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The ARIES-HM3 Randomized Clinical Trial assessed the safety and efficacy of excluding aspirin from the antithrombotic regimen in patients with advanced heart failure who have undergone implantation of a fully magnetically levitated left ventricular assist device (LVAD).
“We can now safely say that not giving aspirin is not only safe from a thromboembolic risk profile but results in improved adverse event rate by a significant reduction in non-surgical bleeding which is a well-known complication related to LVAD therapy,” said Mirnela Byku, M.D., Ph.D., MBA, co-author of the study and director of the UNC Durable Mechanical Circulatory Device Program at the UNC School of Medicine. “Improving not only longevity but also reducing morbidity and improving quality of life is a big focus in the field of MCS.”
Until this study, there had been no consensus in the field about use of or dose of aspirin in the LVAD population. The paper was published in JAMA.
The international clinical trial followed a randomized, double-blind, placebo-controlled design and involved 628 patients across 51 centers in 9 countries. The patients were divided into two groups: one receiving aspirin (100mg/d) and the other receiving a placebo in addition to vitamin K antagonist (VKA) therapy.
A focus was to determine if the likelihood a patient experiences major nonsurgical hemocompatibility-related adverse events (such as stroke, pump thrombosis, major bleeding, or arterial peripheral thromboembolism) within 12 months differed between the two groups.
The results showed not giving aspirin to patients with advanced heart failure, treated with a fully magnetically levitated LVAD who are receiving VKAs, did not make their survival worse. Furthermore, aspirin avoidance was associated with a significant reduction (34%) in major nonsurgical bleeding events.

When entering public restrooms, it’s hard not to dwell on what germs previous users have left behind in the toilet bowl. Imagine, instead, a self-cleaning system that doesn’t require a brightly colored gel. Researchers reporting in ACS Applied Materials & Interfaces have developed a simple, transparent coating that makes surfaces, like porcelain, more water-repellent. They show how this surface treatment effectively prevents bacteria from sticking to the inside of a toilet bowl.
Coatings can be applied to glass and porcelain to ensure water droplets easily slide off, preventing fog or bacterial films from developing, for example. To add this water-repellant property to surfaces, scientists typically engineer microscopic structures, like the tiny barbs and hooks on bird feathers, to trap air or oils between the surface and water droplets. But this approach is typically labor intensive and can change the appearance of the surface. Another approach is to graft slippery polymer chains onto a surface, and those polymers act like a permanent oil slick. However, this technique can involve harsh chemicals and isn’t feasible for use on everyday items. So, Mustafa Serdar Onses and coworkers wanted to find a more practical way to make polymer-grafted surfaces repel water and impede growth of bacterial films.
Their selected approach involved grinding poly(dimethylsiloxane) (PDMS), a silicone oil, in a ball mill for an hour. In the mill, small tungsten carbide balls bombarded the oil at high speeds, breaking apart some of the polymer’s chemical bonds and forming new molecules. The team hypothesized that the milled PDMS would graft quickly onto surfaces, such as glass or porcelain, forming a durable, oily layer.
The researchers brushed the milled oil onto one side of a sterilized toilet’s bowl interior, leaving the other half untreated. Then they poured sterile human urine combined with E. coli and S. aureus bacteria into the toilet and subsequently swabbed what was left behind on both halves of the bowl. Bacteria culture tests showed that the PDMS-treated area inhibited 99.99% of the bacterial growth as compared to the untreated area. Additional experiments showed that both porcelain and glass surfaces coated with the milled PDMS strongly repelled water, suggesting that, in the first test, urine and bacteria slipped right down the treated toilet bowl’s wall. The researchers say that their transparent and colorless toilet bowl treatment method could be a practical way to self-sanitize shared surfaces for public health applications.

