Latest news with #APOE
Yahoo
23-05-2025
- Business
- Yahoo
QGEN Stock Might Gain Following New Partnership With ID Solutions
QIAGEN N.V. QGEN recently entered into a commercial partnership and co-marketing agreement with ID Solutions, a French provider of high-quality digital PCR (dPCR) assays, to expand the availability of dPCR assays for oncology research applications. The latest partnership is likely to expand QIAGEN's position in oncology-focused digital PCR assays, advancing QIAcuity as the platform of choice for cancer research. Following the announcement, shares of QIAGEN remained unchanged at $42.32 yesterday. QIAGEN's long-term business strategy involves entering into strategic alliances as well as making marketing and distribution arrangements with academic, corporate and other partners relating to the development, commercialization, marketing and distribution of certain of their existing and potential products. In line with this, QIAGEN's partnership with McGill University is aimed at enhancing its position in North America's $1.8 billion microbiome research market. Additionally, the company announced a collaboration with Eli Lilly and Company to support the development of a QIAstat-Dx in-vitro diagnostic (IVD) to detect APOE genotypes, which can play a key role in Alzheimer's disease diagnosis. As a result, we expect the new partnership with ID Solutions to positively boost the market sentiment toward QGEN stock. QIAGEN has a market capitalization of $9.16 billion. The company's earnings yield of 5.5% compares favorably to the industry's -33.5%. In the trailing four quarters, it delivered an average earnings surprise of 4.93%. Under the agreement, ID Solutions will manufacture and supply dPCR assays for non-clinical research use on QIAGEN's QIAcuity platforms. These assays are optimized to simultaneously detect multiple mutations in cell-free DNA (cfDNA) from plasma and genomic DNA (gDNA) from formalin-fixed, paraffin-embedded (FFPE) tissue. QIAGEN will commercialize these kits starting with Europe, with the potential for future expansion into other regions. The agreement supports QIAGEN's strategic focus on accelerating the adoption of the QIAcuity dPCR platform in oncology research. The new assays will expand QIAGEN's portfolio and complement the existing PanCancer Kits for detecting multiple hallmark mutations in DNA. The combination of QIAGEN's global reach and automation expertise with the assay development and manufacturing capabilities of ID Solutions will strengthen QIAGEN's position in oncology research. For customers, this partnership translates into streamlined access to ready-to-use assays optimized for QIAcuity in non-clinical oncology research, expanding beyond the current menu, enabling results in less than a day and meeting the growing demand for deeper molecular insights. Image Source: Zacks Investment Research Per the report from Research and Markets, the global digital PCR market was valued at $678.1 million in 2023 and is poised to reach $3.35 billion by 2034, marking a remarkable compound annual growth rate (CAGR) of 15.75% during 2024-2034. The market has been experiencing significant growth, primarily fueled by the rising adoption of personalized medicine to screen and diagnose genetic disorders. Additionally, the growing prevalence of infectious diseases is driving the demand for dPCR. Earlier this month, QIAGEN signed a definitive agreement to acquire Genoox, a provider of AI-powered software that enables clinical labs to scale and accelerate the processing of complex genetic tests. The acquisition adds Franklin — Genoox's flagship cloud-based community platform — to the QIAGEN Digital Insights ('QDI') portfolio. It further strengthens QIAGEN's leadership in genetic interpretation for clinical genomics applications. In the past year, QGEN's shares have lost 5.9% compared with the industry's 17.5% decline. The company currently carries a Zacks Rank #2 (Buy). Some other top-ranked stocks in the broader medical space are AngioDynamics ANGO, STERIS STE and DexCom DXCM. AngioDynamics, carrying a Zacks Rank #1 (Strong Buy) at present, has an estimated earnings growth rate of 23.7% for 2025. You can see the complete list of today's Zacks #1 Rank stocks here. ANGO's earnings surpassed estimates in each of the trailing four quarters, delivering an average surprise of 70.85%. Veracyte's shares have risen 49.2% in the past year compared with the industry's 5.5% growth. STERIS, carrying a Zacks Rank #2 at present, has an estimated growth rate of 10.8% for 2025. STE's earnings surpassed estimates in each of the trailing four quarters, delivering an average surprise of 0.61%. Its shares have risen 34.1% compared with the industry's 7.7% growth in the past year. DexCom, carrying a Zacks Rank #2 at present, has an estimated earnings growth rate of 23.2% for 2025. Its earnings surpassed estimates in two of the trailing four quarters and missed in the other two, delivering an average surprise of 0.47%. DXCM's shares have risen 26.4% against the industry's 15.7% decline in the past year. Want the latest recommendations from Zacks Investment Research? Today, you can download 7 Best Stocks for the Next 30 Days. Click to get this free report AngioDynamics, Inc. (ANGO) : Free Stock Analysis Report DexCom, Inc. (DXCM) : Free Stock Analysis Report QIAGEN N.V. (QGEN) : Free Stock Analysis Report STERIS plc (STE) : Free Stock Analysis Report This article originally published on Zacks Investment Research ( Zacks Investment Research
Yahoo
07-04-2025
- Health
- Yahoo
First-of-Its-Kind Study Identifies How The Brain Could Thwart Alzheimer's
