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How Skin, Lung, and Intestinal Inflammation Could Signal Early Onset of Alzheimer’s Disease

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Amyloid plaques in the brain are a defining feature of Alzheimer’s disease, but what if the roots of the condition start elsewhere in the body?

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Alzheimer’s disease has traditionally been believed to originate in the brain. However, comprehensive genomic analysis indicates that inflammation in distant organs such as the skin, lungs, or intestines may initiate the condition, potentially decades before noticeable memory decline occurs. This shift in understanding could shed light on why Alzheimer’s treatments have been largely ineffective. Current drugs intervene too late; a focus on early-stage inflammation in peripheral organs may be crucial.

“As neuroscientists, we tend to focus on the brain, but this study highlights that the brain is interconnected with the body, and changes elsewhere can impact brain function,” states Donna Wilcock from Indiana University, not involved in the study. “Although Alzheimer’s is a brain disorder, we must consider the entire body when discussing its genesis.”

To explore the genetic underpinnings of Alzheimer’s disease, researchers including Cesar Cunha from Denmark’s Novo Nordisk Foundation Basic Metabolic Research Center analyzed genetic data from the European Alzheimer’s and Dementia Biobank, encompassing over 85,000 individuals with the disease and approximately 485,000 without it. They also evaluated gene activity in 5 million single cells across 40 body regions and 100 brain regions.

The study scrutinized 1,000 genes linked to an increased Alzheimer’s disease risk, surprisingly finding these genes were more abundant in organs like the skin, lungs, and digestive system than in the brain. “It was counterintuitive at first because the expression of these risk genes in brain cells seemed low,” notes Cunha. “Our continued analysis revealed their primary presence in other body parts.”

Many of these Alzheimer’s risk genes are tied to immune regulation and are particularly abundant in barrier tissues like the skin and lungs, which defend against bacteria and toxins through inflammatory responses. “This suggests that Alzheimer’s might initiate due to inflammation in these peripheral organs,” Cunha explains. Genetic variations may even dictate the extent of inflammation and its impact on brain health. Hence, individuals with a family history of Alzheimer’s could be more vulnerable to the disease amidst infections or inflammatory episodes.

Interestingly, the highest expression of these gene variants occurs when individuals reach ages 55 to 60. Inflammation during this period seems likely to trigger Alzheimer’s, corroborated by long-term studies from Hawaii. Inflammatory markers rise in individuals in their late 50s, with those in their 70s and 80s exhibiting increased Alzheimer’s likelihood. “A person could suffer from lung inflammation due to a viral infection at age 55, which might initiate Alzheimer’s 30 years later, but the exact mechanisms remain elusive,” Cunha remarks.

Rezanur Rahman, a researcher at QIMR Berghofer Medical Research Institute, has identified a genetic mutation associated with Alzheimer’s that appears concentrated in the skin and lungs. More research is essential to understand their functional role in symptom progression, Rahman states. “Association does not imply causation.”

Nonetheless, findings imply that individuals with various inflammatory conditions—such as eczema, cold sores, pneumonia, periodontal disease, Lyme disease, syphilis, diabetes, high blood pressure, and intestinal infections—may face heightened Alzheimer’s disease risk in the future. This correlation is particularly robust when inflammation occurs in middle age, around ages 45 to 60, aligning with Cunha’s insights.

Previously, the brain was deemed immune-privileged and largely unaffected by inflammatory processes elsewhere in the body. Bryce Vissel from St. Vincent’s Hospital in Sydney, Australia, among those who first proposed inflammation as a trigger for Alzheimer’s, acknowledges that while initially contentious, new evidence supports that peripheral inflammation from infections or injuries may indeed instigate the disease.Infection or injury can affect brain function.

When inflammation occurs, immune cells are activated, releasing signaling proteins like cytokines that can cross into the brain via the bloodstream. An unpublished study by Vissel and his team indicates that cytokines may disrupt neuronal connections, potentially leading to memory impairment.

Concurrently, research has shown that the blood-brain barrier becomes more permeable with age, allowing inflammatory cytokines and immune cells easier access, which might elucidate why inflammation poses more of a risk during mid-life compared to youth, Cunha notes.

