Publisher Health

Despite a name straight from a Tarantino movie, natural killer (NK) cells are your allies when it comes to fighting infections and cancer. If T cells are like a team of specialist doctors in an emergency room, NK cells are the paramedics: They arrive first on the scene and perform damage control until reinforcements arrive.
Part of our innate immune system, which dispatches these first responders, NK cells are primed from birth to recognize and respond to danger. Learning what fuels NK cells is an active area of research in immunology, with important clinical implications.
“There’s a lot of interest right now in NK cells as a potential target of immunotherapy,” says Joseph Sun, an immunologist in the Sloan Kettering Institute. “The more we can understand what drives these cells, the better we can program them to fight disease.”
Despite a name straight from a Tarantino movie, natural killer (NK) cells are your allies when it comes to fighting infections and cancer. If T cells are like a team of specialist doctors in an emergency room, NK cells are the paramedics: They arrive first on the scene and perform damage control until reinforcements arrive.
Part of our innate immune system, which dispatches these first responders, NK cells are primed from birth to recognize and respond to danger. Learning what fuels NK cells is an active area of research in immunology, with important clinical implications.
“There’s a lot of interest right now in NK cells as a potential target of immunotherapy,” says Joseph Sun, an immunologist in the Sloan Kettering Institute. “The more we can understand what drives these cells, the better we can program them to fight disease.”
First in Line

By delivering small electrical pulses directly to the brain, deep brain stimulation (DBS) can ease tremors associated with Parkinson’s disease or help relieve chronic pain. The technique works well for many patients, but researchers would like to make DBS devices that are a little smarter by adding the capability to sense activity in the brain and adapt stimulation accordingly.
Now, a new algorithm developed by Brown University bioengineers could be an important step toward such adaptive DBS. The algorithm removes a key hurdle that makes it difficult for DBS systems to sense brain signals while simultaneously delivering stimulation.
“We know that there are electrical signals in the brain associated with disease states, and we’d like to be able to record those signals and use them to adjust neuromodulation therapy automatically,” said David Borton, an assistant professor of biomedical engineering at Brown and corresponding author of a study describing the algorithm. “The problem is that stimulation creates electrical artifacts that corrupt the signals we’re trying to record. So we’ve developed a means of identifying and removing those artifacts, so all that’s left is the signal of interest from the brain.”
The research is published in the journal Cell Reports Methods. The work was co-led by Nicole Provenza, a Ph.D. candidate working in Borton’s lab at Brown, and Evan Dastin-van Rijn, a Ph.D. student at the University of Minnesota who worked on the project while he was an undergraduate at Brown advised by Borton and Matthew Harrison, an associate professor of applied mathematics. Borton’s lab is affiliated the Brown’s Carney Institute for Brain Science.
DBS systems typically consist of an electrode implanted in the brain that’s connected to a pacemaker-like device implanted in the chest. Electrical pulses are delivered at a consistent frequency, which is set by a doctor. The stimulation frequency can be adjusted as disease states change, but this has to be done manually by a physician. If devices could sense biomarkers of disease and respond automatically, it could lead to more effective DBS therapy with potentially fewer side effects.
There are several factors that make it difficult to sense and stimulate at the same time, the researchers say. For one thing, the frequency signature of the stimulation artifact can sometimes overlap with that of the brain signal researchers want to detect. So merely cutting out swaths of frequency to eliminate artifacts might also remove important signals. To eliminate the artifact and leave other data intact, the exact waveform of the artifact needs to be identified, which presents another problem. Implanted brain sensors are generally designed to run on minimal power, so the rate at which sensors sample electrical signals makes for fairly low-resolution data. Accurately identifying the artifact waveform with such low-resolution data is a challenge.
To get around that problem, the researchers came up with a way to turn low-resolution data into a high-resolution picture of the waveform. Even though sensors don’t collect high-resolution data, they do collect a lot of data over time. Using some clever mathematics, the Brown team found a way to cobble bits of data together into a high-resolution picture of the artifact waveform.
“We basically take an average of samples recorded at similar points along the artifact waveform,” Dastin-van Rijn said. “That allows us to predict the contribution of the artifact in those kinds of samples, and then remove it.”
In a series of laboratory experiments and computer simulations, the team showed that their algorithm outperforms other techniques in its ability to separate signal from artifact. The team also used the algorithm on previously collected data from humans and animal models to show that they could accurately identify artifacts and remove them.
