Category: 8. Health

When it comes to gastrointestinal health, there’s often a focus on eating probiotic-packed foods. However, all of the other foods you eat—including proteins—can influence the composition of the bacteria in your gut microbiome, too. Some are more beneficial than others. Learn about our registered dietitians’ top picks for digestion-friendly protein and keep reading to find out how dietary protein influences your gut health.

1. Yogurt

Yogurt is a concentrated source of protein that comes with beneficial live cultures (aka probiotics), such as Lactobacillus acidophilus. When consumed regularly, dairy products like yogurt may support the bacterial balance in the gut by increasing Lactobacillus bacteria. Enjoy yogurt on its own, add it to smoothies, fruit parfaits or make frozen yogurt cake and frozen yogurt popsicles.

2. Fermented Cheese

Whether you love Cheddar, Swiss or Parmesan, these cheeses are a good source of protein, and aged cheeses in particular may contain probiotics. Shred these cheeses and add them to salads—like this Apple & Cheddar Side Salad with Mustard Vinaigrette—or a wrap, or add pieces of cheese to a Turkey Apple Cheddar Sandwich.

3. Fish

Fish—especially fatty fish like salmon, tuna, mackerel and sardines—are rich in omega-3 fatty acids. These healthy fats have anti-inflammatory properties and can benefit your microbiome by reducing inflammation in the digestive tract. Certain types of fish, such as salmon, also contain vitamin D, an essential nutrient that may influence the type of bacteria in the intestines, as well as protect intestinal lining from inflammation and injury. Kristen White, RDN, CLT, owner of Food Sensitivity Dietitian, says that fish is also generally easier to digest than red meat, which may be beneficial if you experience digestive issues. Check out our Healthy Fish Recipes for easy-to-prep meal ideas.

4. Poultry

Chicken and turkey are excellent sources of lean proteins. They contain amino acids such as glutamine and tryptophan, known to support a healthy microbiome. For example, tryptophan is metabolized by intestinal bacteria that may help make the intestinal lining strong and durable and reduce inflammation, says , Lina Begdache, Ph.D., RDN, a dietitian and assistant professor of Health and Wellness Studies at Binghamton University, State University of New York. In addition, poultry contains B vitamins that play a role in the production of butyrate, which also supports a healthy intestinal barrier.

5. Beans

Beans are a good source of fiber, an important nutrient that helps promote regular digestion and increase healthy bacteria in the GI tract. One cup of canned black beans provides about 17 grams of this important nutrient and 15 grams of protein. Beans are an excellent source of prebiotics, a nutrient that helps gut bacteria flourish, and research shows that eating more beans improves the growth of good bacteria in the GI tract. Check out all of our healthy bean recipes for inspiration.  

Protein and Gut Health

Research reveals that dietary protein may influence the makeup of the microbiome in the gastrointestinal tract, as well as how it functions. The theory is that not all dietary proteins get digested, and as undigested protein arrives in the colon, some bacteria may use the amino acids (building blocks of proteins) as an energy source, producing byproducts called metabolites. These metabolites may then play a role in metabolism and our immune system.

Are you going for plant- or animal-based protein? That makes a difference in this discussion. Animal proteins are complete proteins, meaning they provide all the essential amino acids in proportions needed for health, says White. These amino acids are crucial for a range of bodily functions, including tissue repair and immune system support.

“Animal proteins are generally well-tolerated and easily digested by most people. [Animal proteins] can be particularly beneficial for individuals with digestive issues or sensitivities, as they are less likely to cause gastrointestinal discomfort than some plant-based proteins,” White explains. 

Although animal proteins are complete, some plant-based and vegetarian proteins, like tofu and quinoa, are also complete proteins. You can still get all of the amino acids you need if eating primarily plant-based proteins, like beans and nuts, but it’s important to eat a wide variety of options to meet your needs. Animal proteins are easy to digest for most people, although many plant-based proteins provide other benefits, such as fiber and healthy fats. Eating a wide variety of protein options is recommended to provide a range of nutrients. 

