's keep showing up for each other and keep working to #ENDALZ — one bite at a time!'
The number of Americans living with Alzheimer's is growing — and growing fast. According to the Alzheimer's Association's 2025 Facts and Figures report, nearly 7 million Americans are living with Alzheimer's and it is estimated that more than half of all Americans know someone with the disease. Additionally, almost 12 million family members and friends serve as dementia caregivers.
About The Fresh Market
Rated by USA Today as one of America's Best Customer Service Companies in 2025, voted #1 in three categories by USA Today's 10Best Readers' Choice Awards for 2024—"Best Grocery Store Bakery," "Best Grocery Store Deli," and "Best Grocery Store Prepared Foods"—and recognized for three consecutive years as the 'Best Grocery Store in America.' The Fresh Market currently operates more than 170 grocery stores in 22 states across the U.S. and one Spirits & Wine store, inspiring guests to discover new flavors and cook with confidence. For more information, please visit www.thefreshmarket.com or follow the company on Facebook, Instagram, TikTok, X and Pinterest.
About the Alzheimer's Association
The Alzheimer's Association is a worldwide voluntary health organization dedicated to Alzheimer's care, support and research. Our mission is to lead the way to end Alzheimer's and all other dementia — by accelerating global research, driving risk reduction and early detection, and maximizing quality care and support. Our vision is a world without Alzheimer's and all other dementia®. Visit alz.org or call 800.272.3900.
About Carla Hall
Chef, best-selling author and television personality Carla Hall has been entertaining audiences with her enthusiasm for life and warm personality for years. She has starred on Food Network shows such as 'BakeAway Camp,' 'Halloween Baking Championship,' 'Holiday Baking Championship' and 'Worst Cooks in America.' She also hosted the Emmy-nominated 'Chasing Flavor with Carla Hall' (HBO Max) and serves as a judge on 'Harry Potter: Wizards of Baking' (HBO Max). She first won over audiences when she competed on Bravo's 'Top Chef' and hosted ABC's 'The Chew' for 7 years.
Her product line, Sweet Heritage by Carla Hall (available through QVC), is designed to bring you kitchen items that are useful, reliable, and complete with a dash of joy and soul. Carla's latest cookbook, Carla Hall's Soul Food: Everyday and Celebration, was published in 2018, landing on annual "Best Cookbook" lists across the country and receiving an NAACP Image Awards nomination. Her second children's book, Carla and the Tin Can Cake Party will be published October 14th.
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Vox
3 minutes ago
- Vox
The one, big unanswered question about Ozempic
covers health for Vox, guiding readers through the emerging opportunities and challenges in improving our health. He has reported on health policy for more than 10 years, writing for Governing magazine, Talking Points Memo, and STAT before joining Vox in 2017. We are nearing a point of no return for GLP-1 drugs. More than one in 10 Americans have already taken a GLP-1 agonist, be it Ozempic, Wegovy or Mounjaro. The medications, originally developed for diabetes treatment, have proven to be remarkably effective in helping people lose weight — and America is in the throes of an obesity crisis. They have shown promise in treating cardiovascular diseases, the country's leading killer and a direct consequence of the obesity epidemic. With each additional study finding yet another application for these drugs, you might find yourself asking: Should I be taking Ozempic? Should everybody take it? Is there anything these drugs can't do? And indeed, right now it can seem like everyone will be taking GLP-1, sooner or later. These drugs currently require regular injections and can cost more than $1,000 out of pocket, but cheaper and more easily used versions are coming. Eli Lilly will soon bring a pill version to the market, with a version expected to debut at a lower price than injectable Ozempic or Wegovy did. A generic GLP-1 agonist is on track to arrive at Canadian pharmacies in 2026 and a US version will likely follow within the next decade. Some of the newer versions in development may prove to be even more effective than the first generation, which will only create more demand among doctors and patients. Put it all together, and we can expect many, many more people taking them. GLP-1 drug prescriptions for adults with commercial insurance increased by a staggering 364 percent from 2019 to 2024, but they were still only prescribed to 4 percent of insured US adults; more than 100 million US adults — 40 percent of the population — are obese, the Wall Street Journal reported earlier this year, and as more insurers cover these drugs for weight loss, more patients will be able to access them. These drugs' power comes from their mysterious ability to control people's compulsions. Patients who take an GLP-1 agonist say that the fatty ultraprocessed foods they used to find irresistible are no longer so tempting, though sometimes those old cravings for unhealthy junk come rushing back after taking the drugs for a while. Substances as habit-forming as coffee no longer hold the same sway. Others notice decreased desires that have nothing to do with their diet — to bite their nails, for example. We are entering the Ozempic era, and even as excitement grows about the possibilities for these medications, now is the time to take seriously the possible risks from this new class of drugs. A lot of people experience brand-new cravings, sometimes for healthier foods. 'Beans — I get cravings for beans. I never really ate them before, now I crave homemade baked beans in a tomato sauce,' Sarah, a charity development worker from Scotland who has been taking a GLP-1 compound for a few months, told me by email. 