Current theories posit that Alzheimer’s disease stems from the accumulation of misfolded beta-amyloid and tau proteins within the brain. Yet, treatments aimed at eliminating these proteins have yielded minimal success, indicating that such accumulation might be a symptom rather than the core issue. “We’ve been trying to treat the result of the disease, not its cause,” Cunha argues.

Cunha likens this to past mistakes in obesity treatments, which initially targeted excess fat directly, failing until genetic research revealed that mutations connected with obesity are often highly expressed in the brain, disrupting appetite and energy balance. This led to the development of the weight-loss medication semaglutide (marketed as Ozempic and Wegovy), which modulates brain pathways to curb appetite.

If Alzheimer’s originates from peripheral inflammation, its treatment would necessitate a paradigm shift, Cunha asserts. Data indicate that midlife vaccinations may offer protective benefits against Alzheimer’s disease. A recent Californian study revealed that adults receiving both doses of the shingles vaccine recommended for individuals aged 50 and older were 50% less likely to develop Alzheimer’s by age 65. Another investigation found that those aged 50 and older treated with the Bacillus Calmette-Guérin (BCG) vaccine for bladder cancer had a 20% reduced risk of onset.

This phenomenon might arise as vaccines bolster the aging immune system and mitigate inflammation, suggests Wilcock. “At age 55, we should invigorate our immune systems and remind them to stay active, as most vaccinations occur in childhood.”

Beyond vaccinations, several lifestyle interventions have been shown to diminish inflammation and avert Alzheimer’s disease. These include adopting a Mediterranean diet, limiting alcohol consumption, exercising, quitting smoking, and managing blood pressure and cholesterol levels.

Professor Cunha emphasizes that the challenge lies in convincing fellow neuroscientists to recognize peripheral inflammation as a potential contributor to Alzheimer’s disease. “I’ve encountered skepticism at academic conferences, being told, ‘If you aren’t focusing on amyloid, you’re not studying Alzheimer’s disease,'” he shares. “After decades entrenched in amyloid research, adapting one’s perspective can be daunting.”

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Source: www.newscientist.com

Discover How Genes Connect Intestinal Motility to Vitamin B1: An Unexpected Nutrient Link

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In a groundbreaking study analyzing data from over 268,000 individuals, researchers have identified that genes associated with thiamine (vitamin B1) metabolism significantly influence intestinal motility. This discovery paves the way for personalized treatments targeting conditions like constipation and irritable bowel syndrome (IBS).

Diaz Muñoz et al. identified key mechanisms involved in intestinal motility, including an overlooked role for vitamin B1. Image credit: Hillman et al., doi: 10.1264/jsme2.ME17017 / CC BY 4.0.

Gastrointestinal motility is crucial for food digestion, nutrient absorption, and waste elimination, all critical components of human health and well-being.

The regulation of motility depends on a multifaceted communication network, which encompasses the gut-brain axis, the immune system, gut microbiota, and is affected by external influences such as diet, physical activity, and medications.

Disruptions in motility control and peristalsis can lead to significant health issues, including IBS and chronic idiopathic intestinal pseudoobstruction, highlighting the importance of understanding these conditions.

In this recent study, Professor Mauro D’Amato from LUM University, CIC bioGUNE-BRTA, and Ikerbasque, along with his colleagues, employed a large-scale genetic approach to identify common DNA variations linked to intestinal motility.

The research utilized questionnaires and genetic data from 268,606 individuals of European and East Asian ancestry, applying computational analysis to pinpoint relevant genes and mechanisms.

The team discovered 21 genomic regions that affect defecation frequency, including 10 previously unknown regions, affirming the biologically plausible pathways involved in intestinal motility regulation.

For instance, they found significant correlations with bile acid regulation, which aids fat digestion and serves as signaling molecules in the intestines, along with neural signaling pathways crucial for intestinal muscle contractions (especially acetylcholine-related signaling).

However, the most striking outcome arose when the researchers pinpointed two high-priority genes focused on vitamin B1 biology, specifically those involved in the transport and activation of thiamine: SLC35F3 and XPR1.

To validate the relevance of the vitamin B1 signal, they further examined dietary data from the UK Biobank.