Published6 days agoShareclose panelShare pageCopy linkAbout sharingBy Lucy WatkinsonBBC NewsWhen five-year-old Cali said the word “spider”, her mother, Cara, had tears in her eyes.It was the first time she had ever heard her daughter clearly say a word. Cali had always found it difficult to form sounds and words, but when she turned two during the Covid lockdown and her parents tried to find her help, it was nearly impossible to access NHS speech therapy services.”The only appointment was over the phone, and they didn’t speak to Cali, they just spoke to me,” Cara says. “I was told to try out some games, and that was the last contact I had with them before she started school last year.” Without help, Cali would get frustrated because she could not make herself understood, and then started to have extreme tantrums in the classroom. Cara heard about a speech and language unit at the University of Reading, where therapy is provided for free but observed by students.When Cali first arrived here a year ago, all of her sounds started with a “y” – so if she was counting, Cali would say, “yun, yoo, yee, your…yait, yine, yen.”But with help from the therapists she has made great progress.”The improvement in her speech is huge,” Cara says. “What they have done has helped us so much.” Children and young people on NHS waiting lists for speech and language therapy65,057 in England6.503 in Scotland2,319 in Wales4,527 in Northern IrelandSource: Latest NHS figuresData from health visitor checks in England for 2022-2023 shows nearly 15% of children aged 24 to 30 months were below the expected level in communication skills, a rise from 11% in 2018.At the age of five, children with speech and language difficulties are six times less likely to achieve expected targets in English, and 11 times less likely to achieve maths targets by the end of primary school. Eight out of 10 children with emotional and behavioural disorders have speech, language and communication needs that have not previously been identified.Listen to: 5 Minutes On – Starting school speechless – A pandemic legacySpecialist centre At the University of Reading speech therapy unit, places are limited and demand is high.”We’re getting families phoning up in tears, saying, ‘we’re desperate, please can you see our child?’,” says Allie Biddle, director of speech and language. “It’s really hard to say ‘we’re sorry we can’t’.”During the pandemic, she says accessing speech and language development services became increasingly challenging for parents whose children were struggling as many places closed down. By the time services had moved online, long waiting lists had built up, meaning children like Cali were left behind.”And unfortunately children’s development does not wait for Covid to go away,” Allie says. Aldine and Adam’s five-year-old daughter Ivy is among those currently being helped by the clinic. They say the stress of the pandemic and not being able to see friends and family took a big toll on Ivy. When the family went out for walks, Ivy wanted to go to talk to other children – but could not because of Covid restrictions.”She had no interaction with anyone her own age, so that slowed down her development,” Aldine says. “Ivy was frustrated and upset at being unable to communicate: she would either bang her head on the wall or hit herself. It was quite horrible.”Aldine says the demands of home-schooling their two other children during Covid while also looking after Ivy meant “things fell by the wayside as a parent”, and she and Adam did not fully realise how compromised Ivy’s development had become.”We know from all our research early intervention is key,” says Allie, “because you are trying to prevent the long-term impact on mental health, not just for the young child but for the family as well.”In the past, she says the difficulties faced by children with speech delays were often able to be resolved quickly with minimum support from services like hers – but that has changed since the pandemic.”We are seeing children who have got virtually all of their sound systems disordered,” she says. “We’ve seen a change in profile in our clinic.”Ivy, who has now been diagnosed with speech dyspraxia, is having to unlearn the many inaccurate word patterns that she developed while learning to speak during the pandemic. She has trouble sounding out “ch” and “g” sounds, and often gets them muddled up, so instead of saying “chair”, Ivy will say, “gair”.Ivy’s new younger brother’s name, Barnaby, was deliberately chosen because it is one that Ivy can say without a problem – but she is making steady progress, and getting help has been “life-changing”, her mother says. She can now make herself understood not only at home, but also at school. Five-year-old Reggie’s mum, Laura, says many people have been judgemental about her son’s speech issues, and would ask why he was not talking. Although his school was supportive, it did not have the resources to give Reggie all the help he needed. But since accessing speech therapy, she has seen a huge change in him.”Now, I have a little boy who doesn’t stop talking. He has so much confidence,” Laura says. “People who’ve not seen him for a while say, ‘I understand everything Reggie said there’. It’s lovely to see.” After a year of speech and language support, the children are all keen to speak now. They are understood by their families and their friends at school, and their confidence has returned. The government says it is looking at a number of ways to improve early identification and support for children with speech and language difficulties. The Department for Education (DfE) said: “We are conscious of the effect the pandemic has had on pupils’ education, which is why we have made almost £5bn available for education recovery. “To help schools spot any language development difficulties early on, we have screened over 500,000 primary school children and helped over 160,000 children in reception classes improve their speech and language over three years, across two-thirds of all primary schools.”In September, NHS England joined forces with the DfE to launch a project called Early Language and Support for Every Child, which is based in early years and primary school settings. It is testing out new ways of identifying and supporting children with speech, language and communication needs.More on this story’My baby’s first word was mask’Published10 November 2021Lockdowns hurt child speech and language skillsPublished27 April 2021Child speech delays increase following lockdownsPublished7 November 2022’Raising a child with speech issues was isolating’Published20 OctoberWhat is the UK Covid inquiry and how does it work?Published27 minutes agoAround the BBCSpeech delay in children and toddlers- Frequently asked questions – BBC Tiny Happy People

The Second Plague Pandemic of the mid-14th century, also known as the Black Death, killed 30-60 percent of the European population and profoundly changed the course of European history. New research led by Penn State and the University of Adelaide suggests that this plague, potentially through resulting changes in diet and hygiene, may also be associated with a shift in the composition of the human oral microbiome toward one that contributes to chronic diseases in modern-day humans.