Training the brain's immune system to recognize and clear toxic material is rapidly emerging as an promising way to put the brakes on Alzheimer's disease. Unfortunately researchers haven't been clear on how this method of protection operates on a cellular level. An international team of researchers analyzed brain samples taken from people who had died with Alzheimer's, some of whom had also received approved Alzheimer's immunotherapy treatments. The therapies encourage cleaning cells called microglia to attack the clumps of amyloid-beta proteins that are thought to be involved in neurodegeneration. Microglia responses to amyloid beta can lead to inflammation, which in turn risks damage to brain tissues. The researchers wanted to know why immunotherapy turned microglia into ruthless cleaning machines in some cases but not others. "Our study is the first to identify the mechanisms in microglia, the brain's immune cells, that help limit the spread of amyloid in certain brain regions following treatment with amyloid-targeting drugs," says neuroscientist David Gate, from the Northwestern University Feinberg School of Medicine. The team observed microglia not only remove amyloid beta protein clumps but also contain the inflammatory response necessary for this removal, helping the brain recover. These insights were obtained in part through a technique called spatial transcriptomics, which can highlight activity of targeted genes. The genes linked to supercharged microglia included APOE and TREM2, both of which have been identified as being related to Alzheimer's disease in earlier studies. While it's early days for this field of research, the findings from the study could potentially lead to new ways to put a stop to amyloid beta build-up and the development of Alzheimer's symptoms. "A long-standing question in the field of Alzheimer's therapeutics is if we coax these immune cells into removing the amyloid, are they just always going to be in that amyloid-removal mode?" says Gate. "The answer we found is no, they can remove the amyloid and then go back to being good and appear to actually help the brain heal." Putting the body's own defense force through a better training scheme is always going to be preferable to introducing additional chemicals into the brain, and the researchers hope that the disease brakes can be applied before Alzheimer's gets a grip. And while the immunotherapies we mentioned at the top are approved by regulators and can help battle Alzheimer's disease, there's a lot of room for improvement in terms of increasing their success rate and reducing the risk of associated side effects. "I think everyone agrees that, although these drugs are becoming more effective, they ultimately do not cure Alzheimer's disease patients," says Gate. "These drugs stimulate the immune cells of the brain to remove amyloid beta, but we believe that the data in our publication can be utilized to make these drugs work even better." The research has been published in Nature Medicine. Long-Term Meditation May Reduce Stress And Aging, Study Suggests This Traditional African Diet Appears to Boost The Immune System 'Misokinesia' Phenomenon Could Affect 1 in 3 People, Study Shows
The Independent
27-03-2025
- Health
- The Independent
Study finds the age at which human brain starts ageing faster
The human brain appears to undergo accelerated ageing once a person reaches the age of 44, with the deterioration hitting a peak around 67 and plateauing around 90, according to a new study. A better understanding of these critical transition points may lead to new interventions against neurological conditions like Alzheimer's, researchers say. 'Understanding exactly when and how brain aging accelerates gives us strategic time points for intervention,' said Lilianne Mujica-Parodi, lead author of the study from Stony Brook University (SBU). The study, published in the journal PNAS, assessed the communication between brain regions in over 19,300 individuals across four large-scale datasets. It found that brain networks degrade in a nonlinear trajectory with clear transition points – rather than a late-life clinical onset or a gradual linear decline as previously thought. The research follows previous findings that signal transmission by the brain's neurons is impacted by a loss of energy within the nerve cells. 'We've identified a critical midlife window where the brain begins to experience declining access to energy but before irreversible damage occurs, essentially the 'bend' before the 'break,'' said Dr Mujica-Parodi, who is the director of SBU's Laboratory for Computational Neurodiagnostics (LCNeuro). During midlife, the brain's nerve cells continue to function despite being metabolically stressed due to insufficient fuel, researchers say. This stress is mainly due to insulin resistance within the nerve cells, scientists found. 'However, by later ages, neurons' prolonged starvation may have triggered a cascade of other physiological effects,' Dr Mujica-Parodi explained. 'Therefore, providing an alternative fuel during this critical window can help restore function,' she said. Scientists found that the metabolic stress experienced by neurons is consistently followed by inflammatory ones as well as changes within blood vessels supplying nutrients to the brian. Researchers discovered two key proteins – insulin-dependent glucose transporter GLUT4 and the known Alzheimer's risk factor APOE – are implicated in these aging patterns. However, they also found that another protein – neuronal ketone transporter MCT2 – could be a protective factor in preventing stress from these changes. The study suggests MCT2 could serve a beneficial role in enhancing the brain's ability to utilise ketones – an alternative brain fuel that neurons can metabolise without insulin. In another experiment, scientists administered careful doses of glucose and ketones to 101 