A study involving 98,449 participants revealed that increased dietary thiamine intake correlated with more frequent bowel movements.

Crucially, the relationship between thiamine consumption and bowel frequency exhibited variations based on genetic factors, specifically the combined genetic score of SLC35F3 and XPR1.

This suggests that genetic variations in thiamine metabolism may impact how vitamin B1 intake affects bowel habits in the general population.

“By utilizing genetic data, we’ve created a roadmap for the biological pathways influencing intestinal pace,” said Dr. Cristian Díaz Muñoz from CIC bioGUNE-BRTA.

“The data strongly highlights vitamin B1 metabolism alongside established mechanisms like bile acids and neural signaling.”

This research also confirms a significant biological link between bowel frequency and IBS, a widespread condition affecting millions globally.

“Issues with intestinal motility are at the core of irritable bowel syndrome, constipation, and other common motility disorders, yet the underlying biology remains challenging to decipher,” noted Professor D’Amato.

“These genetic findings point to specific pathways, particularly those involving vitamin B1, as vital areas for further research, including laboratory experiments and meticulously designed clinical trials.”

For more details, refer to the study published in the Journal on January 20, 2026.

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C. Diaz Muñoz et al. Genetic analysis of defecation frequency suggests a link to vitamin B1 metabolism and other pathways regulating intestinal motility. Intestine published online January 20, 2026. doi: 10.1136/gutjnl-2025-337059

Source: www.sci.news

CAR-T Cell Therapy: A Natural Approach to Revitalizing Aging Intestinal Health

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The Importance of a Strong Intestinal Lining for Optimal Health

Shutterstock/3dMediSphere

As we age, the cells that line our intestines gradually lose their ability to regenerate, impacting our immune health. However, recent research has successfully reversed this decline in older mice using genetically modified immune cells.

This innovative approach, known as CAR T-cell therapy, is primarily used to target specific blood cancers. It entails collecting a patient’s T cells, reprogramming them in a laboratory to identify and eliminate cancerous cells, and then reintroducing them into the bloodstream. Emerging variations of this therapy show promise not only in combatting solid tumors but also in preventing arterial blockages and treating autoimmune diseases like lupus.

In a groundbreaking study, Cemil Beyaz and his team at Cold Spring Harbor Laboratory, New York, explored the application of this therapy for revitalizing the aging gut. They focused on targeting damaged cells, known as senescent cells, which accumulate over time, fail to proliferate, and secrete substances that exacerbate inflammation and promote further aging. The researchers aimed their intervention at a protein called uPAR, prevalent on aging cells.

“The decline in gut health we observe with aging is linked to diminished stem cell fitness responsible for renewing the intestinal lining every three to five days,” Beyaz states. “We posited that eliminating these ‘unfit’ senescent cells would enhance the regenerative ability and overall functionality of stem cells in older mice.”

To validate this hypothesis, the researchers engineered CAR T cells from older mice to specifically recognize and eliminate uPAR on senescent cells. Upon reintroducing these modified cells, the researchers noted a significant increase in both the activity and number of stem cells maintaining tissue function, reaching levels comparable to those observed in younger mice. The treated older mice also exhibited marked improvements in intestinal barrier integrity and reduced inflammation compared to a separate cohort that received CAR T-cell therapy targeting different mechanisms.

“By removing senescent cells, we not only inhibited the aging process but also witnessed a reversal, with tissues displaying characteristics similar to those of young mice,” said team member Corina Amor, also from Cold Spring Harbor Laboratory.

“This therapy could potentially reverse age-related declines in bowel function, decreasing vulnerability to diseases such as intestinal infections, compromised intestinal integrity, and even cancer,” explained Tuomas Tammera from Memorial Sloan Kettering Cancer Center, who was not part of the study. However, he emphasized that ensuring the treatment’s effectiveness and safety in humans remains crucial.

Onur Eskiokaku, a researcher at Cold Spring Harbor Laboratory, highlighted the importance of determining the optimal dosage before advancing to human trials. “While uPAR is abundant in aged, defective cells, it may also be present in healthy tissues under certain conditions,” he noted.

It’s important to remember that senescent cells aren’t all detrimental; they play roles in tumor suppression and wound healing. “We are investigating the implications of depleting uPAR expression in other tissues,” mentioned Jesse Poganic from Harvard Medical School.