“Modern microbiomes are linked to a wide range of chronic diseases, including obesity, cardiovascular disease, and poor mental health,” said Laura Weyrich, associate professor of anthropology, Penn State. “Uncovering the origins of these microbial communities may help in understanding and managing these diseases.”
According to Weyrich, dietary changes are believed to have influenced oral microbiome evolution through time; however, few studies have directly examined the history of human oral microbiomes in a single population. Weyrich noted that some studies have used the microbiomes of living Indigenous people who practice traditional subsistence lifestyles as a proxy for the microbiomes of pre-industrialized peoples. Yet, this strategy is faulty, she said, because modern-day non-industrialized populations may not have microbes that accurately reflect those that existed in the ancestors of industrialized peoples.
Additionally, she said, “This research places unnecessary responsibilities and obligations on Indigenous communities to participate in microbiome research, where the benefits of these studies may not directly serve Indigenous peoples.”
A more accurate and ethically responsible method is to directly examine the oral microbiomes preserved within calcified dental plaque, known as calculus, from the ancestors of Industrialized people with the permission and collaboration of decedent populations and stakeholders. In the largest study to date of ancient dental calculus, Weyrich and her colleagues collected material from the teeth of 235 individuals who were buried across 27 archaeological sites in England and Scotland from about 2,200 B.C. to A.D. 1853.
The findings published today (Nov. 29) in Nature Microbiology.
The researchers processed the samples in an ultra-sterile, ancient DNA laboratory to minimize contamination. They identified 954 microbial species and determined that they fell within two distinct communities of bacteria — one dominated by the genus Streptococcus — which is common in the oral microbiomes of modern Industrialized peoples — and the other by the genus Methanobrevibacter — which is now largely considered extinct in healthy Industrialized people.

Exploring the origins of these two communities, the team found that almost 11% of the total variation in microbiome species composition could be explained by temporal changes, including the arrival of the Second Plague Pandemic. But how could the Second Plague Pandemic contribute to changes in the oral microbiome?
“We know that survivors of the Second Plague Pandemic earned higher incomes and could afford higher-calorie foods,” said Weyrich. “It’s possible that the pandemic triggered changes in people’s diets that, in turn, influenced the composition of their oral microbiomes.”
The team used a novel approach to investigate whether a change in diet could have influenced the emergence of the Streptococcus group and the extinction of the Methanobrevibacter group. They assembled a list of functional differences among the bacteria in the two groups that could be linked to diet; for example, functions linked to high or low-dietary fiber digestion, carbohydrate metabolism and lactose — a sugar in milk — metabolism.
The researchers found that the bacteria in the Streptococcus-dominated group had more functional traits that are significantly linked with low-fiber, high-carbohydrate diets, as well as dairy consumption — all of which characterize modern-day diets. By contrast, the Methanobrevibacter-dominated group were missing traits associated with dairy and sugar consumption, which characterized the diets of some ancient humans.
The team further determined that the Streptococcus group was associated with the presence of periodontal disease, which is characterized by infections and inflammation of the gums and bones around the teeth. When this disease progresses, bacteria can enter the bloodstream through gum tissue and potentially cause respiratory disease, rheumatoid arthritis, coronary artery disease and blood sugar issues in diabetes. The Methanobrevibacter group, on the other hand, was associated with the presence of skeletal pathologies.