“I think one big advantage to our method is that even when the signal of interest closely resembles the simulation artifact, our method can still tell the difference between the two,” Provenza said. “So that way we’re able to get rid of the artifact while leaving the signal intact.”
Another advantage, the researchers say, is that the algorithm isn’t computationally expensive. It could potentially run in real time on current DBS devices. That opens the door to real-time artifact-filtering, which would enable simultaneous recording and stimulation.
“That’s the key to an adaptive system,” Borton said. “Being able to get rid of the stimulation artifact while still recording important biomarkers is what will ultimately enable a closed-loop therapeutic system.”
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Simulators have long been used for training surgeons and surgical teams, but traditional simulator platforms typically have a built-in limitation: they often simulate one or a limited number of conditions that require performance of isolated tasks, such as placing an intravenous catheter, instead of simulating and providing opportunities for feedback on the performance of multiple interventions that a trauma victim may require at the same time. To overcome this limitation, the Advanced Modular Manikin (AMM), an innovative simulation platform that allows integration of other simulation devices, was developed and field testing was conducted, with support from the Department of Defense (DoD).
The DoD subcontracted with the American College of Surgeons (ACS) Division of Education to conduct field testing of the AMM. The results have been published online in advance of print by the Journal of the American College of Surgeons. Robert M. Sweet, MD, FACS, MAMSE, of the department of surgery at the University of Washington, served as principal investigator (PI) of the DoD contract to build the AMM. Ajit K. Sachdeva, MD, FACS, FRCSC, FSACME, MAMSE, Director, Division of Education, American College of Surgeons, served as the PI for the subcontract to conduct field testing.
The investigators reported that members of trauma teams at a testing site preferred the integrated AMM platform including a “peripheral” simulator over the “peripheral” simulator alone, in terms of realism, physiologic responses, and feedback they receive on the multiple and overlapping interventions they perform on a simulated trauma patient. Corresponding study author Dimitrios Stefanidis, MD, PhD, FACS, FASMBS, FSSH, of the department of surgery at Indiana University School of Medicine, Indianapolis, described the AMM as “more of a platform rather than a manikin.”
The DoD supported development of the AMM through a contract with the University of Minnesota and the University of Washington. The goal was to create an open-source simulation platform that permits integration of a number of simulators, known as “peripherals,” into a singular, comprehensive training platform. A Steering Committee composed of leaders and staff of the ACS Division of Education and the Research and Development Committee of the ACS-Accredited Education Institutes, along with leaders from the Development Team of the AMM Project created the model for field testing the AMM.
“The AMM platform, along with the ‘peripherals,’ can help to address the need for more robust simulators that focus on open procedures and interprofessional teamwork,” Dr. Sachdeva explained. “The ability to integrate the anatomic and physiologic elements of the simulation is an important advance. The experience with the trauma scenario may readily be extended to other surgical procedures and settings.”
Corresponding author Dr. Stefanidis explained that with most traditional simulators, instructors have to manipulate vital signs to respond to specific actions of the learner. He pointed out that the AMM promotes “a learner experience that is more based on the actual physiology of what’s happening to the patient.” The AMM platform allows different members of the trauma team to perform different tasks concurrently — one inserts a breathing tube, another starts an intravenous line, another performs a splenectomy. “All of these interventions impact the physiology,” he said.
The researchers evaluated team experience ratings of 14 trauma teams consisting of 42 individual members who performed tasks on the integrated AMM platform and the standalone “peripheral” simulator. Team experience ratings were higher for the integrated AMM platform as compared with the standalone “peripheral” simulator. Among the team members, surgeons and first responders rated their experience significantly higher than anesthesiologists, who noted higher workload ratings. In focus groups, the team members said they preferred the AMM platform because of its increased realism, and for the way it responded physiologically to their actions and the feedback it provided.
Dr. Stefanidis explained how the AMM can potentially aid in training trauma teams. “Trauma requires exemplary teamwork,” he said. “When we see patients who are injured, there are typically multiple providers who take care of them simultaneously — trauma surgeons, emergency room physicians, anesthesiologists, orthopedic surgeons, neurosurgeons, nurses, respiratory therapists, etc. So, it’s extremely important to also be able to train these teams in a low-stress simulation environment, such as by using the AMM, where they can hone their skills, individually and as a team, and perform at their best when faced with the very high-stress clinical environment.”
The AMM platform offers other benefits for improving the training and proficiency of trauma teams, said the field study PI, Dr. Sachdeva. “Specific training models could be standardized and the situation made increasingly complex in this safe simulation environment,” he said.