'It used to bother me if a cafe served beans on a cooked breakfast; now beans is the main part of my breakfast.' Swapping salad greens for carbs sound like a clear win — in fact, it sounds almost too good to be true. In the long term, what does it mean to modulate our desire? Are we sure we can suppress the harmful compulsion to eat too much without compromising the productive ones — such as the desire to succeed or the pleasure we find in personal relationships? How might these drugs impact our experience of joy and pain? What might that do to impact the messy human experience of…simply living? 'What are the very long-term effects of these drugs? The literature will say, 'Well, there isn't really bad long-term effects because some people have been taking it for diabetes for 10 years, and they don't have bad effects,'' Kent Berridge, a professor of psychology and neuroscience at the University of Michigan, told me. 'And I think that's a fair argument. But then 10 years is not 20 years or 30 years.' We are entering the Ozempic era, and even as excitement grows about the possibilities for these medications, now is the time to take seriously the possible risks from this new class of drugs. In my conversations with some of the top experts on the science of cravings, they offered a cautious outlook in regard to messing with our brain's desire pathways. But they were also optimistic that these drugs could deliver benefits to many Americans without turning us into emotionless robots. Why GLP-1s work for so many different medical conditions In the 1980s, scientists had identified the naturally occurring hormone GLP-1 and its importance in regulating people's digestion. By the end of the decade, investigators had confirmed that the hormone encouraged insulin production — offering the potential to treat people with diabetes, who struggle to produce insulin that regulates their blood sugar. Then just a few years later, a scientist identified a peptide from the Gila monster that was similar to the human hormone GLP-1 but came in a more stable form, offering therapeutic potential. By the mid-2000s, the first GLP-1 agonist drugs were approved for diabetes, but the daily injections required and the narrow focus kept the market small. In 2017, the Food and Drug Administration approved Ozempic — a weekly injection, rather than a daily shot. By that point, doctors had already begun to notice that some patients who took the GLP-1 agonists experienced a reduced appetite with resulting weight loss. Researchers began to study the weight-loss effects and they were stunned: One of the first studies found users lost 15 percent of their body weight, on average, in little more than a year, a wildly larger percentage than from any other weight loss drug or tool. The Ozempic fervor had begun. Specialty pharmacies started to sell off-brand compounded versions of the drugs. The FDA then approved Wegovy, an Ozempic successor, for weight loss in 2021, and in 2023, Zepbound got the green light for weight-loss prescriptions. As their astonishing weight-loss effects became clear, research into GLP-1 agonists and their health benefits exploded. Today, the list of possible benefits is genuinely astounding. But how, exactly, do they work? First, a drug like Ozempic mimics the natural GLP-1 hormone in your gut, which slows down digestion in the stomach and gastrointestinal tract. Those who take it feel fuller earlier and longer, and it's easier for them to eat less. The better regulation of blood sugar also prevents massive swings in glucose, which can induce hunger. As a result of its effect on digestion, the most common clinical side effects reported with Ozempic and its peers are nausea, vomiting, diarrhea and constipation. In clinical trials for GLP-1 treatment for diabetes or obesity, between 4 and 12 percent of patients experienced constipation; a similar share of patients endured vomiting and diarrhea. There have been reports of other rare but serious physical side effects: The drugs have been linked to an elevated risk of eye disease among older patients, for example. Some people who lose weight quickly experience temporary hair loss, a symptom that a small number of patients on GLP-1 medications have anecdotally reported. But scientists have also discovered these drugs can affect your brain directly, with sometimes surprising and unpredictable effects on people's cravings — for food and for other things. Naturally occurring GLP-1 secretes from in a person's intestines into their blood and it disappears within a matter of minutes, destroyed by enzymes in the blood, Berridge said. As a result, it does not cross into people's brains very easily. The drug form, GLP-1 agonists, on the other hand, can cross this barrier. When a person takes Ozempic or Wegovey or whichever GLP-1 they've been prescribed, the semaglutide endures for a long time, giving it more time to cross into the brain. Once the chemical is in that person's brain, it can turbocharge neurons in your brainstem that naturally produce some very small amounts of GLP-1. Those neurons then release the hormone into many other parts of the brain and disrupt the release of dopamine, which produces that little surge of pleasure that makes eating a sweet sugary piece of cake so damn good or finishing a half marathon after months of training so satisfying. 