Additionally, treating aging in otherwise healthy individuals is not commonplace. The complexity and expense associated with CAR-T therapy, coupled with ongoing safety concerns, suggest that widespread application for reversing aging effects is not imminent, according to Joanna Neves at the Center at King’s College London. “Safety standards for preventative treatments must be more stringent than those for oncology.”

Beyaz asserts that addressing the age-related decline in intestinal function has long posed a challenge, with no effective solutions currently available, especially when the intestinal barrier’s regenerative capability is compromised. This research marks a significant step forward, indicating that the removal of unfit cells can restore crucial functions.

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Source: www.newscientist.com

Intestinal Parasites Found in Roman Soldiers Stationed at Hadrian’s Wall

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Third-century baths and sanitary facilities at Vindolanda, a Roman stronghold near Hadrian’s Wall in England

Vindolanda Trust

Although the Romans were recognized for their sophisticated sanitation systems, those stationed in major forts in northern England likely endured numerous digestive illnesses caused by parasites.

The Vindolanda Fortress, situated close to Hadrian’s Wall and inhabited by Roman soldiers from the 1st to 4th century AD, was likely not suitable for individuals with sensitive stomachs, as excavations of waste pits at this location indicate.

Piers Mitchell and his team from the University of Cambridge collected and examined nearly 60 sediment samples from the communal toilets believed to have been utilized in the 3rd century.

Utilizing microscopy, they discovered the eggs of two intestinal parasites: roundworms and whipworms. Additionally, they identified a one-celled parasite called duodenal giardia through specific antibodies that bind exclusively to proteins found in this organism.

All three parasites can lead to gastrointestinal issues, which can be particularly severe for children, the elderly, and immunocompromised individuals.

“Even with our efforts to implement Roman conveniences like baths and toilets, we still faced diarrhea and intestinal parasitic diseases,” Mitchell remarked.

Structures such as toilets, baths, aqueducts, and fountains primarily served to enhance air quality and maintain visible cleanliness, he explains. “They lacked microscopes and therefore were unaware of many infections that plagued them.”

Whipworm eggs discovered in a sewer pipe in Vindolanda

Marissa Ledger

Excavations at another nearby fort, occupied in the 1st century AD and believed to have defensive ditches, also revealed roundworms and whipworms.

“The contents of the sewage drains consist of mixed fecal matter from various individuals utilizing the toilets, making it difficult to determine the infection rate among soldiers,” Mitchell states. “However, the presence of parasite eggs along the sewer drains implies that a considerable number of individuals using the facilities were likely infected.”

Roundworms and whipworms are also found throughout the Roman Empire; giardia, however, has only been identified in the Roman contexts in Turkey and Italy, according to Mitchell.

If asked whether he would like a glass of water during the time the fort was operational, he would certainly decline. “They might say, ‘How about a beer instead?'”

Exploring Hadrian’s Wall and Roman Innovations: England

Embark on an immersive walking tour tracing the paths of the Romans along Hadrian’s Wall, one of Britain’s most iconic ancient sites and a UNESCO World Heritage gem.

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Source: www.newscientist.com

Gastric Bypass Surgery Potentially Lowers Intestinal Cancer Risk

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Gastric bypass surgery is primarily utilized for weight loss, but it may provide other advantages

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A widely recognized form of weight loss surgery may lower the risk of colorectal cancer by changing the levels of bile acids in the bloodstream. These findings could pave the way for new bowel cancer treatments.

During gastric bypass surgery, the stomach is surgically altered to create a small upper pouch and a larger lower pouch. The small intestine is then connected to the upper pouch, allowing food and digestive juices to bypass most of the upper stomach and small intestine. Post-surgery, patients often feel fuller and experience quicker weight loss.

Earlier research indicated that this procedure is associated with a decreased risk of colorectal cancer; however, the underlying reasons remained unclear. To investigate further, Rebecca Kesselling of the University of Freiburg, Germany, and her team fed mice a high-fat diet until they reached approximately 50% of their starting weight. They then performed a partial gastric bypass on some of the mice, while the remaining mice underwent a sham surgery that did not alter their digestive systems.