“Our research suggests that modern-day oral microbiomes may reflect past changes in diet, resulting from the Second Plague Pandemic,” said Weyrich. “Importantly, this work helps to inform our understanding of modern-day chronic, noncommunicable diseases.”
Other Penn State authors of the paper include Abigail Gancz, graduate student; Michelle Nixon, assistant research professor of information sciences and technology; Sterling Wright, graduate student; Emily R. Davenport, assistant professor of biology; and Justin Silverman, assistant professor of information sciences and technology. Other co-authors include Andrew Farrer, graduate student, University of Adelaide; Luis Arriola, graduate student, University of Adelaide; C. Adler, senior lecturer, School of Dentistry, University of Sydney; Neville Gully, assistant dean learning and teaching, Adelaide Dental School, University of Adelaide; Alan Cooper; Kate Britton, professor of archaeology, University of Aberdeen; and Keith Dobney, head, School of Historical and Philosophical Inquiry, University of Sydney.
The Australian Research Council, National Science Foundation and Penn State supported this research.

Researchers have uncovered a mechanism that safeguards the biallelic expression of haploinsufficient genes, shedding light on the importance of having two copies of each chromosome. A study by the lab of Asifa Akhtar identified the epigenetic regulator MSL2 an “anti-monoallelic” factor that maintains biallelic gene dosage. This discovery not only reveals a communication system between parental alleles but also points to potential therapeutic strategies for diseases associated with haploinsufficient genes.
Have you ever wondered why we carry two copies of each chromosome in all of our cells? During reproduction, we receive one from each of our parents. This means that we also receive two copies, or alleles, of each gene — one allele per chromosome or parent.
Both alleles are able to produce messenger RNA, which is the recipe needed to make proteins and keep cells running. Scientists hypothesize that having two alleles for each gene is the cell’s in-built redundancy system. If there is ever a mutation or drop in messenger RNA production from the allele carried on one of the chromosomes, the allele on the second chromosome will serve as a backup and will be able to step up to produce sufficient messenger RNA output to compensate for loss of the first allele. This redundancy enables us as humans to be largely resistant to the effects of recessive mutations.
However, a class of genes known as haploinsufficient genes, rely on the continuous expression of two intact alleles. If just one allele of a haploinsufficient gene is compromised, it will lead to human disease. It was therefore hypothesized that the cell may have a special “safety” mechanism to safeguard the messenger RNA expression from this special class of genes. A study featured in the scientific journal Nature led by Asifa Akhtar discovered exactly such a mechanism.
MSL2 is an epigenetic dosage-sensor
The researchers found that the epigenetic regulator MSL2 guarantees the expression of both alleles of specific haploinsufficient genes, ensuring the right messenger RNA dosage. This is crucial because genes require different dosage depending on the tissues they are expressed in. With MSL2, the team has identified, for the first time, a protein that can sense these dosage-sensitive genes and ensure their biallelic expression in the relevant tissue or developmental stage.
“We were always wondering whether the copy of the gene on the chromosome coming from the mother could communicate with the second copy on the chromosome coming from the father. Our findings imply an underlying communication between the two alleles and we speculate that MSL2 ensures that mom and dad can talk to each other — at least molecularly,” says Asifa Akhtar, Director at the Max Planck Institute of Immunobiology and Epigenetics in Freiburg.

Tracking down the allelic regulator with a genetic trick
Fascinated by their discovery of a mechanism which safeguards the biallelic expression of haploinsufficient genes, the researchers investigated how this MSL2 mechanism works at the molecular level. To tackle this, the team used a trick. “We crossed genetically distant mouse strains with each other — a bit like crossing a Chihuahua with a Great Dane. This allowed us to see which alleles were inherited from the mother and which from the father,” says Yidan Sun, the first author of the paper, explaining the method of allele-specific gene expression analysis. With this hybrid mouse system, the team could analyze the activity of individual alleles. She adds: “In contrast to the standard method of expression data analysis, in which the gene products are summed over the two alleles, this gave us the resolution necessary to track the expression status of each allele individually.”
A future for novel therapeutic strategies to address diseases
Their experiments demonstrated that when MSL2 was lost in hybrid mouse cells, certain haploinsufficient genes could only achieve monoallelic expression. This implies that in mammalian cells, MSL2 is necessary for the biallelic expression of genes, ensuring their functionality and, consequently, the overall health of the organism. Interestingly, many of the haploinsufficient genes regulated by MSL2 are associated with neurological disorders.