'The drugs are getting into these structures and it turns out that they suppress cravings in all of these places, including the reward-system ones,' Berridge said. Scientists began to make this connection when observational studies reported that people who took a GLP-1 agonist for its diabetes or weight-loss effects also reported consuming less alcohol or fewer illicit drugs than they did before. Researchers started to probe further, experimenting with injecting microdoses of a semaglutide directly into the brains of animals in lab studies, and they have found a decrease in all kinds of cravings, including powerful compulsions for cocaine and heroin. These findings have introduced the startling possibility that, beyond food, we could control some of the most uncontrollable urges that people struggle with, often to the detriment of their health. But they also bring us to the big question: If we can turn down the volume of our desire, how might that change the very emotions that make us human, the experience of our deepest joys and pleasures? What the science on desire can tell us about GLP-1s I've started to think of the dilemma these drugs present this way: Can I cut off the part of my brain that compels me to reach for a bag of potato chips at night, without compromising the desire to sit down and read books with my children? Unfortunately, we simply don't know yet. Scientists aren't exactly sure how these complex human desires interact. The desire to eat, for example, is one of our oldest evolutionary impulses, Berridge, the Michigan neuroscientist, told me. Can we really mess with that ancient part of our brain without unintended consequences? There are at least two ways of thinking about what the answer might be. First, the (maybe) good news: Berridge's research has focused on the distinction between wanting something and liking it. He told me if Ozempic can eliminate our unchecked wanting of something that's bad for us — such as fatty, processed foods or alcohol, for example — but still maintain our enjoyment of it, that would suggest people who take it are not suddenly at risk of losing all of the pleasure in their lives, including other things that also cause a surge of dopamine in our brains, like finishing a creative writing project after months of work or cherishing conversations with your friends. This is a concept that my former colleague Brian Resnick explored last year: GLP-1s have the ability to manipulate a figurative 'dial of desire' in our brains, which could be leveraged for good. In the 1980s, Berridge worked on a series of experiments with a colleague, Terry Robinson, in which they eliminated dopamine in rats. What they observed was the rats stopped voluntarily eating, drinking, and seeking other rewards set up by the investigators. However, when they were given something sweet to eat, their faces would react positively to the taste, just as they normally would. That reactivity, the researchers postured, was a proxy for their joy. The rats could also still become averse to new sensations, which again affirmed a capacity for strong emotions, even if their compulsiveness had been removed. Berridge told me he actually doubted their findings at first — how could you like something but not want it? — but it continued to be replicated in experiments by other investigators over the years. In one particularly revealing experiment from 2005, participants were given cocaine and a dopamine-blocking drug. They still liked the cocaine when they were given it, but their desire for additional cocaine was dampened when the dopamine was blocked. The study was small, but it affirmed Berridge and Robinson's initial insight: Dopamine appears to influence the wanting of things, rather than the liking of them. Early studies of Ozempic patients indicate most participants still enjoy their food despite their compulsion to eat being reduced. Some of them, including some of the patients I spoke with, also found themselves desiring healthier foods. 'That's encouraging,' Berridge told me. 'I would say that's a good thing.' However, another way of understanding desire would raise more cause for concern. Jackie Andrade, a psychology professor at the University of Plymouth, has worked with colleagues on the Elaborated Intrusion Theory, which proposes that all our cravings are not unique brain processes but part of our general motivation. According to this theory, when we encounter certain 'triggers' — such as a physical sensation or some environmental cue — the trigger leads to a burst of spontaneous thoughts about an object of our desires. And when we begin mentally picturing our desire, our craving for it only increases. Here is the key finding, Andrade told me: The object of desire — whether it be alcohol, chocolate, or cigarettes — is less important than the underlying mental processes involved in craving. The brain mechanisms are the same regardless of the craving, based on their observations of people's brain patterns when being presented with different triggers. We crave something because the image of it in our minds is briefly pleasurable and thinking about whatever it is boosts our mood, which in turn strengthens the craving and our awareness that we don't have it. This explains one of the conundrums about desire: Our desires are thoughts and thoughts require mental effort. So why aren't they easier to shake? This cycle of environmental triggers — seeing a billboard advertising fast food or attending a cookout with chips and dip on display — leads to our imagining the craving, which leads to both pleasure if we satisfy it and frustration if we don't, which is why we feel such strong impulses to resolve the cravings. But, at least according to the Plymouth researchers' work, there is not a clear distinction between a craving for a piece of pizza and a craving for something more productive. 'From our research, the cognitive processes are the same for both,' Andrade said. 'Could we have less driven entrepreneurs or marathon runners because they're on these drugs and they're too chilled out to want to do anything? Right now, we don't know.' What we still need to figure out about these drugs Even as their usage explodes, the reality behind these drugs and how they affect our desires is still a mystery. Pills are likely to have the same effect as injections on cravings, Berridge told me, so long as the GLP-1 agonist is still crossing into people's brains. 'In what sense is it reducing wanting? Because there's a couple of possible ways. One way would be to subtract a degree of intensity from every want,' Berridge said. 'So addictive wants go down, but then so do the everyday desires in life and even eagerness to go out into the world and face it and do things. That would be bad if it was a general subtraction in intensity of wanting.' 