Researchers world-wide are focused on clearing the toxic mutant Huntingtin protein that leads to neuronal cell death and systemic dysfunction in Huntington’s disease (HD), a devastating, incurable, progressive neurodegenerative genetic disorder. Scientists in the Buck Institute’s Ellerby lab have found that the targeting the protein called FK506-binding protein 51 or FKBP51 promotes the clearing of those toxic proteins via autophagy, a natural process whereby cells recycle damaged proteins and mitochondria and use them for nutrition.
Publishing in Autophagy , researchers showed that FKBP51 promotes autophagy through a new mechanism that could avoid worrisome side effects associated with rapamycin, an immune-suppressing drug which also extends lifespan in mice. They show both rapamycin and the small pharmacological inhibitor of FKBP51, SAFit2, protect HD neurons but that the mechanisms of the two drugs are distinct.
The possibility of avoiding the negative side effects of rapamycin
Researchers focused on a family of binding proteins called FKBP’s and specifically on FKBP51, which was most changed in mouse and human stem cell models of HD. During the course of the study scientist found that FKBP51 acts on a pathway independent of mTOR (mammalian Target of Rapamycin), which is associated with rapamycin. Scientists also identified a small molecule, SAFit2, which crossed the blood-brain barrier and promoted autophagy and reduced the toxic disease-causing protein through that mTOR-independent pathway.
“Rapamycin can have both positive and negative effects and this new molecule could give us a way to go after the toxic proteins without those complications,” said Buck Professor Lisa Ellerby, PhD, director of the study, who added that the findings are also significant for the aging field. “We know that FKBP’s get dysregulated during aging, a phenomena which likely contributes to the accumulation of toxic proteins associated with other age-related diseases. SAFit2, which is neuroprotective, could give us another option to promote autophagy and clear out disease-causing proteins or proteins accumulated during disease and aging which are correlated with other conditions.” FKPB51 has been implicated in Parkinson’s and Alzheimer’s diseases as well as post-traumatic stress disorder and schizophrenia.
The first author of the work, Barbara Bailus, PhD, is a former postdoc in the Ellerby lab. “The fact that SAFit2 crosses the blood brain barrier is significant,” said Bailus, who is now an Assistant Professor of Genetics at the Keck Graduate Institute in Claremont, CA. “In our mouse models of HD, the small molecule interacted with FKPBP51 and cleared toxic proteins in both the cortex and the striatum which is part of the neural circuit necessary for voluntary movement.”
The Ellerby lab will do pre-clinical work with SAFit2, which was developed by a collaborator, Dr. Felix Hausch, PhD, at the Technical University in Darmstadt, Germany.
Current status of clinical trials for HD
The recent failure of an experimental drug tested in Europe and Canada against HD highlights the desperation of patients who are forced to deal with a malady that usually sees it victims dying about 20 years following the onset of observable symptoms. The drug was developed by Ionis and Roche, and is an antisense oligonucleotide (ASO). It was designed to silence the gene responsible for HD, and had to be injected into the fluid-filled space between the thin layers of tissue that cover the brain and spinal cord. While the details of the failed trial are not published yet, Ellerby says the drug appeared not to diffuse into the entire brain, the ASOs may have unanticipated toxic effects and the ASOs do not reach all affected peripheral tissues. HD affects coordination and leads to cognitive decline and psychiatric problems.
“While we had hoped that this drug would ultimately work for patients in desperate need of treatment, those of us in the field have been aware that we need less invasive treatments for HD that are more likely to be easily tolerated,” said Ellerby. “I don’t know if we’ll be able to do that with this small molecule, but at this point it does show potential and we look forward to evaluating its effects in pre-clinical experiments.”

Observational studies have suggested that increased vitamin D levels may protect against COVID-19. However, these studies were inconclusive and possibly subject to confounding. A study published in PLOS Medicine by Guillaume Butler-Laporte and Tomoko Nakanishi at McGill University in Quebec, Canada, and colleagues suggests that genetic evidence does not support vitamin D as a protective measure against COVID-19.
The ability of vitamin D to protect against severe COVID-19 illness is of great interest to public health experts, but has limited supporting evidence. To assess the relationship between vitamin D levels and COVID-19 susceptibility and severity, researchers conducted a Mendelian randomization study using genetic variants strongly associated with increased vitamin D levels. The authors analyzed genetic variants of 4,134 individuals with COVID-19, and 1,284,876 without COVID-19, from 11 countries to determine whether genetic predisposition for higher vitamin D levels were associated with less-severe disease outcomes in people with COVID-19.