Considerations When Choosing Protein 

• Change up your proteins: Eat a variety of animal- and plant-based proteins for balanced nutrition. Along with the animal proteins on this list, check out these plant-based foods that have more protein than an egg.
• Think about cooking methods: “How these proteins are prepared can significantly impact their effects on gut health,” says White. Both White and Begdache recommend cooking methods such as grilling, baking, poaching and steaming to retain more nutrients and support heart and overall health.
• Go for natural proteins over supplements: Protein powders and shakes have their place, and they can help you meet your protein needs. However, there’s a benefit to choosing food when you can, including a wider array of nutrients. 
• While protein may play a key role in gut health, Begdache advises not to consume protein foods in large amounts without sources of fiber-rich carbohydrates, like fruits, vegetables, whole grains or legumes.
• A high-protein, low-fiber diet may change the gut microbiome by altering the types of metabolites produced by intestinal bacteria. “The healthy microbes that live in the GI tract feed on undigested complex carbohydrates like fiber,” Begdache explains. “High-protein foods, [generally] tend to lack these complex fibers; therefore, their presence in the gut may change the composition of the gut microbiota into a less health-favorable one,” she says. Conversely, a high-fiber diet that includes complex carbohydrate foods may help protect the gut microbiome and reduce inflammation.
• Begdache also indicates that protein digestion in the stomach differs from one person to another. “People with low stomach acid or pancreatic problems may not digest proteins effectively. Consequently, the more undigested proteins enter the colon, the less advantageous these proteins are,” she adds.

Our Expert Take

What you eat—including protein choices—may influence the health and balance of your gut microbiome. Eating a wide variety of protein sources, particularly gut-healthy options like yogurt, fish, poultry, beans and fermented cheese, can help diversify and maintain the concentration of beneficial bacteria in the gut.

A recently published case report in the journal Neurocase describes an unusual and distressing psychiatric condition that developed in a 50-year-old woman shortly after a stroke. With no history of mental illness, she suddenly became consumed by the belief that her husband was unfaithful—an unshakable conviction that ultimately escalated into violence. Doctors diagnosed her with Othello syndrome, a rare form of psychosis involving delusional jealousy. The case sheds light on how specific types of brain damage can dramatically alter perception, emotion, and behavior.

Othello syndrome is a rare psychiatric disorder characterized by the fixed, false belief that a partner is being unfaithful. This belief persists despite clear evidence to the contrary. Named after the jealous protagonist in Shakespeare’s Othello, the condition is a form of delusional jealousy, a subset of psychotic disorders.

While jealousy is a common human emotion, it becomes pathological when it is based on no real evidence, dominates the person’s thoughts, and results in harmful behavior. Othello syndrome has been observed in people with psychiatric disorders, substance use problems, and some neurological conditions. In rare cases, it can emerge after a stroke, particularly when the stroke affects brain regions involved in judgment, emotional regulation, and attention.

The woman described in the case report had lived a stable life with her husband for over 30 years. She had no history of psychiatric illness, substance abuse, or previous strokes. The only known health issue was hypertension, which had not been adequately controlled. One day, while preparing a meal, she experienced a sudden, intense headache followed by confusion and memory problems. These symptoms led her to seek emergency medical care.

Magnetic resonance imaging revealed that she had experienced a rare type of stroke known as a bilateral paramedian thalamic infarct. This type of stroke is caused by a blockage in a unique artery known as the artery of Percheron. Instead of supplying only one side of the brain, this artery provides blood to both sides of a deep brain structure called the thalamus. In her case, the damage was more pronounced on the right side. The thalamus plays a key role in regulating attention, emotion, and the integration of sensory and cognitive information. When this area is damaged, it can have far-reaching effects on a person’s behavior and personality.

