In a retrospective study of 40 individuals with Parkinson disease, lower visual equilibrium scores (as measured by the sensory organization test, condition 2) were significantly associated with a higher frequency of falls.
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Reduced Glaucoma Risk Connected to Migraine Medication Use
Individuals with migraines have been known to have a higher risk of glaucoma development, and a new study published in Neurology suggests that use of preventative medication for migraines may be connected with reduced instance of glaucoma development.
“Glaucoma is a leading cause of blindness, and evidence has linked migraine with an increased risk of glaucoma, with both conditions affecting the capacity of the blood vessels in the brain to alter blood flow in response to stimuli,” said the study lead, Chien-Hsiang Weng, MD, clinical associate professor at Brown University.
Weng and his team surmised that drugs that help to regulate blood vessel function to prevent migraines may also help prevent the development of glaucoma. The researchers focused on assessing the efficacy of calcitonin gene-related peptide inhibitors (CGRPi), which included six medications: erenumab, fremanezumab, galcanezumab, eptinezumab, atogepant, and rimegepant.
“Since CGRP inhibitors help regulate blood vessel contraction and inflammation in the nervous system, there has been hope that these drugs could benefit eye health in people at risk of glaucoma,” said Weng.
In this retrospective cohort study, the researchers collected data from a healthcare database including individuals who were prescribed migraine prevention drugs with at least one refill between 2018 and 2024. These individuals were tracked for three years to identify glaucoma diagnoses.
The researchers analyzed data from over 73 thousand participants, 36,822 of which were prescribed drugs from the CGRPi group to prevent migraine, and an equivalent number of people prescribed non-CGRPi drugs (including valproate, topiramate, flunarizine, candesartan, lisinopril, metoprolol, propranolol, nadolol, amitriptyline and venlafaxine). To prevent confounding the data, the researchers point out that “Crossovers were not allowed, and the non-CGRPi group included only individuals who never used CGRPi.”
Primary analysis using the Cox proportional hazards model showed that within the first three years from the first prescription of the migraine medication, 153 people (0.42%) in the CGRPi group developed glaucoma, compared to 223 people (0.61%) of those in the non-CGRPi group.
When adjusted for glaucoma risk factors including migraine frequency, history of high blood pressure, and age, individuals taking CGRPi drugs have a 25% lower risk of developing glaucoma compared with those taking the non-CGRPi drugs.
Not all CGRPi drugs showed equal effectiveness in reducing the risk of developing glaucoma. The authors specify that “only users of monoclonal antibody CGRPi show a reduced risk of glaucoma compared with non-CGRPi users (HR 0.77; 95% CI 0.61–0.98).”
Additionally, not all participants responded to the CGRPi medications equally. “The reduced risk of glaucoma associated with CGRPi is also observed in older adults, women, and those with chronic migraine or migraine without aura.”
This study presented a broad overview of the comparison of the potential effectiveness of two drug groups in preventing glaucoma. While this study shows a promising correlation between reduced risk of developing glaucoma when some individuals use specific CGRPi drugs, more directed and focused studies would be required to confirm a causative impact of CGRPi treatment reducing glaucoma risk.
“Further studies are needed to confirm these results, but the findings may help us better understand both migraine and glaucoma,” confirmed Weng.
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Digital PCR Playbook: Applications and Challenges Across Research and Clinical Labs
Alex Zevin, PhD
Director, Genomics Shared Resource
Fred Hutchinson Cancer Center
Panelist
Alex Zevin, PhD
Alex Zevin, PhD, began serving as the director of the Genomics Shared Resource at Fred Hutch in December 2022. Before that, he was a research scientist at ArcherDX where he developed NGS in vitro diagnostic devices including several clinical trial assays and an approved companion diagnostic. He also previously worked at InBios International and developed a rapid test for detection of anthrax.
Zevin has a bachelor’s degree in biochemistry from Colorado State University and a PhD in molecular biology from Arizona State University where he developed methods to characterize bacterial communities in engineered systems and conducted postdoctoral research at the University of Washington studying host-microbe interactions in non-human primate models.
Broadcast Date:
- Time:
Digital PCR has emerged as a powerful approach for precise nucleic acid quantification, but it is constrained by limited dynamic range and the difficulty of multiplexing. Newer platforms, like Countable Labs’ single-molecule counting PCR, address both by offering precise quantification across a broad range of target abundances while simplifying multiplexing through single-molecule isolation and fluorescent imaging across millions of spatially fixed compartments.
In this GEN webinar, Alex Zevin, PhD, director of Fred Hutchinson Cancer Center’s Genomics Shared Resource, draws on hands-on experience with managing a suite of nucleic acid quantification technologies, including standard qPCR, digital droplet PCR, and Countable PCR, to share practical guidance for labs considering or expanding their PCR quantification capabilities. Key insights from the webinar include:
- How single-molecule counting differs from conventional digital PCR—and the sensitivity, precision, and multiplexing advantages it enables
- Real-world applications suited to single-molecule counting PCR, including validating NGS results, replacing or supplementing existing assays, and generating clinically actionable data
- Common challenges for converting qPCR and dPCR assays to single-molecule counting PCR, and how to overcome them
A live Q&A session will follow the presentations offering you a chance to pose questions to our expert panelist.