participants at different stages along their aging trajectory. They found that unlike glucose, the ketone molecules effectively stabilised deteriorating brain networks with effects that differed significantly across critical age transition points. For instance, while ketones showed moderate benefits in young adults, the molecules were found to have maximum benefits during the midlife 'metabolic stress' period between 40 and 59 years. These findings can 'revolutionise' approaches to preventing neurodegenerative diseases like Alzheimer's, scientists say. With dementia cases projected to triple by 2050, new insights from the study offer hope for preventive strategies, researchers say. A metabolic intervention developed from the findings, such as ketogenic diets or supplements, might start working 'well before cognitive symptoms appear' as opposed to current treatments that typically target symptoms only after they emerge. 'This represents a paradigm shift in how we think about brain aging prevention,' said Botond Antal, another author of the study. 'Rather than waiting for cognitive symptoms, which may not appear until substantial damage has occurred, we can potentially identify people at risk through neurometabolic markers and intervene during this critical window,' Dr Antal said.
The National
14-03-2025
- Health
- The National
Genetic variant triples health risks from pollution for some in the UAE
People in the UAE with a specific genetic variant are at greater risk from air pollution than those without it, a study has found. Scientists have found that the harmful effects of tiny particulate matter in the air are nearly three times as severe among people with the variant. Researchers said people known to have the gene type, APOE rs429358, should take extra precautions to reduce their exposure to air pollution. It is a variant of a gene called Apolipoprotein E. As with other genes, everyone has two copies of Apolipoprotein E, one inherited from each parent. The prevalence of the variant in the global human population is about 14 per cent, meaning that it accounts for about one in seven Apolipoprotein E genes. The study was conducted by Dr Hassa Iftikhar, a researcher at Huazhong University of Science and Technology in China. The report looked at 3,000 people in the UAE, including citizens and foreign residents, and it found that those with the variant were 2.8 times more likely to suffer from heart problems when exposed to air pollution. It did not give a breakdown of how many of the participants were Emirati. In particular, PM2.5, particulate matter up to 2.5 micrometres in diameter, is especially harmful because the particles are so small that they travel deep into the lungs and can enter the bloodstream. 'While air pollution is a well-known risk factor for coronary artery disease, our study highlights that genetic susceptibility plays a crucial role in amplifying this risk,' said the study. 'This means that for individuals with the APOE rs429358 variant, exposure to PM2.5 poses a disproportionately higher threat compared to those without this genetic marker.' Dr Iftikhar said pollutants and the genetic predisposition together increased inflammation and another harmful biochemical effect called oxidative stress. These damage blood vessels and cause plaque to build-up in arteries, increasing the risk of heart attacks or strokes. While many other studies have highlighted the risks of air pollution, and of genetic variants increasing a person's risk of cardiovascular disease, the new research is among the smaller number of studies revealing how those factors interact. 'Individuals with this genetic variant should be more proactive in minimising exposure to air pollution, especially in urban areas with high PM2.5 levels,' Dr Iftikhar said. This could include using N95 face masks when commuting in areas with poor air quality, she said. She also recommended avoiding outdoor exercise when pollution levels are high. Other measures include having a diet that reduces inflammation, having plenty of exercise and undergoing regular medical check-ups. 'While routine screening for APOE rs429358 is not yet a standard clinical practice, our study suggests that individuals with a family history of cardiovascular diseases or those living in high-pollution regions could benefit from knowing their genetic risk," she said. Dr Iftikhar said authorities could also take action to reduce pollution, such as increasing green spaces, cutting vehicle emissions and enhancing air quality monitoring. A recent report from air purifier company IQAir found that the UAE is the 17th most-polluted country in the world in terms of PM2.5 levels. A year earlier the country was the seventh most polluted. Prof Uwe Schlink, a senior researcher at the Department Urban and Environmental Sociology in the Helmholtz Centre for Environmental Research in Germany, said previous research showed very young children and the elderly are especially at risk from PM2.5. Prof Schlink, who was not involved in the UAE study, said that to reduce the risks, people could 'seek out places without air pollution', although that is not always easy. 'Here, the use of wearable sensors can provide feedback on air quality and motivate and support people to avoid high exposure during their daily routine,' he said. Another researcher, Prof Frank Kelly, of the School of Public Health at Imperial College London, said that, where possible, people could ensure their indoor air was clean by using purifiers. 'For those who are in more constantly polluted environments, one of the approaches is to ensure that there's better quality air indoors through air purification or ensure the fabric of the building is sealed during [times when pollution is high],' he added.