During her hospital stay, the woman was sometimes agitated, experienced visual hallucinations, and had trouble moving her eyes vertically—symptoms consistent with damage to the thalamus. After about two weeks, she was discharged from the hospital. Only a few days later, she began accusing her younger sister of having an affair with her husband. The accusations came out of nowhere, as her sister had only come to visit after the hospital stay. The woman told friends and family that her husband’s supposed infidelity was the cause of her illness. Over time, her suspicions shifted. She no longer accused her sister, but now believed her friend’s daughter was involved with her husband.

Her behavior became increasingly erratic. She would try to check her husband’s phone without his knowledge. She stayed up late watching him, sometimes waking him in the middle of the night to accuse him of cheating. These outbursts escalated into two separate violent incidents in which she attacked him with a bladed weapon. Although she later denied these attacks, her jealousy remained intense and unrelenting.

A psychiatric evaluation revealed signs of cognitive decline, such as impaired memory, reduced attention span, and a narrowed focus on her jealous suspicions. On two common cognitive screening tools—the Mini-Mental State Exam and the Montreal Cognitive Assessment—she scored well below the threshold for normal function. The clinicians ruled out other possible causes, such as dementia, drug intoxication, or metabolic disorders. The timing of her symptoms and brain imaging supported the conclusion that her psychiatric symptoms were linked to the stroke. Doctors diagnosed her with Othello syndrome stemming from her thalamic infarct.

She was initially treated with quetiapine, an antipsychotic medication, which appeared to improve her symptoms for a few months. But she relapsed, and her jealous beliefs returned with the same intensity. Her care team then switched her to another antipsychotic, olanzapine, which led to much greater improvement. Over the course of the following year, she continued to take the medication at a reduced dose, with no reappearance of symptoms. She eventually recognized that her past beliefs were false, and she no longer viewed her husband with suspicion.

Although this case is striking, it is not without precedent. Psychotic symptoms can emerge after a stroke, although they are far less common than anxiety or depression. Among people who develop post-stroke psychosis, delusional jealousy is one of the more frequently observed subtypes. The brain regions most commonly associated with these delusions include areas of the right hemisphere, particularly the frontal and parietal lobes, as well as the thalamus.

The thalamus acts as a central relay station in the brain. It connects with both cognitive regions, such as the prefrontal cortex, and emotional areas, such as the limbic system. Damage to the thalamus, particularly on the right side, can disrupt networks responsible for attention, self-monitoring, and emotional processing. This kind of disruption can impair judgment and heighten suspicious thoughts. In this case, the patient’s stroke likely disrupted the normal communication between brain regions responsible for interpreting social cues and regulating emotional responses, paving the way for delusional jealousy.

The researchers emphasized that the patient’s test results showed no signs of underlying dementia or small vessel disease. This helped rule out alternative explanations for her cognitive problems. Instead, the stroke itself appeared to be the primary cause of her psychiatric symptoms. The selective damage to her thalamus seemed to explain not only her delusional thinking but also her memory and attention problems.

This case also illustrates how Othello syndrome can pose a danger not only to mental well-being but to physical safety. The woman’s false beliefs led to violent behavior against a loved one. Because of the risks associated with this syndrome, recognizing the signs early and initiating treatment is essential.

At the same time, the authors of the study acknowledged the limitations of a single case. Case reports cannot establish how common a condition is or how often it is caused by a particular type of brain injury. Nor can they predict how other individuals might respond to the same treatment. Each brain injury is unique, and many factors influence how symptoms develop and change over time.

However, case studies remain a valuable part of medical science. They allow researchers and clinicians to document rare conditions, identify patterns, and generate hypotheses that can later be tested in larger studies. In particular, unusual cases like this one can help draw attention to the diverse ways that brain injury can manifest—not just as physical or cognitive disability, but also as profound changes in personality and behavior.

The study, “Jealousy’s stroke: Othello syndrome following a percheron artery infarct,” and Ghita Hjiej, Maha Abdellaoui, Hajar Khattab, Kamal Haddouali, Salma Bellakhdar, Bouchera El Moutawakil, Mohammed Abdoh Rafai, and Hicham El Otmani.

People often clock thousands of steps a day yet still wonder why the scale or their blood pressure hardly budges. A simple twist on walking, first tested in Japan, may be the missing ingredient.