'On the other hand, it is possible that that's not what it's doing, but rather it's lowering the ceiling,' he continued. 'So really intense peaks of wanting can't go so high, but things below that ceiling can still remain normal.' In other words, GLP-1 agonists can only decrease the intense peaks of our cravings, which could allow us to, for example, not binge-eat or overdrink — without eliminating a more normal intensity of wanting for other things. The problem is, Berridge said: 'I don't know of any actual studies that have asked this question.' He said he would like to see a study that measures people's motivation to pursue a wide range of incentives, both mild and intense ones, when on and off one of these drugs. Researchers at the University of Plymouth are setting up studies that would evaluate behavioral changes in people who take the GLP-1 medications. We need more evidence, because what we have right now is circumstantial and inconclusive anecdotes. Peruse the many Reddit communities devoted to these weight-loss drugs and you'll see the subject of cravings come up a lot. Some people describe food cravings that come back after a few months of taking Ozempic or Wegovy. Others report strange new cravings they never experienced before, such as a sudden taste for milk. Some of the changes are expected — decreased desire for nicotine or alcohol — but some are puzzling: One user, a true crime aficionado, described a reduced desire to look at dark or gory materials online after being on a GLP-1 agonist. Others responded by sharing that they were less compelled to shop online or stopped biting their nails. Sarah, the charity development worker from Scotland, told me she started taking a GLP-1 drug three months ago after she gained weight during perimenopause and was struggling to lose it. She's since lost 18 pounds. There have been some physical side effects — fatigue and acid reflux — and she's noticed a significant shift in her cravings. Whereas she used to mix salads with pasta, she finds she no longer craves the carbs. Mashed potatoes used to be one of her favorite foods, but she hasn't eaten that once since going on the medication. At the same time, she has new hankerings for beans and green apples — which she told me she found puzzling because she says she used to hate the sound of teeth crunching into an apple. 'I don't get the same emotions from food,' she told me over email. 'It's nice, I enjoy it, but I don't feel food in the same way.' She, like many other patients, also says she no longer experiences the same desire to drink alcohol. She told me she drinks at most one night on the weekend and no longer attends happy hours with her colleagues like she used to, when she would have a few drinks midweek. 'I don't go and not drink, I just don't go,' she told me. 'Drunk people are tedious when you're sober!' GLP-1s are genuinely promising, but they also reveal our insatiable desire to find a wonder drug that takes care of all of our problems in one pill. Andrade said we should resist that temptation, even if Ozempic and its peers could play a role in helping to address important health crises. Research has consistently found that weight loss tends to be more sustainable when it includes behavioral changes in addition to pharmaceutical interventions. Ideally, you would do both: work on modifying your behavior, while medication assists. Losing weight isn't just about eating less, but eating healthier and exercising more in order to enjoy the health benefits that those positive activities produce. If Ozempic affects all kinds of motivation, patients may not be as driven to adopt those other desirable behaviors. 'If people are taking these drugs, are they more motivated to, say, become more physically active or to eat more healthily? Or are they less motivated because the drugs are doing it for them?' Andrade said. 'There's the risk that people might not want to make changes. If you've still got a bad diet and a sedentary lifestyle, you're building up other problems that are maybe a little bit more hidden because the obesity is not there.' This is already an ongoing subject of concern: Some studies have suggested that people who stop taking Ozempic gain back much of the weight they lost; that may be because they are not adopting desirable new behaviors — better eating, more activity — alongside their taking the drug. On the flip side, some doctors say they also worry about people who take the drugs for reasons other than weight loss but end up undereating and increasing the related health risks of undernourishment. Are these findings a canary in the coal mine for other unexpected and undesirable side effects related to the drug's effects on cravings? It's a genuinely vexing question. After all, many people take these drugs because they do have a problematic compulsive behavior — they eat too much. Getting those cravings under control is the point of getting a prescription. But are people also losing other less obvious desires? Are they losing, in a sense, a part of themselves? The evidence for now is mixed. One Reddit user joked they felt like they were getting mental health care they didn't know they needed. Two Reddit users shared that they had cut down from multiple cups of coffee in the morning to one (or less). 'I'm kind of bummed about it,' one said. 'I love my coffee.' 'Same. I love coffee,' the other poster replied.
Business Upturn
4 hours ago
- Business Upturn
Roche presents new insights in Alzheimer's disease research across its diagnostics and pharmaceutical portfolios at AAIC