“But what adds a fascinating layer to this discovery is the tissue- and cell-type specificity of these genes. Looking at the organism as a whole, it makes you wonder whether a backup system orchestrated by epigenetic factors such as MSL2 might explain why people, even with similar lifelong habits like smoking or diet, have different health outcomes or disease risks,” says Meike Wiese, one of the first authors of the study.
An evolutionarily conserved mechanism that regulates gene dosage
“My lab started out studying dosage compensation in fruit flies, which is the process by which males with one X chromosome can achieve the same level of gene products as females with two X chromosomes. Over the years we have been fascinated by how male fruit flies with just one X chromosome do double duty to produce the same messenger RNA compared to the females with two X chromosomes. Without this double dose males simply die! It looks like this strategy has been cleverly adapted by mammals. Our results clearly illustrate how the same tools, like MSL2, are again used in evolution to regulate dosage of genes. Gene dosage matters, and our study provides a new level of understanding of how the cells in our body ensure that we get the right dose of messenger RNAs,” says Asifa Akhtar.
What truly excites the scientists is that this discovery opens new directions to delve deeper into understanding the modulation of gene dosage within our cells. MSL2, as revealed, may just be one example of such an allelic regulator, suggesting the existence of other factors performing similar roles. This newfound knowledge carries profound implications for understanding diseases and holds promise for developing potential treatments.

New research being presented this week at the annual meeting of the Radiological Society of North America (RSNA) links soccer heading — where players hit the ball with their head — to a measurable decline in the microstructure and function of the brain over a two-year period.
“There is enormous worldwide concern for brain injury in general and in the potential for soccer heading to cause long-term adverse brain effects in particular,” said senior author Michael L. Lipton, M.D., Ph.D., professor of radiology at Columbia University’s Vagelos College of Physicians and Surgeons and affiliate professor of biomedical engineering at Columbia University. “A large part of this concern relates to the potential for changes in young adulthood to confer risk for neurodegeneration and dementia later in life.”
While previous research has examined adverse effects on the brain related to soccer heading at a single point in time, this new study looked at brain changes over two years.
The study included 148 young adult amateur soccer players (mean age 27, 26% women). The research team developed a specialized questionnaire for players to determine how often they hit the soccer ball with their head.
“When we first started, there was no method for assessing the number of head impacts a player experienced,” Dr. Lipton said. “So, we developed a structured, epidemiological questionnaire that has been validated in multiple studies.”
The questionnaire consists of a series of questions about how often an individual plays, practices and heads the ball, and in what type of situations. Two-year heading exposure was categorized as low, moderate or high.
The players were assessed for verbal learning and memory and underwent diffusion tensor imaging (DTI), an MRI technique, at the time of enrollment and two years later. DTI characterizes the microstructure of the brain by tracking the microscopic movement of water molecules through the tissue.

Compared to the baseline test results, the high-heading group (over 1,500 headers in two years) demonstrated an increase of diffusivity in frontal white matter regions, and a decrease of orientation dispersion index (a measure of brain organization) in certain brain regions after two years of heading exposure. The analysis adjusted for variables including age, sex, education and concussion history.
“Our analysis found that high levels of heading over the two-year period were associated with changes in brain microstructure similar to findings seen in mild traumatic brain injuries,” Dr. Lipton said. “High levels of heading were also associated with a decline in verbal learning performance. This is the first study to show a change of brain structure over the long term related to sub-concussive head impacts in soccer.”
Dr. Lipton and colleagues also presented another study today in which they used DTI to investigate the association between repetitive head impacts from soccer heading and verbal learning performance.
For the second study, researchers analyzed heading over 12 months prior to DTI and verbal learning performance testing in 353 amateur soccer players (age 18-53, 27% female). Unlike previous research that has focused on deep white matter regions, this study employed a new technique, using DTI parameters to evaluate the integrity of the interface between the brain’s gray and white matter closer to the skull.
“Importantly, our new approach addresses a brain region that is susceptible to injury but has been neglected due to limitations of existing methods,” Dr. Lipton said. “Application of this technique has potential to disclose the extent of injury from repetitive heading, but also from concussion and traumatic brain injury to an extent not previously possible.”