To isolate the weight-loss effects of gastric bypass surgery, the team grouped the gastric bypass mice alongside half of the sham-operated mice. Over six weeks, the gastric bypass mice lost about 20% of their body weight on average.

Subsequently, the researchers implanted colorectal cancer cells into the colons of the mice. After an additional six weeks, it was observed that colon tumors in the gastric bypass mice were two-thirds smaller than those in the mice that either continued gaining weight or lost weight solely through diet.

Additionally, cancer spread to the liver was seen in only one out of twenty gastric bypass mice, while it occurred in most of the sham-operated mice.

“Both sham groups exhibited similar tumor levels, but weight loss alone could not account for the lower cancer risk, suggesting that gastric bypass involves additional factors,” Kesselling explains.

The researchers speculated that this might be attributed to alterations in bile acids, which are compounds that aid in fat digestion. These molecules are typically produced by the liver, move through the gallbladder, stomach, and small intestine, and then return to the liver via the bloodstream.

“Bile acids are reintroduced into the small intestine during bypass surgery,” Kesselling states, implying that this process may lead to variations in intestinal bacteria that chemically modify these molecules.

The mice that underwent gastric bypass surgery displayed lower levels of specific bile acids, known as primary bile acids, in both their colon and bloodstream compared to the sham group.

To further explore whether changes in bile acids influenced cancer risk, the team conducted a similar experiment with another group of mice. Instead of gastric bypass, these mice had surgery that redirected bile acids to the latter part of the small intestine without altering the stomach.

Significantly, the team noted that this surgery also lowered primary bile acid levels in the bloodstream and decreased the size and spread of colorectal tumors as effectively as gastric bypass surgery. This was supported by an additional experiment, where they identified that primary bile acids promote the growth of colorectal cancer cells in laboratory settings.

The results indicate that focusing on primary bile acids may hold promise for cancer treatment. “We might be able to leverage various oral medications designed to reduce these bile acids to replicate some of the advantageous effects of gastric bypass surgery,” notes Vance Albaf from Louisiana State University.

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Source: www.newscientist.com

Paleontologists Discover Fossilized Intestinal Contents from Sauropod Dinosaurs

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Diamantinasaurus Mathilde, which existed approximately 94 million years ago during the mid-Cretaceous period, primarily consumed conifers, ferns, flowering plants, and utilized intestinal microorganisms for digestion almost entirely. You can learn more about it at the Winton Formation in Queensland, Australia.

Artist’s impression of Diamantinasaurus Mathilde (Judy). Image credit: Travis Tischler.

Understanding dinosaur diets is essential for grasping their paleontology and their roles in Mesozoic ecosystems.

Nevertheless, while many non-avian dinosaurs are interpreted as herbivores based on their anatomy, only a few fossils provide tangible evidence in the form of coprolites (fossilized intestinal contents).

Out of the thousands of herbivorous non-avian dinosaur specimens identified globally, only three have shown likely or atypical gut contents, all of which belong to armored theropod dinosaurs preserved in marine layers.

Other herbivorous non-avian dinosaur specimens with fossilized gut contents include hadrosaurid ornithopods found in river environments.

Thus, the intestinal contents of sauropod dinosaurs—arguably the most ecologically significant large terrestrial herbivores during the Jurassic and Cretaceous periods—remain largely unexplored due to their immense size.

“Since the 19th century, paleontologists have universally classified sauropods as herbivores,” stated Dr. Stephen Polopat, deputy director of the Western Australian Centre for Organic and Isotope Geochemistry at Curtin University.

“However, the specific plants they consumed and the heights from which they fed remained largely unknown until now.”

Dr. Polopat and his team examined the fossilized intestines of a specimen of Diamantinasaurus Mathilde informally referred to as Judy.

This fossil was discovered at a site near Winton and excavated in 2017 by museum staff and citizen scientists at the Australian Dinosaurs’ Museum of Natural History.

Among Judy’s stomach contents, paleontologists identified pinus and bracts from tall coniferous trees, as well as leaves and fruits originating from small seeds and flowering plants.

“The findings indicated that sauropods consumed a variety of plants from different levels above the ground, contributing to their long-term survival and adaptability,” Dr. Polopat remarked.