The results showed no evidence for an association between genetically predicted vitamin D levels and COVID-19 susceptibility, hospitalization, or severe disease, suggesting that raising circulating vitamin D levels through supplementation may not improve COVID-19 outcomes in the general population. However, the study had several important limitations, including that the research did not include individuals with vitamin D deficiency, and it remains possible that truly deficient patients may benefit from supplementation for COVID-19 related protection and outcomes. Additionally, the genetic variants were obtained only from individuals of European ancestry, so future studies will be needed to determine the relationship with COVID-19 outcomes in other populations.
According to the authors, “Vitamin D supplementation as a public health measure to improve outcomes is not supported by this study. Most importantly, our results suggest that investment in other therapeutic or preventative avenues should be prioritized for COVID-19 randomized clinical trials.”
Dr. Butler-Laporte notes, “Most vitamin D studies are very difficult to interpret since they cannot adjust for the known risk factors for severe Covid-19 (e.g. older age, institutionalization, having chronic diseases) which are also predictors of low vitamin D. Therefore, the best way to answer the question of the effect of vitamin D would be through randomized trials, but these are complex and resource intensive, and take a long time during a pandemic. Mendelian randomization can provide more clear insights into the role of risk factors like vitamin D because they can decrease potential bias from associated risk factors like institutionalization and chronic disease. In the past Mendelian randomization has consistently predicted results of large, expensive, and timely vitamin D trials. Here, this method does not show clear evidence that vitamin D supplementation would have a large effect on Covid-19 outcomes.”
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A new study analyzing the association between an individual’s genetics (genotype) and their observable characteristics resulting from the interaction of genetics and the environment (phenotype), contributes new knowledge to the understanding of human complex traits and diseases.
The study titled, “An atlas of alternative polyadenylation quantitative trait loci (3′aQTLs) contributing to complex trait and disease heritability,” was recently published in Nature Genetics. Led by University of California, Irvine professor of bioinformatics Wei Li, PhD, the Grace B. Bell chair of the Department of Biological Chemistry at UCI’s School of Medicine, this new research unlocks how much differences in people’s genes account for differences in their traits and what can be attributed to the effects of the surrounding environment.
“Our research is of particularly importance as it offers interpretations that explain how natural variations can shape human phenotypic diversity and tissue-specific diseases,” said Li. “Our most exciting finding was that certain events in human genes can explain a substantial proportion of trait heritability.”
It was well known that 3′-UTR alternative polyadenylation (APA) occurs in approximately 70 percent of human genes and substantively impacts cellular processes such as proliferation, differentiation and tumorigenesis. But, until now, the association of APA events with disease risk and complex human traits was not well understood.
Genome-wide association studies have identified thousands of noncoding variants associated with human traits and diseases. However, the functional interpretation of these variants has proven to be a major challenge. In this study, researchers constructed a multi-tissue atlas of human 3′ UTR alternative polyadenylation (APA) quantitative trait loci (3′aQTLs), containing approximately 0.4 million common genetic variants associated with the APA of target genes, identified in 46 tissues isolated from 467 individuals (Genotype-Tissue Expression Project).
“From our findings we could show that specific molecular features associated with human phenotypic variations contribute substantially to the molecular mechanisms underlying human complex traits and diseases,” explained Li.
The research team is continuing to study these molecular mechanisms to test the novel 3′aQTLs genes for diabetes, prostate cancer, Alzheimer’s Disease and Amyotrophic lateral sclerosis (ALS).
The study was supported in part by the Cancer Prevention Research Institute of Texas and the National Institutes of Health.
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Evidence of sleep-dependent low-frequency (0.1 Hz) global brain activity in the clearance of Alzheimer’s disease-related toxin buildup is presented in research published on 1st June 2021 in the open access journal PLOS Biology by Xiao Liu and colleagues at The Pennsylvania State University. This neuronal activity was more strongly linked with cerebrospinal fluid flow in healthy controls than higher risk groups and patients, and the findings could serve as a potential imaging marker for clinicians in evaluating patients.
The development of Alzheimer’s disease is believed to be driven by the buildup of the toxic proteins amyloid-β and tau in the brain. The brain’s glymphatic system plays a crucial role in clearing these toxins and previous work has shown a possible relationship between sleep-dependent global brain activity and the glymphatic system by showing this activity is coupled by cerebrospinal fluid flow essential for the glymphatic system.