The researchers found that the normally sharp gray matter-white matter interface was blunted in proportion to high repetitive head impact exposure.

“We used DTI to assess the sharpness of the transition from gray matter to white matter,” Dr. Lipton said. “In various brain disorders, what is typically a sharp distinction between these two brain tissues becomes a more gradual, or fuzzier transition.”
He added that gray matter-white matter interface integrity may play a causal role in the adverse association between repetitive head impacts and cognitive performance.
“These findings add to the ongoing conversation and contentious debate as to whether soccer heading is benign or confers significant risk,” he said.
Co-authors on the first study are Molly F. Charney, M.D., Kenny Ye, Ph.D., Roman Fleysher, Ph.D., Liane E. Hunter, M.D., Ph.D., Shimon Garrel, B.S., Bluyé Demessie, A.B., M.S., Joan Y. Song, B.S.E., M.S., Molly E. Zimmerman, Ph.D., Walter F. Stewart, Ph.D., Mimi Kim, Sc.D., and Richard B. Lipton, M.D.
Co-authors on the second study are Joan Y. Song, B.S.E., M.S., and Roman Fleysher, Ph.D.

Researchers have developed an AI model that can predict where a drug molecule can be chemically altered.
A team of researchers from LMU, ETH Zurich, and Roche Pharma Research and Early Development (pRED) Basel has used artificial intelligence (AI) to develop an innovative method that predicts the optimal method for synthesizing drug molecules. “This method has the potential to significantly reduce the number of required lab experiments, thereby increasing both the efficiency and sustainability of chemical synthesis,” says David Nippa, lead author of the corresponding paper, which has been published in the journal Nature Chemistry. Nippa is a doctoral student in Dr. David Konrad’s research group at the Faculty of Chemistry and Pharmacy at LMU and at Roche.
Active pharmaceutical ingredients typically consist of a framework to which functional groups are attached. These groups enable a specific biological function. To achieve new or improved medical effects, functional groups are altered and added to new positions in the framework. However, this process is particularly challenging in chemistry, as the frameworks, which mainly consist of carbon and hydrogen atoms, are hardly reactive themselves. One method of activating the framework is the so-called borylation reaction. In this process, a chemical group containing the element boron is attached to a carbon atom of the framework. This boron group can then be replaced by a variety of medically effective groups. Although borylation has great potential, it is difficult to control in the lab.
Together with Kenneth Atz, a doctoral student at ETH Zurich, David Nippa developed an AI model that was trained on data from trustworthy scientific works and experiments from an automated lab at Roche. It can successfully predict the position of borylation for any molecule and provides the optimal conditions for the chemical transformation. “Interestingly, the predictions improved when the three-dimensional information of the starting materials were taken into account, not just their two-dimensional chemical formulas,” says Atz.
The method has already been successfully used to identify positions in existing active ingredients where additional active groups can be introduced. This helps researchers develop new and more effective variants of known drug active ingredients more quickly.

Adults diagnosed with coronary heart disease, especially before the age of 45, may be at increased risk of developing dementia, Alzheimer’s disease and vascular dementia later in life, according to new research published today in the Journal of the American Heart Association, an open access, peer-reviewed journal of the American Heart Association.
“Coronary heart disease has previously been associated with dementia risk in older adults, however, this is believed to be the first large-scale study examining whether the age of coronary heart disease onset may impact the risk of developing dementia later in life,” said Fanfan Zheng, Ph.D., senior study author and researcher in the School of Nursing at the Chinese Academy of Medical Sciences & Peking Union Medical College in Beijing, China.
“In previous research, we found that adults experienced accelerated cognitive decline after new diagnoses of coronary heart disease,” she said.
The researchers assessed the potential relationship between age at coronary heart disease onset and the development of dementia by analyzing health data from the UK Biobank.