This “Japanese walking” exercise methodology, called interval walking training (IWT), swaps steady strolling for bursts of brisk movement, then recovery‑paced steps.

Cardiometabolic researcher Kristian Karstoft of the University of Copenhagen’s Center for Healthy Aging has spent more than a decade tracking its effects.

Why pace changes matter

Most walkers cruise at one comfortable speed and never raise their heart rate high enough to stimulate deeper adaptations.

Switching between fast and slow bouts nudges the body to use oxygen more efficiently, a trait measured by VO2peak.

That oxygen boost drives down resting blood pressure and encourages muscles to burn more sugar for fuel. It also keeps a session feeling manageable because the recovery intervals prevent the distress that can accompany continuous hard effort.

Regular shifts in speed even appear to sharpen insulin action, regulating blood sugar swings that set the stage for diabetes.

Scientists call that improvement better glycemic control, a term describing how tightly the body keeps glucose within a healthy range.

How “Japanese walking” works

Japanese physiologists outline a straightforward walking recipe, alternating three minutes at roughly seventy percent of personal maximum effort with three minutes around forty percent. Completing five of these cycles takes about half an hour.

“Additionally, interval walking training is a great way to meet the recommended 150 minutes a week of moderate‑intensity aerobic activity,” noted Sarah F. Eby, the sports medicine specialist at Mass General Brigham and assistant professor at Harvard Medical School.

That schedule, performed on at least five days each week, fits neatly into current public‑health advice to accumulate one hundred fifty minutes of moderate exercise. 

A simple watch or phone app can cue the switches, though early Japanese volunteers used a waist‑worn beeper nicknamed JD Mate. Supportive shoes and a safe sidewalk are the only other requirements.

Proof in older adults

In a seminal five‑month experiment involving adults averaging sixty‑three years old, IWT raised VO2peak ten percent and drove systolic pressure down nine millimeters of mercury compared with either continuous walking or no exercise.

Knee strength climbed as much as seventeen percent, a critical buffer against falls. Body mass index dipped and fasting glucose improved within weeks, suggesting metabolic changes arrive quickly.

What surprised the investigators most was adherence. Ninety‑five percent of more than eight hundred participants kept the habit for the full study window.

Those who logged at least four sessions a week enjoyed the biggest gains, reinforcing the idea that consistency outranks intensity.

The pattern held over nearly two years, although adherence slipped for volunteers starting with higher waistlines.

Benefits of IWT Japanese walking

A Danish trial later pitted IWT against energy‑matched continuous walking in adults living with type 2 diabetes.

Only the interval group shrank abdominal fat and cut twenty‑four‑hour glucose fluctuations, despite similar caloric burn.

“Compared to energy‑expenditure and time‑duration matched continuous walking training, IWT is superior for improving physical fitness, body composition, and glycemic control in individuals with type 2 diabetes,” stated Karstoft.

Follow‑up mechanistic work pointed toward enhanced glucose effectiveness, meaning muscles absorbed sugar without extra insulin. 

Safety and sticking with it

Because walking remains fully aerobic, lactate rarely spikes and the risk of cardiac complications stays low. No serious adverse events surfaced across dozens of trials, even among recent joint‑replacement patients cleared by their surgeons.

Digital prompts can help sustain motivation once novelty fades. Yet data from a Danish smartphone roll‑out show that unsupervised users averaged only nine minutes of fast walking per week after a year, underscoring the value of social or clinical follow‑up.

Coaching, group strolls, or gamified leaderboards may lift engagement, particularly for people carrying extra weight.

Researchers are testing whether regular phone calls paired with step‑count feedback can duplicate laboratory adherence in the real world.

Getting started today

Consult your clinician if you have chronic conditions, then pick a flat route and set a timer for thirty minutes. Begin with one minute brisk, one minute relaxed for fifteen cycles, or even shorter bursts until comfort builds.

“Studies specifically looking at the benefits of interval walking training have found improved physical fitness, muscle strength, and glycemic control,” said Eby.