Using 118 subjects in the Alzheimer’s Disease Neuroimaging Initiative project, the researchers measured this global brain activity and cerebrospinal fluid flow as well as looking at behavioral data. Individuals underwent resting-state fMRI sessions two years apart, and the team compared their findings with neurobiological and neuropsychological markers related to Alzheimer’s disease, such as levels of the toxic protein amyloid-β.
The strength of the connection between brain activity and cerebrospinal fluid flow was weaker in individuals at a higher risk or who had already developed Alzheimer’s disease. Additionally, this weaker connection was associated with higher levels of amyloid-β and disease-related behavioral measures two years later. This suggests an important role for sleep-dependent global brain activity in the clearance of brain waste, and its connection to cerebrospinal fluid flow could be helpful as a future marker for clinical evaluation.
Dr. Liu adds, “The study linked the coupling between the resting-state global brain activity and cerebrospinal fluid flow to Alzheimer’s disease pathology. The finding highlights the potential role of low-frequency (

For patients who have experienced certain common types of stroke, a small chip inserted under the skin may help physicians predict their likelihood of experiencing a second stroke, and therefore their likelihood of benefiting from preventive therapy. The findings come from a recent clinical trial published in the Journal of the American Medical Association and led by investigators at Massachusetts General Hospital (MGH) and Northwestern University Feinberg School of Medicine.
Each year, approximately 800,000 strokes occur in the United States, and as many as one-fourth occur in people who experienced a previous stroke. Investigators have been searching for ways to identify patients who are likely to experience a recurrent stroke, as these individuals could be candidates for taking certain medications such as blood thinners. One group of patients who face an elevated risk of recurrent strokes are those with atrial fibrillation — an irregular and often rapid heart rate — that often goes undetected and untreated. (Irregular heartbeats can allow blood to pool in the heart, which can cause clots to form and travel to the brain.)
Recent research has shown that a small chip inserted under the skin can monitor the heart rate and rhythm, and help physicians detect atrial fibrillation in patients who previously experienced what’s called a cryptogenic stroke, one with no identified cause despite thorough patient testing. Now investigators have tested the chip — less than 1¾? long and 1/6? thick and called an insertable cardiac monitor — in patients who experienced a stroke caused by narrowing of a large artery like the carotid artery, or blockage of a small artery deep in the brain where atrial fibrillation would be unexpected.
In the Stroke of Known Cause and Underlying Atrial Fibrillation (STROKE AF) trial, 492 patients were randomized and completed 12 months of follow-up after receiving either an insertable cardiac monitor within 10 days of an initial stroke or usual care consisting of external cardiac monitoring through electrocardiograms or other tracking methods.
The chip detected atrial fibrillation in 12.1% of patients, compared with 1.8% detected through usual care. The team noted that the episodes of atrial fibrillation were not brief, with most lasting at least one hour. Most stroke experts would recommend that patients with this degree of atrial fibrillation start taking blood thinners to prevent a future stroke.
“We found that a significant minority of patients with stroke not thought to be related to atrial fibrillation actually have atrial fibrillation, but we can only find it with an implantable monitor,” says lead author Richard A. Bernstein, MD, PhD, a professor of Neurology at Northwestern University Feinberg School of Medicine.
Adds senior author Lee H. Schwamm, MD, C. Miller Fisher Chair of Vascular Neurology at MGH: “Based on the study findings, we believe that patients with stroke who are similar to those in the STROKE AF Trial should now undergo long-term cardiac monitoring with an insertable cardiac monitor to identify unsuspected atrial fibrillation.”
Schwamm notes that for every eight patients monitored, clinicians could expect to find atrial fibrillation in one of them in the first year. “This could dramatically change the treatment recommendations by their doctor,” he says.
Next steps in this research include identifying patient factors that predict the development of atrial fibrillation and the duration and extent of the arrhythmia. Additional studies are being explored to further understand the association of silent atrial fibrillation and recurrent stroke of all types.
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Researchers have discovered a gene, OTUD7A, that impacts the development of Ewing sarcoma, a bone cancer that occurs mainly in children. They have also identified a compound that shows potential to block OTUD7A protein activity. The finding, by scientists at the University of North Carolina and the Lineberger Comprehensive Cancer Center, appeared online June 1, 2021, in Advanced Science.