By GlobeNewswire Published on July 28, 2025, 10:00 IST Trontinemab's Phase Ib/IIa Brainshuttle™ AD study continues to show rapid and robust clearance of amyloid plaques, with 91% becoming amyloid PET negative and ARIA-E remaining <5% Design of the Phase III TRONTIER 1 and 2 studies of trontinemab in early symptomatic Alzheimer's disease featured, with initiation planned in 2025 Plans for new Phase III trial investigating trontinemab in preclinical Alzheimer's disease, in people at high risk of cognitive decline New real-world data support Elecsys pTau217 as a standalone blood test, comparable to a PET scan, for rule-in and rule-out identification of amyloid pathology Basel, 28 July 2025 – Roche (SIX: RO, ROG; OTCQX: RHHBY) announced today that new data from its Alzheimer's development portfolio is being presented at the Alzheimer's Association International Conference (AAIC) in Toronto, Canada (July 27-30). These data exemplify the comprehensive approach Roche is taking in addressing Alzheimer's across the entire patient journey. Featured oral presentations include the latest results from the ongoing Phase Ib/IIa Brainshuttle™ AD study, which continue to support rapid and robust reduction of amyloid plaques, and design of the Phase III TRONTIER 1 and 2 studies of investigational trontinemab for early symptomatic Alzheimer's disease, with initiation planned later this year. As part of its growing Alzheimer's development programme, Roche announced today its plans for an additional Phase III trial to investigate trontinemab in preclinical Alzheimer's disease. The trial will focus on individuals at risk of cognitive decline, with the goal of potentially delaying or preventing the progression of the disease to symptomatic stages. 'Alzheimer's disease represents one of the greatest challenges in healthcare today and tackling it requires early detection and effective therapeutics,' said Levi Garraway, M.D., Ph.D., Roche's Chief Medical Officer and Head of Global Product Development. 'Trontinemab is designed to target a key driver of Alzheimer's disease biology more effectively in the brain. Combining new treatment avenues with advanced diagnostics may enable earlier and potentially more effective intervention. With plans for Phase III trials in both early symptomatic and preclinical Alzheimer's disease, we are advancing science with the goal of delaying —and ultimately preventing—progression of this devastating condition.' Late-breaking oral and poster presentations highlight the potential of Roche's Elecsys® pTau217 as a reliable and accessible blood-based biomarker test, providing comparable results to PET scan and cerebrospinal fluid (CSF) diagnostics for rule-in and rule-out diagnosis of amyloid pathology, a hallmark of Alzheimer's disease, across care settings. The test, which received Breakthrough Device Designation from the U.S. Food and Drug Administration last year, will also be utilised in Roche's TRONTIER studies. 'Blood based testing for Alzheimer's disease has the potential to greatly improve patient access and decrease the time to definitive disease diagnosis,' said Matt Sause, CEO of Roche Diagnostics. 'Our data show that the Elecsys pTau217 test performs comparably to PET scans but can be performed with a simple blood draw and analyzed in a routine clinical laboratory. This has the potential to transform the diagnosis of Alzheimer's and provide clear answers to caregivers, patients, and their families.' Up to 75% of people living with symptoms of Alzheimer's disease globally have not been diagnosed, and those who have, waited an average of 2.8 years1, and even less have received any form of treatment. Diagnostics play a crucial role in addressing the global challenge of Alzheimer's, not only to detect and identify people with the disease early, even before the first symptoms, but also to rule out those who may or may not benefit from specific treatments. Pharmaceuticals In a 90-minute Featured Research session, designs were shared for the Phase III studies, TRONTIER 1 and 2, which will initiate later this year, investigating the efficacy and safety of investigational trontinemab in people with early Alzheimer's disease. The primary endpoint will measure the change in cognition and function based on the Clinical Dementia Rating – Sum of Boxes scale after 18 months of treatment. Secondary endpoints will include assessments of cognition, function, behavioural symptoms, and quality of life. A pre-screening study, TRAVELLER, based on a brief clinical assessment and a plasma biomarker, which will be identified using the Elecsys pTau217 test, has also been initiated, to enable broader community outreach and extend access to these trials to more diverse populations representative of Alzheimer's disease. New data on the latest results for trontinemab from the completed dose-expansion part of the 1.8 mg/kg and 3.6 mg/kg cohorts from the ongoing Phase Ib/IIa Brainshuttle AD study continued to show rapid and robust reduction of amyloid plaques in the brain as measured by amyloid positron emission tomography (PET). In the 3.6 mg/kg cohort, trontinemab reduced amyloid levels below the 24 centiloid positivity threshold in 91% of participants (n=49/54) after 28 weeks of treatment; 72% (n=39/54) achieved deep clearance below 11 centiloids. These data were reinforced by early and significant reductions in fluid biomarkers of Alzheimer's disease, including total tau, phosphorylated Tau (pTau)181, pTau217, and neurogranin measured in CSF and continues to show a favourable safety and tolerability profile. Amyloid-related imaging abnormalities-edema/effusion (ARIA-E) continued to be observed in <5% of participants (blinded data; N=4/149 across 1.8 and 3.6mg/kg dose cohorts). All cases were radiographically mild, one was associated with mild and transient symptoms. Diagnostics Roche will present data on a new study comparing the pTau217/Ab42 plasma ratio to the high-throughput, fully automated Elecsys pTau217 assay. The presentation will report on the accuracy of these tools in detecting amyloid pathology. Together with the high throughput and full automation of the assay, these data will assess the potential of Elecsys pTau217 as an accurate standalone rule-in and rule-out test that could be scaled up for broad implementation in routine clinical practice worldwide. Additionally, results from a cohort-based