Yahoo
03-03-2025
- Health
- Yahoo
Living a long time isn't just about good genes, a new study says. 4 lifestyle changes that can improve your longevity.
If you have a parent or grandparent who's reached their 90s or even become a centenarian, someone's probably said to you, 'Oh, you have good genes!' But if longevity doesn't seem to run in your family, fret not: Lifespan has more to do with your lifestyle and environment than with your genetics, according to a study published in the journal Nature Medicine. In other words, there's a lot you can do to take control of your own destiny when it comes to longevity, regardless of how long your relatives lived. Here's what to know. Using data on nearly half a million people from the U.K., Oxford University researchers looked for patterns in who died prematurely, or before the age of 75. They also looked at markers of biological aging in a smaller subset of the study group (over 45,000 people). Their analysis included comparisons of genetic risk factors for disease as well as what some scientists have termed the 'exposome.' Our DNA makes up our genome, whereas the exposome is made up of all the exposures we encounter throughout life. This includes everything from what we eat, drink and inhale to the neighborhoods we live in. See for yourself — The Yodel is the go-to source for daily news, entertainment and feel-good stories. By signing up, you agree to our Terms and Privacy Policy. While genetics accounted for less than 2% of the difference in people's risks of death, environmental factors were behind 17% of the disparity, the scientists found. Smoking, socioeconomic status — a measure of factors like income, neighborhood, education and occupation — physical activity levels and living conditions had the greatest influence on someone's biological aging and risk of death. Some of these factors — such as how much money you make or whether you can afford to own a home in a nice neighborhood — are hard to change. But overall, 23 out of 25 of the environmental variables the researchers looked at are modifiable. And many of them are pretty simple. No, they definitely do. But to what extent varies a lot depending on the specific genes, the diseases that they put you at risk for and what you do throughout your life. For example, which variants of the APOE gene you carry is highly predictive of your risk for Alzheimer's disease; the same goes for BRCA1 and BRCA2 variants and breast cancer. And these diseases can have a lot to do with your biological aging and life expectancy. But even these genes are influenced by your behavior and environment. And, in most cases, our choices and the lives we lead have a huge impact on what those genes will mean for our health. 'Someone put a comment on our paper, saying 'genetics loads the dice, but it's up to us to play our hand,'' Austin Argentieri, a research fellow at Massachusetts General Hospital who led the new study while he was a researcher at Oxford Population Health, tells Yahoo Life. Even if your genetic makeup predisposes you to diseases that could cut your life short, 'in most cases, you can mitigate that risk through lifestyle, behavior, or taking different drugs or treatments,' explains Argentieri. By now, it's hardly a surprise that smoking is bad for you. But, aside from a person's age, smoking has a greater bearing on longevity and aging than any other factor — genetic or environmental — according to the new study. Second to age, the factor that most influenced mortality risk was 'smoking pack years,' meaning the number of packs of cigarettes a person smoked daily, for how many years. And smoking status — whether someone currently, formerly or never smoked — was the fourth-most-influential factor (sex was third; men are more likely to die earlier than women). 'If you can do one thing, don't smoke,' says Argentieri. People who are tired frequently or don't get very much sleep at night are more likely to both age quickly and die prematurely. How much sleep you need varies from person to person, but for most adults, you should aim to get seven to nine hours a night. And try to have good 'sleep hygiene' by going to bed and waking at consistent times, having a bedtime routine, keeping your room dark and keeping your phone away from your bed. After tiredness, physical activity 'is close in the running for the top' factor influencing biological aging and risk of death, says Argentieri. That's in part because many of the chronic conditions that accelerate aging and lead to early death are cardiometabolic diseases, such as heart disease, diabetes and stroke. Obesity increases risks for these conditions, while exercise, in combination with a healthy diet, can reduce those risks. Diet may have more influence, but 'that doesn't mean that exercise shouldn't be part of the plan,' Valter Longo, a University of Southern California professor of gerontology who studies how nutrition and fasting can influence longevity, tells Yahoo Life. In combination with other habits, exercising can help you live healthier, for longer. The study found that while what people ate didn't have much effect on their biological aging, it was predictive of their risk of death. That may be because many people change their diets to be healthier because they have a health problem, such as prediabetes. But Longo's research suggests that eating a diet that consists of lots of plants and fish and little red meat is associated with a longer life. A diet that includes sufficient but low levels of protein helps to prevent aging acceleration by altering the way certain genes associated with the breakdown of our bodies work, Longo says (though this changes around age 65, when we need more protein, he notes).