The analysis found: Among the 432,667 participants in the study, there were 5,876 cases of dementia, 2,540 cases of Alzheimer’s disease and 1,220 cases of vascular dementia that occurred over an average of 13 years of follow-up. Compared with participants who did not have coronary heart disease, participants with coronary heart disease had higher risks of developing dementia from any cause, Alzheimer’s disease and vascular dementia. After adjusting the analysis for demographic and lifestyle factors, participants with coronary heart disease had a 36% increased risk of developing dementia, a 13% increased risk of developing Alzheimer’s and a 78% greater risk of developing vascular dementia. Earlier coronary heart disease-onset was associated with a 25% increased risk of dementia, a 29% increased risk of Alzheimer’s disease and a 22% increased risk of vascular dementia. The risk of dementia rose in direct proportion to the younger age of coronary heart disease onset (per 10-year decrease in age). Participants diagnosed with coronary heart disease before age 45 had a significantly increased risk of developing dementia compared to their counterparts who did not have coronary heart disease.”What surprised us most was the linear relationship between age of coronary heart disease onset and dementia. This shows the huge detrimental influence of premature coronary heart disease on brain health,” Zheng said. “As more people live longer and are diagnosed with coronary heart disease at a younger age, it’s likely there will be a large increase in the number of people living with dementia in years to come. Health care professionals should be aware of individuals diagnosed with coronary heart disease at a young age. The next step is to determine whether modifying cardiovascular risk early in life will promote better brain health later in life.”
Study details and background: The UK Biobank is a large, biomedical database and research resource with health records of about 500,000 adults — enrolled from 2006 until 2010 — who live in the U.K and received health care through the U.K.’s National Health Service. The researchers accessed the data in May 2022 and analyzed health records through October to December 2022. The researchers analyzed health records for a total of 432,667 adults (average age of 57 years when they became participants in the UK Biobank; 54.6% were female); 11.7% — 50,685 adults — had coronary heart disease at time of enrollment and through the follow-up period. 240 adults who had coronary heart disease were excluded due to missing data about the age at which they were diagnosed with CHD. The researchers adjusted the analysis for demographic factors including age, sex, race and education. They also adjusted for lifestyle factors, including smoking status, alcohol consumption and whether participants engaged in moderate or vigorous exercise for over 10 minutes at least twice per week. Health factors considered included baseline body mass index; levels of low-density lipoprotein cholesterol; hypertension status; diabetes status; use of statins; and if they were a carrier for the APOE4 gene, which increases an individual’s risk of developing Alzheimer’s. Data on age of coronary heart disease onset and subsequent incident dementia were collected over an average of 13 years of follow-up. The researchers controlled for confounding bias, which suggests associations where they may not exist. They then evaluated the association between coronary artery disease onset in different age groups and the development of dementia. 50,445 of the participants with coronary heart disease were divided into three groups based on age of heart disease onset — before age 45; 45 to 59; and 60 and older — and then matched to counterparts who did not have coronary heart disease to gauge the possible relationship between coronary heart disease and dementia.According to the American Heart Association’s 2023 Statistical Update, coronary heart disease caused 382,820 deaths in 2020. The estimated rate of dementia (alone, not including Alzheimer’s) in U.S. adults, 65 years of age and older, was 10.5% in 2012, with a rate of 7.3% in males and 12.9% in females, according to the Aging, Demographics and Memory Study, which is a supplemental study of the long-running Health and Retirement Study in the U.S.
The study’s limitations included that it is an observational study, meaning the findings do not confirm cause and effect, and that more than 94% of the study population from the UK Biobank self-identified as white, meaning the findings may not be generalizable to people of other races or ethnicities.

People with personality traits such as conscientiousness, extraversion and positive affect are less likely to be diagnosed with dementia than those with neuroticism and negative affect, according to a new analysis by researchers at the University of California, Davis and Northwestern University. The difference was not linked to physical damage to brain tissue found in dementia patients, but more likely to how certain personality traits help people navigate dementia-related impairments.
The work is published Nov. 29 in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.
Previous studies have tried to establish links between personality traits and dementia, but these were mostly small and represented only specific populations, said Emorie Beck, assistant professor of psychology at UC Davis and first author on the paper.
“We wanted to leverage new technology to synthesize these studies and test the strength and consistency of these associations,” Beck said. If those links hold up, then targeting personality traits for change in interventions earlier in life could be a way to reduce dementia risk in the long term, she said.
Beck and colleagues analyzed data from eight published studies including over 44,000 people, of whom 1,703 developed dementia. They looked at measures of the “big five” personality traits (conscientiousness, extraversion, openness to experience, neuroticism and agreeableness) and subjective wellbeing (positive and negative affect, and life satisfaction) compared to clinical symptoms of dementia (performance on cognitive tests) and brain pathology at autopsy.