model of healthcare utilisation in the U.S. demonstrated that using the Elecsys® pTau181 blood-based rule-out test in primary care scenarios improved diagnostic accuracy and reduced resource use compared with the current standard-of-care clinical, cognitive and imaging tests. If made available in primary care settings, the Roche Elecsys® pTau181 blood test has the potential to reliably avoid the need for further confirmatory testing in nearly all people who receive a negative result. This will avoid the need for these people to undergo unnecessary testing using CSF or PET, which often come with long wait times and high cost, resulting in further delays to diagnosis and cost to healthcare systems. Medicine Abstract title Presentation number (type) Presentation date (session) Time Abstracts will be available on the AAIC website. Pharmaceuticals Next wave of innovation in Alzheimer's disease therapeutics: The value of novel active transport mechanisms Featured Research Session (FRS), Talk 1 Room 718 27 Jul 2025, 2pm – 3.30pm EDT Cath Mummery, Roberto Villaseñor, Jens Niewoehner, Scarlett Barker, Luka Kulic Latest results from the dose-expansion part (Part 2) of the Brainshuttle™ AD study of trontinemab in people with Alzheimer's disease Featured Research Session (FRS), Talk 2 Room 71827 Jul 2025, 2pm – 3.30pm EDT Luka Kulic, Fabien Alcaraz, Gregory Klein, Stephen Salloway, Carsten Hofmann, João A. Abrantes, Stella Yilmaz, Denise Sickert, Maddalena Marchesi, Jakub Wojtowicz, Andres Schneider, Ruth Croney, David Agnew, Silke Ahlers, Paul Delmar, Hanno Svoboda, Iris Wiesel Interim biomarker results for trontinemab, a novel Brainshuttle™ antibody in development for the treatment of Alzheimer's disease Featured Research Session (FRS), Talk 3 Room 718 27 Jul 2025, 2pm – 3.30pm EDT Gregory Klein, Gil Rabinovici, Henrik Zetterberg, Matteo Tonietto, Tobias Bittner, Daria Rukina, Fabien Alcaraz, Carsten Hofmann, Maddalena Marchesi, Jakub Wojtowicz, Ruth Croney, David Agnew, João A. Abrantes, Franziska Schaedeli Stark, Silke Ahlers, Paul Delmar, Hanno Svoboda, Iris Wiesel, Luka Kulic TRONTIER 1 and TRONTIER 2: Pivotal trials of trontinemab in early symptomatic Alzheimer's disease Featured Research Session (FRS), Talk 4 Room 71827 Jul 2025, 2pm – 3.30pm EDT Janice Smith, Catherine Mummery, Jeffrey L. Cummings, Gil Rabinovici, Stephen Salloway, Reisa Sperling, Henrik Zetterberg, Angeliki Thanasopolou, Christopher Lane, Paul Delmar, Gregory Klein, Ruth Croney, Jakub Wojtowicz, Carsten Hofmann, Luka Kulic, Hideki Garren Diagnostics Evaluating the Impact on Diagnostic Performance and Healthcare Resource Utilization of Introducing a plasma rule-out test in the Alzheimer's Disease Diagnostic Pathway Poster #102729 July 27, 7:30am- 4:15pm EDT Sophie Roth , Gustaf Ortsäter, Joana Amorim Freire Location tbc Evaluating the Clinical Performance of the Elecsys pTau217 Plasma Immunoassay to Detect Amyloid Pathology in a Routine Clinical Practice Cohort Poster #96679 July 28, 7:30 am – 4:15 pm EDT Sayuri Hortsch , Niels Borlinghaus, Alexander Jethwa, David Caley, Annunziata Di Domenico, Craig Ritchie Clinical performance and effect of pre-analytical variation of plasma pTau217 alone versus the plasma pTau217/Aβ42 ratio for the identification of amyloid pathology Oral Developing Topics #108585 3-23-DEV Developing Topics on Tau Biomarkers July 29, 2025: 2:00 PM – 3:30 PM Christopher M. Rank, Joana Amorim Freire, Alexander Jethwa, Annunziata Di Domenico, Christina Rabe, Marc Suárez-Calvet , Colin L. Masters, Tobias Bittner Accuracy of cerebrospinal fluid biomarker ratios to determine amyloid positron-emission tomography status: a diagnostic test accuracy meta-analysis Poster #100941 July 28, 7:30 am – 4:15 pm EDT Pablo Martinez-Lage, Eino Solje, Julian G. Martins, Sraboni Sarkar Equity in diagnosis through adequate clinical trial design in diagnostic performance studies Poster #102804 July 30, 7:30am-4:15pm EDT Imke Kirste , David Caley, Clara Quijano Rubio, Margherita Carboni Investigating Differences in Patients Enrolled in a Clinical Study Based on Referral Type Poster #108110 July 30, 7:30am-4:15pm EDT Sophie Roth , Laura Schlieker, Sayuri Hortsch, Joana Amorim Freire,David Caley About trontinemab Trontinemab is an investigational Brainshuttle bispecific 2+1 amyloid-beta targeting monoclonal antibody specifically engineered for enhanced access to the brain to enable rapid reduction of amyloid in people with Alzheimer's disease. Trontinemab is designed for the efficient transport across the blood-brain barrier to target aggregated forms of amyloid beta and remove amyloid plaques in the brain. The uniqueness of trontinemab is based on Roche's proprietary Brainshuttle technology combining an amyloid beta-binding antibody with a transferring receptor (TfR1) shuttle module. As a result, high central nervous system (CNS) exposure of trontinemab may be achieved at low doses, leading to a rapid and deep amyloid clearance. Due to its unique properties, trontinemab might unlock the full potential of disease-modifying monoclonal antibodies by effectively penetrating the brain and potentially leading to slowing of disease progression. About Roche in Alzheimer's Disease With more than two decades of scientific research in Alzheimer's disease, Roche is working towards a day when we can detect and treat the disease early, in order to slow down, stop or even prevent its progression to preserve what makes people who they are. Today, the company's Alzheimer's disease portfolio spans investigational medicines for different targets, types and stages of the disease, including trontinemab. On the diagnostics side, it also includes approved and investigational tools, including digital and blood-based tests and CSF assays, aiming to more effectively detect, diagnose and monitor the disease. Yet the global challenges of Alzheimer's disease go well beyond the capabilities of science, and making a meaningful impact requires collaboration both within the Alzheimer's community and