She advises ramping up gradually so each brisk interval still allows a short phrase before breath runs out.

Track sessions on a calendar; seeing streaks grow is strangely satisfying. Celebrate milestones such as a lower belt notch or an easier climb up the porch steps.

A final word for anyone who thinks walking is too gentle to matter, remember that pace, not mileage, drives adaptation.

The Japanese approach proves that swapping a few calm blocks for a confident stride can steer health markers in the right direction long before you break into a jog.

The study is published in Applied Physiology, Nutrition, and Metabolism.

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Summary: A groundbreaking study shows that the human hippocampus continues producing new neurons well into late adulthood. Researchers identified neural progenitor cells—the precursors to neurons—in adults up to 78 years old, confirming ongoing neurogenesis in the memory center of the brain.

Using advanced sequencing, imaging, and machine learning techniques, they traced how these cells develop and where they reside in the hippocampus. The findings may pave the way for regenerative therapies targeting cognitive and psychiatric disorders.

Key Facts:

• Neural progenitor cells persist in the hippocampus into late adulthood, enabling neurogenesis.
• Newly formed neurons localize to the dentate gyrus, a hub for memory and learning.
• Individual variation in neurogenesis could inform treatments for brain disorders.

Source: Karolinska Institute

A study in the journal Science presents compelling new evidence that neurons in the brain’s memory centre, the hippocampus, continue to form well into late adulthood.

The research from Karolinska Institutet in Sweden provides answers to a fundamental and long-debated question about the human brain’s adaptability.

The hippocampus is a brain region that is essential for learning and memory and involved in emotion regulation. Back in 2013, Jonas Frisén’s research group at Karolinska Institutet showed in a high-profile study that new neurons can form in the hippocampus of adult humans.

The researchers then measured carbon-14 levels in DNA from brain tissue, which made it possible to determine when the cells were formed.

Identifying cells of origin

However, the extent and significance of this formation of new neurons (neurogenesis) are still debated. There has been no clear evidence that the cells that precede new neurons, known as neural progenitor cells, actually exist and divide in adult humans.

“We have now been able to identify these cells of origin, which confirms that there is an ongoing formation of neurons in the hippocampus of the adult brain,” says Jonas Frisén, Professor of Stem Cell Research at the Department of Cell and Molecular Biology, Karolinska Institutet, who led the research.

From 0 to 78 years of age

In the new study, the researchers combined several advanced methods to examine brain tissue from people aged 0 to 78 years from several international biobanks. They used a method called single-nucleus RNA sequencing, which analyses gene activity in individual cell nuclei, and flow cytometry to study cell properties.

By combining this with machine learning, they were able to identify different stages of neuronal development, from stem cells to immature neurons, many of which were in the division phase.

To localise these cells, the researchers used two techniques that show where in the tissue different genes are active: RNAscope and Xenium. These methods confirmed that the newly formed cells were located in a specific area of the hippocampus called the dentate gyrus. This area is important for memory formation, learning and cognitive flexibility.

Hope for new treatments

The results show that the progenitors of adult neurons are similar to those of mice, pigs and monkeys, but that there are some differences in which genes are active. There were also large variations between individuals – some adult humans had many neural progenitor cells, others hardly any at all.

“This gives us an important piece of the puzzle in understanding how the human brain works and changes during life,” explains Jonas Frisén.

“Our research may also have implications for the development of regenerative treatments that stimulate neurogenesis in neurodegenerative and psychiatric disorders.”

The study was conducted in close collaboration with Ionut Dumitru, Marta Paterlini and other researchers at Karolinska Institutet, as well as researchers at Chalmers University of Technology in Sweden.

Funding: The research was funded by the Swedish Research Council, the European Research Council (ERC), the Swedish Cancer Society, the Knut and Alice Wallenberg Foundation, the Swedish Foundation for Strategic Research, the StratRegen programme, the EMBO Long-Term Fellowship, Marie Sklodowska-Curie Actions and SciLifeLab. Jonas Frisén is a consultant for the company 10x Genomics. See the scientific article for a complete list of potential conflicts of interest.