About 250 children and young adults are diagnosed with Ewing sarcoma each year in the U.S. About half of those diagnosed will ultimately succumb to the disease, pointing to the need for better therapies.
“Our primary research focus targeted the EWS-FLI1 fusion protein found in about 85 percent of Ewing sarcoma patients,” said UNC Lineberger’s Pengda Liu, PhD, assistant professor of Biochemistry and Biophysics in the UNC School of Medicine and co-lead author. “This protein, made up of pieces of two other proteins, is unique to Ewing sarcoma and only produced in cancer cells, making it an excellent target for treatment.”
Critical relationships between proteins contribute to the development of cancers such as Ewing sarcoma. So, it was a seminal discovery when the UNC researchers found that OTUD7A controls the cancer-causing fusion protein.
Armed with this knowledge, the scientists went on the hunt for small molecule compounds that could block OTUD7A’s activity. Their collaborator, Atomwise Inc., used an artificial intelligence program known as AtomNet to screen four million small molecules to find ones that could fit into a pocket in OTUD7A. One compound they identified, 7Ai, showed a good ability to reduce tumor formation in mice that were grafted with human Ewing sarcoma cells. The compound did not appear to be toxic and was well-tolerated. Also, 7Ai did not kill normal cells that were tested in lab culture experiments.
“Treatment with 7Ai could provide a new targeted therapeutic option for patients who become resistant to chemotherapy. Developing an effective drug will require more lab work and then clinical studies, however,” said Liu.
“By deeply exploring the key cellular processes that lead to cancer, unexpected potential therapeutic avenues can result,” said co-author Ian Davis, MD, PhD, G. Denman Hammond Professor of Childhood Cancer and co-leader of the Cancer Genetics Program at UNC Lineberger. “Once the basic science validated our biological approaches, the application of computational virtual screening enabled us to quickly identify a lead molecule for further testing and validation.”
The researchers are currently working with the UNC Eshelman School of Pharmacy to improve 7Ai’s potency and specificity.
“I am particularly indebted to a UNC student with metastatic Ewing sarcoma who made it a priority to donate tissue that could be used for research,” said Davis, who is also the associate division chief of pediatric hematology-oncology. “We’re also appreciative of funding for our research through an NIH Beau Biden Pediatric Cancer Moonshot grant, which came about after the cancer-related death of President Biden’s son.”
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A new analysis of adults aged 80 years and older shows that a healthier lifestyle is associated with a lower risk of cognitive impairment, and that this link does not depend on whether a person carries a particular form of the gene APOE. Xurui Jin of Duke Kunshan University in Jiangsu, China, and colleagues present these findings in the open-access journal PLOS Medicine.
The APOE gene comes in several different forms, and people with a form known as APOE ε4 have an increased risk of cognitive impairment and Alzheimer’s disease. Previous research has also linked cognitive function to lifestyle factors, such as smoking, exercise, and diet. However, it has been unclear whether the benefits of a healthy lifestyle are affected by APOE ε4, particularly for adults over 80 years of age.
To clarify the relationship between APOE ε4 and lifestyle, Jin and colleagues examined data from 6,160 adults aged 80 or older who had participated in a larger, ongoing study known as the Chinese Longitudinal Healthy Longevity Survey. The researchers statistically analyzed the data to investigate links between APOE ε4, lifestyle, and cognition. They also accounted for sociodemographics and other factors that could impact cognition.
The analysis confirmed that participants with healthy lifestyles or intermediately healthy lifestyles were significantly less likely to have cognitive impairment than those with an unhealthy lifestyle, by 55 and 28 percent, respectively. In addition, participants with APOE ε4 were 17 percent more likely to have cognitive impairment than those with other forms of APOE.
A previous study suggested that in individuals at low and intermediate genetic risk, favorable lifestyle profiles are related to a lower risk of dementia compared to unfavorable profiles. But these protective associations were not found in those at high genetic risk. However, the investigation showed the link between lifestyle and cognitive impairment did not vary significantly based on APOE ε4 status which represented the genetic dementia risk. This suggests that maintaining a healthier lifestyle could be important for maintaining cognitive function in adults over 80 years of age, regardless of genetic risk.
This cross-sectional study emphasized the importance of a healthy lifestyle on cognitive health. While further research will be needed to validate these findings among different population, this study could help inform efforts to boost cognitive function for the oldest of adults.
In the next step, the team will explore this association using the AD polygenetic risk score (AD-PRS) and explore the interactive relationship between AD-PRS and lifestyle on cognition with the longitudinal data.
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