outside of healthcare. Roche will continue to work together with numerous partners with the hope to transform millions of lives. About Roche Founded in 1896 in Basel, Switzerland, as one of the first industrial manufacturers of branded medicines, Roche has grown into the world's largest biotechnology company and the global leader in in-vitro diagnostics. The company pursues scientific excellence to discover and develop medicines and diagnostics for improving and saving the lives of people around the world. We are a pioneer in personalised healthcare and want to further transform how healthcare is delivered to have an even greater impact. To provide the best care for each person we partner with many stakeholders and combine our strengths in Diagnostics and Pharma with data insights from the clinical practice. For over 125 years, sustainability has been an integral part of Roche's business. As a science-driven company, our greatest contribution to society is developing innovative medicines and diagnostics that help people live healthier lives. Roche is committed to the Science Based Targets initiative and the Sustainable Markets Initiative to achieve net zero by 2045. Genentech, in the United States, is a wholly owned member of the Roche Group. Roche is the majority shareholder in Chugai Pharmaceutical, Japan. For more information, please visit All trademarks used or mentioned in this release are protected by law. References [1] Roche Global Media Relations Phone: +41 61 688 8888 / e-mail: [email protected] Hans Trees, PhD Phone: +41 79 407 72 58 Sileia Urech Phone: +41 79 935 81 48 Nathalie Altermatt Phone: +41 79 771 05 25 Lorena Corfas Phone: +41 79 568 24 95 Simon Goldsborough Phone: +44 797 32 72 915 Karsten Kleine Phone: +41 79 461 86 83 Kirti Pandey Phone: +49 172 6367262 Yvette Petillon Phone: +41 79 961 92 50 Dr Rebekka Schnell Phone: +41 79 205 27 03 Roche Investor Relations Investor Relations North America Loren KalmPhone: +1 650 225 3217 e-mail: [email protected] Attachment Media Investor Release AAIC 2025 English Disclaimer: The above press release comes to you under an arrangement with GlobeNewswire. Business Upturn takes no editorial responsibility for the same. Ahmedabad Plane Crash GlobeNewswire provides press release distribution services globally, with substantial operations in North America and Europe.
Business Wire
5 hours ago
- Business Wire
Genentech and Roche Present New Insights in Alzheimer's Disease Research Across Its Diagnostics and Pharmaceutical Portfolios at AAIC
SOUTH SAN FRANCISCO, Calif.--(BUSINESS WIRE)--Genentech, a member of the Roche Group (SIX: RO, ROG; OTCQX: RHHBY) announced today that new data from its Alzheimer's development portfolio is being presented at the Alzheimer's Association International Conference (AAIC) in Toronto, Canada (July 27-30). These data exemplify the comprehensive approach Roche is taking in addressing Alzheimer's across the entire patient journey. Featured oral presentations include the latest results from the ongoing Phase Ib/IIa Brainshuttle™ AD study, which continue to support rapid and robust reduction of amyloid plaques, and design of the Phase III TRONTIER 1 and 2 studies of investigational trontinemab for early symptomatic Alzheimer's disease, with initiation planned later this year. As part of its growing Alzheimer's development program, Roche announced today its plans for an additional Phase III trial to investigate trontinemab in preclinical Alzheimer's disease. The trial will focus on individuals at risk of cognitive decline, with the goal of potentially delaying or preventing the progression of the disease to symptomatic stages. 'Alzheimer's disease represents one of the greatest challenges in healthcare today and tackling it requires early detection and effective therapeutics,' said Levi Garraway, M.D., Ph.D., chief medical officer and head of Global Product Development. 'Trontinemab is designed to target a key driver of Alzheimer's disease biology more effectively in the brain. Combining new treatment avenues with advanced diagnostics may enable earlier and potentially more effective intervention. With plans for Phase III trials in both early symptomatic and preclinical Alzheimer's disease, we are advancing science with the goal of delaying—and ultimately preventing—progression of this devastating condition.' Late-breaking oral and poster presentations highlight the potential of Roche's Elecsys ® pTau217 as a reliable and accessible blood-based biomarker test, providing comparable results to PET scan and cerebrospinal fluid (CSF) diagnostics for rule-in and rule-out diagnosis of amyloid pathology, a hallmark of Alzheimer's disease, across care settings. The test, which received Breakthrough Device Designation from the U.S. Food and Drug Administration last year, will also be utilized in Roche's TRONTIER studies. 'Blood based testing for Alzheimer's disease has the potential to greatly improve patient access and decrease the time to definitive disease diagnosis,' said Matt Sause, CEO of Roche Diagnostics. 'Our data show that the Elecsys pTau217 test performs comparably to PET scans but can be performed with a simple blood draw and analyzed in a routine clinical laboratory. This has the potential to transform the diagnosis of Alzheimer's and provide clear answers to caregivers, patients, and their families.' Up to 75% of people living with symptoms of Alzheimer's disease globally have not been diagnosed, and those who have, waited an average of 2.8 years, and even less have received any form of treatment. Diagnostics play a crucial role in addressing the global challenge of Alzheimer's, not only to detect and identify people with the disease early, even before the first symptoms, but also to rule out those who may or may not benefit from specific treatments. Pharmaceuticals In a 90-minute Featured Research session, designs were shared for the Phase III studies, TRONTIER 1 and 2, which will initiate later this year, investigating the efficacy and