About this neurogenesis research news

Author: Press Office
Source: Karolinska Institute
Contact: Press Office – Karolinska Institute
Image: The image is credited to Neuroscience News

Original Research: Closed access.
“Identification of proliferating neural progenitors in the adult human hippocampus” by Jonas Frisén et al. Science

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Abstract

Identification of proliferating neural progenitors in the adult human hippocampus

Continuous adult hippocampal neurogenesis is involved in memory formation and mood regulation but is challenging to study in humans.

Difficulties finding proliferating progenitor cells called into question whether and how new neurons may be generated.

We analyzed the human hippocampus from birth through adulthood by single-nucleus RNA sequencing.

We identified all neural progenitor cell stages in early childhood. In adults, using antibodies against the proliferation marker Ki67 and machine learning algorithms, we found proliferating neural progenitor cells.

Furthermore, transcriptomic data showed that neural progenitors were localized within the dentate gyrus.

The results contribute to understanding neurogenesis in adult humans.

Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer’s disease.

Alzheimer’s is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It’s not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen.

Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it’s only been regarded as an energy backup for the liver and the muscles.

“This new study challenges that view, and it does so with striking implications,” says molecular biologist Pankaj Kapahi, from the Buck Institute. “Stored glycogen doesn’t just sit there in the brain, it is involved in pathology.”

Related: Insulin Isn’t Just Made by The Pancreas. Here’s Another Location Few Know About.

Building on links previously found between glycogen and neurodegeneration, the researchers spotted evidence of excessive glycogen levels both in tauopathy models created in fruit flies (Drosophila melanogaster) and in the brain cells of people with Alzheimer’s.

Further analysis revealed a key mechanism at play: tau proteins interrupt the normal breakdown and use of glycogen in the brain, adding to the dangerous build-up of both tau and glycogen, as well as lowering protective neuron defense barriers.

Crucial to this interaction is the activity of glycogen phosphorylase or GlyP, the main enzyme tasked with turning glycogen into a fuel the body can use. When the researchers boosted GlyP production in fruit flies, glycogen stores were utilized once more, helping to fight back against cell damage.

“By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies,” says Buck Institute biologist Sudipta Bar.

The team wondered if a restricted diet – already associated with better brain health – would help. When fruit flies affected by tauopathy were put on a low-protein diet, they lived longer and showed reduced brain damage, suggesting that the metabolic shift prompted by dieting can help boost GlyP.

It’s a notable set of findings, not least because it suggests a way that glycogen and tau aggregation could be tackled in the brain. The researchers also developed a drug based around the 8-Br-cAMP molecule to mimic the effects of dietary restriction, which had similar effects on flies in experiments.

The work might even tie into research involving GLP-1 receptor agonists such as Ozempic, designed to manage diabetes and reduce weight loss, but also now showing promise for protecting against dementia. That might be because these drugs interact with one of glycogen’s pathways, the researchers suggest.

“By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell’s inner chemistry to fight age-related decline,” says Kapahi.

“As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain’s hidden sugar code could unlock powerful tools for combating dementia.”

The research has been published in Nature Metabolism.

Combining zanidatamab-hrii (Ziihera) with chemotherapy as frontline treatment produced clinically meaningful and enduring activity in a small cohort of patients with HER2-positive advanced gastroesophageal adenocarcinoma, according to primary results from a phase 2 study (NCT03929666) published in Lancet Oncology.¹

The study treatment yielded a confirmed objective response rate (ORR) of 76.2% (95% CI, 60.5%-87.9%) among 42 evaluable patients, which included complete responses (CRs) in 3 patients (7%) and partial responses (PRs) in 29 (69%). The median duration of response (DOR) was 18.7 months (95% CI, 10.4-44.1), and the post hoc median time to first response was 1.3 months (IQR, 1.3-1.4).