“The stomach contents we analyzed belonged to a 12-meter-long sub-adult sauropod.”

“Our research shows that several types of sub-adult sauropods could feed at varying heights and adapt to diverse climatic, environmental, and vegetation changes during the Jurassic and Cretaceous periods.”

“We also verified that sauropods exhibited bulk-feeding, similar to methods utilized by herbivorous reptiles and birds today.”

“This implies they did not chew their food but swallowed it whole, allowing their digestive systems to process it completely.”

“Any meal would have lingered in their gastrointestinal tracts for as long as two weeks before being excreted.”

“Finally, the ability to observe sauropod stomach contents for the first time corroborated prior hypotheses regarding their dietary behavior.”

“Sauropods were remarkable creatures that roamed the planet for over 130 million years. Understanding their dietary patterns is crucial for comprehending their impact on the Earth’s ecosystem, particularly concerning plants and other herbivorous species.”

“Further research is necessary, and ideally, we aim to discover additional sauropod fossils containing stomach contents to ascertain whether their feeding habits evolved as they matured, especially regarding their consumption of growing plants.”

Professor Kliti Grice, founder of Curtin University’s Western Australian Centre for Organic and Isotope Geochemistry, expressed:

“Utilizing advanced organic geochemical methods, we confirmed the existence of both angiosperms and growth structures within the diet of this sauropod.”

The team’s research paper is published in the journal Current Biology.

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Stephen F. Polopat et al. 2025. The contents of the fossilized intestine reveal the feeding habits of sauropod dinosaurs. Current Biology 35 (11): 2597-2613; doi: 10.1016/j.cub.2025.04.053

Source: www.sci.news

COVID-19 vaccines may be less effective due to intestinal parasites

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Duodenal hookworms (Ancylostoma duodenale) cause one of the most common intestinal parasitic infections worldwide.

Katerina Conn/Shutterstock

People with intestinal parasitic infections, quarter This has been suggested by experiments in mice infected with the parasite, which had significantly weaker immunity after receiving a COVID-19 vaccination compared to mice not infected with the parasite.

Previous studies have shown that people with intestinal parasitic infections have a weakened immune response to vaccines for diseases such as tuberculosis and measles because the parasites suppress the processes that vaccines trigger to confer immunity, such as activating pathogen-killing cells. Intestinal parasitic infections are most common in tropical and subtropical regions, where they often occur because of limited access to clean water and sanitation.

Scientists have not tested whether these pathogens reduce the effectiveness of COVID-19 vaccines. Michael Diamond Researchers at Washington University in St. Louis, Missouri, vaccinated 16 mice with a COVID-19 mRNA vaccine, half of which had been infected 12 days earlier with an intestinal parasite that lives only in rodents. They gave each mouse a booster shot three weeks after the first vaccination.

About two weeks after the booster shot, the researchers analyzed the animals' spleens to measure concentrations of CD8+ T cells, specialized white blood cells that are important for eliminating other cells infected with the SARS-CoV-2 virus. They found that the spleens of mice infected with the intestinal parasite had about half the number of cells as mice without the parasite, suggesting a weakened immune response to the vaccine.

The researchers repeated the vaccination process in another group of 20 mice, half of which were infected with the intestinal parasite, exposing them to the highly infectious Omicron variant of the SARS-CoV-2 virus. After five days, the lungs of vaccinated rodents infected with the intestinal parasite had, on average, about 20% more virus than uninfected ones.

These findings suggest that intestinal parasites may reduce the effectiveness of COVID-19 vaccines in people, but different types of intestinal parasites are known to affect immunity differently, the researchers say. Keke Fairfax The University of Utah researchers said it's unclear whether the parasite's infection in humans would have the same effect on vaccinating against COVID-19 as it did in mice, and the situation is further complicated by the fact that humans tend to harbor multiple types of intestinal parasites at the same time, they said.

Still, understanding how to alter the immune response to vaccination is important given the prevalence of parasitic infections, and these findings suggest that researchers may need to further evaluate the vaccine's effectiveness in parts of the world where a high proportion of the population is infected with intestinal parasites, Fairfax says.

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Source: www.newscientist.com