Personality is typically thought to be linked to dementia risk through behavior, Beck said. For example, people who score high on conscientiousness may be more likely to eat well and take care of their health, which results in better health in the long term.
The researchers found that high scores on negative traits (neuroticism, negative affect) and low scores on positive traits (conscientiousness, extraversion, positive affect) were associated with a higher risk of a dementia diagnosis. High scores on openness to experience, agreeableness, and life satisfaction had a protective effect in a smaller subset of studies.

Link to diagnosis but not pathology
To their surprise, however, no link was found between these personality traits and actual neuropathology in the brains of people after death.
“This was the most surprising finding to us,” Beck said. “If personality is predictive of performance on cognitive tests but not pathology, what might be happening?”
One explanation is that some personality traits could make people more resilient to the damage caused by diseases such as Alzheimer’s. People with higher levels of some traits may find ways, whether they are aware of it or not, to cope with and work around impairments. Other work by members of the study team has shown that some people with quite extensive pathology can show little impairment on cognitive tests.
The researchers also looked at other factors that could moderate the relationship between personality and dementia risk and neuropathology, including age, gender and educational attainment.
“We found almost no evidence for effects, except that conscientiousness’s protective effect increased with age,” Beck said.
Many factors contribute to the development of dementia. Among those that aren’t directly related to genetics, this study is a first step in teasing out the associations between personality and dementia, Beck said. The researchers plan to continue and expand the work, including looking at people who show little impairment in the face of a lot of pathology. They also hope to look at other everyday factors that might play a role in developing dementia.
Part of the work was conducted while Beck was a postdoctoral researcher at Northwestern University in Chicago. Coauthors are: Tomiko Yoneda, UC Davis and Northwestern; Daniel Mroczek and Eileen Graham, Northwestern; Bryan James, David Bennett and John Morris, Rush University Medical Center, Chicago; Jason Hassenstab, Washington University School of Medicine, St. Louis; Mindy Katz and Richard Lipton, Albert Einstein College of Medicine, the Bronx.
The work was supported by grants from the National Institute on Aging.

Recent findings at Cold Spring Harbor Laboratory (CSHL) shine a new light on pancreatic cancer.
More than 90% of pancreatic cancer cases are attributed to an aggressive, deadly form of the disease called pancreatic ductal adenocarcinoma, or PDAC. Researchers have a poor understanding of how our immune system interacts with PDAC. So, coming up with treatments is tricky. It’s thought patients do not show a natural immune response to the cancer because the tumor environment somehow prevents that response. Many are unconvinced that PDAC interacts with the immune system at all.
CSHL scientists have now confirmed that pancreatic cancer does trigger a response in our immune system. However, the T cells that help fight off most diseases have a hard time infiltrating PDAC tumors. These findings could help guide future efforts for developing treatments.
For this study, CSHL Professor Douglas Fearon worked with a team including lead author Min Yao, Professor Matthew Weiss from the Zucker School of Medicine, and CSHL Partners for the Future program participant Sophia Shen from Cold Spring Harbor High School. They first set out to find a new antigen present only in PDAC tumors and not in normal tissue. The body makes cells called antibodies that recognize specific antigens and help destroy them. Identifying a new PDAC antigen could help explain why some patients have better outcomes than others.
The team sequenced plasma cells in pancreatic tumor samples taken from seven Northwell Health patients. They then created synthetic antibodies based on that sequence. The idea was that the synthetic antibodies would point the team toward the new PDAC antigen behind the body’s immune response. But they didn’t find the one they were looking for. Instead, they found 25 antibodies that responded to antigens from cancer cells and normal cells produced in the body. These antibodies were consistent across patients.
“I was surprised at the clarity of the data, that we had a number of antibodies react with the same antigen from multiple patients,” Fearon says.
Previously, researchers had believed that pancreatic cancer suppresses immunity. Some have even explored vaccination as a possible solution. Based on his team’s findings, Fearon says that strategy likely isn’t needed.
“Pancreatic cancer is not immunologically silent. That’s the message,” explains Fearon. “Pancreatic tumors are already immunogenic. We have a challenge in allowing the immune response to attack the cancer.”
Now that scientists better understand the problem, they can try to develop workable solutions. For the pancreatic cancer community, that’s real progress and a welcome development unto itself.