Data showed a median progression-free survival (PFS) of 12.5 months (95% CI, 8.2-21.8), with estimated PFS rates of 57% (95% CI, 40%-70%) at 12 months and 31% (95% CI, 17%-46%) at 24 months. Additionally, treatment elicited a median overall survival (OS) of 36.5 months (95% CI, 23.6-not estimable [NE]), a 12-month OS rate of 87% (95% CI, 72%-94%), and a 24-month OS rate of 65% (95% CI, 49%-77%).

“[F]irst-line treatment with zanidatamab plus chemotherapy demonstrated rapid and durable antitumor activity with promising survival outcomes in patients with HER2-positive advanced gastroesophageal adenocarcinoma. Zanidatamab plus chemotherapy in the first-line setting was well tolerated with a manageable safety profile when incorporating antidiarrheal prophylaxis in the first 7 days of treatment,” lead study author Elena Elimova, MD, from the Department of Gastrointestinal Medical Oncology at Princess Margaret Cancer Centre in Toronto, Ontario, Canada, wrote with coauthors in the publication.¹ “If these results are confirmed in a large-scale, randomized, phase 3 trial, zanidatamab could represent a substantial advancement in the treatment of HER2-positive advanced gastroesophageal adenocarcinoma.”

In the open-label, multi-center phase 2 study, patients received zanidatamab in combination with capecitabine plus oxaliplatin (CAPOX), 5-fluorouracil (5-FU) plus cisplatin (FP), or leucovorin plus 5-FU and oxaliplatin (mFOLFOX6). In the CAPOX and FP groups, patients received zanidatamab at 30 mg/kg, 1800 mg with a weight of less than 70 kg, or 2400 mg with a weight of 70 kg or higher every 3 weeks. In the mFOLFOX6 group, patients received zanidatamab at 20 mg/kg, 1200 mg with a body weight under 70 kg, or 1600 mg with a weight of at least 70 kg every 2 weeks.

In part 1 of the trial, investigators evaluated the safety and tolerability of zanidatamab plus chemotherapy to determine a recommended phase 2 dose; the primary end points of this part were dose-limiting toxicities and dose reductions. In part 2 of the trial, the primary end point was investigator-assessed confirmed ORR per RECIST v1.1 criteria. Secondary efficacy endpoints across parts 1 and 2 of the trial included disease control rate, DOR, clinical benefit rate, PFS, and OS.

Patients 18 years and older with unresectable, locally advanced, recurrent, or metastatic HER2-expressing gastroesophageal adenocarcinoma and measurable disease per RECIST v1.1 guidelines were eligible for enrollment on the trial.² Other eligibility criteria included having an ECOG performance status of 0 or 1, adequate organ function, and adequate cardiac left ventricular function.

The median patient age was 58 years (IQR, 55-63), and most of the population was male (85%), White (61%), and not Hispanic (93%). Additionally, most patients had an ECOG performance status of 0 (57%), gastric anatomical subtype disease (41%), stage IV disease at initial diagnosis (83%), and measurable disease (93%). Prior neoadjuvant or adjuvant chemotherapy was reported in 11% of patients.

In a subgroup of patients with centrally confirmed HER2-positive disease (n = 41), zanidatamab-based therapy produced a confirmed ORR of 84% (n = 31/37; 95% CI, 68.0%-93.8%). Furthermore, the median PFS was 15.2 months (95% CI, 9.5-33.4) in this subgroup, and the median OS was 36.5 months (95% CI, 23.6-NE).

In a post hoc analysis of patients who enrolled on the trial before and after the implementation of antidiarrheal prophylaxis, 61% (n = 14/23; 95% CI, 38.5%-80.3%) and 95% (n = 18/19; 95% CI, 74.0%-99.9%) experienced confirmed responses. Those who received antidiarrheal prophylaxis experienced longer treatment duration and exposure.

Treatment-related adverse effects (TRAEs) affected 100% of patients, with the most common grade 3/4 TRAEs consisting of diarrhea (39%) and hypokalemia (22%). Additionally, 17% of patients had serious TRAEs, the most common of which was diarrhea (7%).