safety of investigational trontinemab in people with early Alzheimer's disease. The primary endpoint will measure the change in cognition and function based on the Clinical Dementia Rating – Sum of Boxes scale after 18 months of treatment. Secondary endpoints will include assessments of cognition, function, behavioral symptoms, and quality of life. A pre-screening study, TRAVELLER, based on a brief clinical assessment and a plasma biomarker, which will be identified using the Elecsys pTau217 test, has also been initiated, to enable broader community outreach and extend access to these trials to more diverse populations representative of Alzheimer's disease. New data on the latest results for trontinemab from the completed dose-expansion part of the 1.8 mg/kg and 3.6 mg/kg cohorts from the ongoing Phase Ib/IIa Brainshuttle AD study continued to show rapid and robust reduction of amyloid plaques in the brain as measured by amyloid positron emission tomography (PET). In the 3.6 mg/kg cohort, trontinemab reduced amyloid levels below the 24 centiloid positivity threshold in 91% of participants (n=49/54) after 28 weeks of treatment; 72% (n=39/54) achieved deep clearance below 11 centiloids. These data were reinforced by early and significant reductions in fluid biomarkers of Alzheimer's disease, including total tau, phosphorylated Tau (pTau)181, pTau217, and neurogranin measured in CSF and continues to show a favourable safety and tolerability profile. Amyloid-related imaging abnormalities-edema/effusion (ARIA-E) continued to be observed in <5% of participants (blinded data; N=4/149 across 1.8 and 3.6 mg/kg dose cohorts). All cases were radiographically mild, one was associated with mild and transient symptoms. Diagnostics Roche will present data on a new study comparing the pTau217/Ab42 plasma ratio to the high-throughput, fully automated Elecsys pTau217 assay. The presentation will report on the accuracy of these tools in detecting amyloid pathology. Together with the high throughput and full automation of the assay, these data will assess the potential of Elecsys pTau217 as an accurate standalone rule-in and rule-out test that could be scaled up for broad implementation in routine clinical practice worldwide. Additionally, results from a cohort-based model of healthcare utilization in the U.S. demonstrated that using the Elecsys ® pTau181 blood-based rule-out test in primary care scenarios improved diagnostic accuracy and reduced resource use compared with the current standard-of-care clinical, cognitive and imaging tests. If made available in primary care settings, the Roche Elecsys ® pTau181 blood test has the potential to reliably avoid the need for further confirmatory testing in nearly all people who receive a negative result. This will avoid the need for these people to undergo unnecessary testing using CSF or PET, which often come with long wait times and high cost, resulting in further delays to diagnosis and cost to healthcare systems. About trontinemab Trontinemab is an investigational Brainshuttle bispecific 2+1 amyloid-beta targeting monoclonal antibody specifically engineered for enhanced access to the brain to enable rapid reduction of amyloid in people with Alzheimer's disease. Trontinemab is designed for the efficient transport across the blood-brain barrier to target aggregated forms of amyloid beta and remove amyloid plaques in the brain. The uniqueness of trontinemab is based on Roche's proprietary Brainshuttle technology combining an amyloid beta-binding antibody with a transferring receptor (TfR1) shuttle module. As a result, high central nervous system (CNS) exposure of trontinemab may be achieved at low doses, leading to a rapid and deep amyloid clearance. Due to its unique properties, trontinemab might unlock the full potential of disease-modifying monoclonal antibodies by effectively penetrating the brain and potentially leading to slowing of disease progression. About Roche in Alzheimer's Disease With more than two decades of scientific research in Alzheimer's disease, Roche is working towards a day when we can detect and treat the disease early, in order to slow down, stop or even prevent its progression to preserve what makes people who they are. Today, the company's Alzheimer's disease portfolio spans investigational medicines for different targets, types and stages of the disease, including trontinemab. On the diagnostics side, it also includes approved and investigational tools, including digital and blood-based tests and CSF assays, aiming to more effectively detect, diagnose and monitor the disease. Yet the global challenges of Alzheimer's disease go well beyond the capabilities of science, and making a meaningful impact requires collaboration both within the Alzheimer's community and outside of healthcare. Roche will continue to work together with numerous partners with the hope to transform millions of lives. About Genentech in Neuroscience Neuroscience is a major focus of research and development at Genentech. Our goal is to pursue groundbreaking science to develop new treatments that help improve the lives of people with chronic and potentially devastating diseases. Genentech and Roche are investigating more than a dozen medicines for neurological disorders, including multiple sclerosis, spinal muscular atrophy, neuromyelitis optica spectrum disorder, Alzheimer's disease, Huntington's disease, Parkinson's disease and Duchenne muscular dystrophy. Together with our partners, we are committed to pushing the boundaries of scientific understanding to solve some of the most difficult challenges in neuroscience today. About Genentech Founded more than 40 years ago, Genentech is a leading biotechnology company that discovers, develops, manufactures and commercializes medicines to treat patients with serious and life-threatening medical conditions. The company, a member of the Roche Group, has headquarters in South San Francisco, California. For additional information about the company, please visit