The median duration of grade 1/2 or grade 3 diarrhea was 6.5 days (IQR, 2-29) and 3 days (IQR, 2-5), respectively, among patients who enrolled on the trial before the implementation of antidiarrheal prophylaxis. The median durations were 3 days (IQR, 2-13) and 4.5 days (IQR, 3-8) among those who entered the trial following the implementation of antidiarrheal prophylaxis.

References

1. Elimova E, Ajani J, Burris H, et al. Zanidatamab plus chemotherapy as first-line treatment for patients with HER2-positive advanced gastro-oesophageal adenocarcinoma: primary results of a multicentre, single-arm, phase 2 study. Lancet Oncol. 2025;26(7):847-859. doi:10.1016/S1470-2045(25)00287-6
2. A safety and efficacy study of ZW25 (Zanidatamab) plus combination chemotherapy in HER2-expressing gastrointestinal cancers, including gastroesophageal adenocarcinoma, biliary tract cancer, and colorectal cancer. ClinicalTrials.gov. Updated March 13, 2025. Accessed July 1, 2025. https://tinyurl.com/y9d77aay

For decades, doctors have tackled heart disease by focusing on well-known risk factors—high blood pressure, high cholesterol, and diabetes. Medications like aspirin and statins have helped millions, yet heart disease remains the leading cause of death in the United States. Alarmingly, many people still suffer heart attacks even when these traditional risk factors are well-managed.

Now, researchers at the University of Michigan have identified a new piece of the puzzle that could explain why.

Their study highlights a protein called suPAR (soluble urokinase plasminogen activator receptor), produced by the immune system. Unlike cholesterol or blood pressure, suPAR appears to directly cause atherosclerosis—the buildup of plaque in the arteries that can lead to heart attacks and strokes.

Atherosclerosis affects more than a billion people worldwide. It occurs when fatty deposits accumulate along artery walls, restricting blood flow and increasing the risk of serious cardiovascular events.

SuPAR is produced in the bone marrow and acts like an inflammation “thermostat” in the body. Scientists already knew that people with elevated suPAR levels had a higher risk of heart disease, but this study is the first to show that suPAR may be a direct cause of the disease.

The research began with an analysis of over 5,000 people without known heart disease. Those with higher suPAR levels were significantly more likely to develop atherosclerosis, regardless of their cholesterol or blood pressure levels.

To find out why some people have higher suPAR levels, the team examined genetic data from 24,000 individuals. They identified a specific genetic variant in the PLAUR gene, which produces suPAR. People with this variant had both higher suPAR levels and a greater risk of developing atherosclerosis.

Using a method called Mendelian randomization—which leverages genetic data to explore cause-and-effect relationships—the researchers confirmed their findings in more than 500,000 participants from the UK Biobank and two additional datasets. The link between the PLAUR variant, elevated suPAR, and atherosclerosis was consistently strong.

To further validate their discovery, the team conducted experiments on mice. Those given high levels of suPAR developed significantly more plaque in their aortas—the main arteries leading from the heart—than mice with normal levels. This provided compelling evidence that suPAR actively contributes to artery damage.

What makes this discovery particularly significant is that suPAR is not affected by current heart disease treatments. Statins, for example, do not lower suPAR levels. This opens the door to a completely new treatment approach, targeting a mechanism not addressed by existing drugs.

Led by Dr. Salim Hayek, the researchers are now working on therapies aimed at safely reducing suPAR levels, with the goal of preventing or slowing the progression of heart disease.

This breakthrough may also shed light on the close link between heart and kidney disease. Prior studies have associated suPAR with kidney damage, and in the U.S., about 1 in 7 people have kidney disease—two-thirds of whom also have heart disease. In fact, more than 40% of heart disease patients show signs of kidney dysfunction. If suPAR contributes to both, targeting it could offer dual benefits.

Published in the Journal of Clinical Investigation, this study may redefine how doctors understand and treat heart disease—offering new hope to millions of people who continue to face it, despite following all the right steps.