Produced with support from:
The post Digital PCR Playbook: Applications and Challenges Across Research and Clinical Labs appeared first on GEN – Genetic Engineering and Biotechnology News.
Cellular Origins Collaborates with Immatics on Automation for Cell Therapy Manufacturing
Cellular Origins agreed to collaborate with Immatics in utilizing Cellular Origins’ automated mobile robotic platform, Constellation®, within certain parts of the company’s manufacturing processes. The collaboration will explore how automation technologies can further contribute to more efficient and scalable manufacturing processes for next-generation cell therapies.
“Following the first cell therapy approvals in 2017, there has been widespread success in treating blood cancers, while progress in solid tumors has been more limited. Immatics is now working to advance clinically validated approaches that could expand treatment options for these,” said Edwin Stone, PhD, CEO, Cellular Origins. “Current manual manufacturing methods can limit the number of patients who are able to access approved therapies,” he added.
“Effective cell therapies for solid-tumor patients is one of the most exciting developments in our field but will need the manufacturing challenges to be addressed to deliver on its potential. Our partnership with Immatics aims to support the scalable and cost-effective manufacturing of their therapies so that more patients could potentially benefit.”
“Immatics has generated extensive data demonstrating the potential of precision targeting PRAME, a target expressed in more than 50 cancers,” noted Ali Mohamed, PhD, senior vice president of CMC, Immatics. “As we continue to advance our programs, it is important that we also develop manufacturing capabilities that can support future scale. We are pleased to collaborate with Cellular Origins to explore how the Constellation platform and our integrated manufacturing processes could support the scalable production of our therapies as we move toward potential approvals.”
The post Cellular Origins Collaborates with Immatics on Automation for Cell Therapy Manufacturing appeared first on GEN – Genetic Engineering and Biotechnology News.
Broader Immune Targeting Increases Immunotherapy Benefit in Colorectal Cancer
Researchers at the Icahn School of Medicine at Mount Sinai and the Mount Sinai Tisch Cancer Center have identified a potential strategy to overcome resistance to immunotherapy in colorectal cancer (CRC) by restoring coordinated interactions between T cells and macrophages within the tumor microenvironment. The findings, published in Cell Reports Medicine, suggest that durable responses to immune checkpoint blockade (ICB) depend not only on activating T cells, but also on reestablishing communication between immune cell populations that work together to eliminate tumors. The study showed that a combination strategy targeting TREM2, LAG3, CTLA4, and PD-1 achieved up to 100% tumor clearance in mismatch repair-deficient colorectal cancer models and more than 70% clearance in mismatch repair-proficient tumors, which are typically resistant to immunotherapy.
“Our findings show that it’s not enough to simply activate the immune system,” said co-senior author Nina Bhardwaj, MD, PhD, director of immunotherapy and professor of medicine at the Icahn School of Medicine. “You also need to restore the communication between immune cells so they can work together effectively against the tumor.”
Currently, anti-PD-1 therapies improve outcomes in some patients with mismatch repair-deficient tumors, but about half of patients with advanced mismatch repair-deficient CRC and most mismatch repair-proficient colorectal cancers fail to respond. In this study, researchers searched for ways to define the immune resistance pathways that limit responses and determine which pathways would need to be targeted simultaneously to overcome immune escape and generate immune memory.
To understand the mechanisms of resistance, the team used orthotopic and patient-derived colorectal cancer models along with murine tumor models and human mismatch repair-deficient colorectal cancer spheroid cultures. The study employed single-cell transcriptomics, spatial analyses, spectral flow cytometry, machine learning, and imaging approaches to characterize immune cell populations and their interactions within tumors.
The analysis of the data identified distinct immune signatures associated with treatment response and resistance. Tumor control during anti-PD-1 therapy was associated with colocalization of MHC-positive, C1Q-positive, CXCL9-positive macrophages and TCF-positive, PRF1-positive T cells. By contrast, resistant tumors contained exhausted T cells expressing TIM3, LAG3, TIGIT, and PD-1, as well as TREM2-positive macrophages concentrated in regions that excluded T cells.
The findings provides a new understanding of effective immunotherapy responses by showing that robust checkpoint blockade activity requires coordinated interactions among multiple immune cell types and not just activation of T cells alone. Specifically, it showed that macrophage remodeling and communication between macrophages and T cells are central components of successful anti-tumor immunity.
In lab studies, the team tested several therapeutic targets individually and in combination, including PD-1, TIM3, TIGIT, LAG3, CTLA4, TREM2, and IFITM. Single-agent targeting of TIM3, TIGIT, LAG3, TREM2, or PD-1 limited tumor growth in mismatch repair-deficient colorectal cancer models, but responses improved when therapies were combined.
The most effective treatment combined blockade of PD-1, LAG3, CTLA4, and TREM2. This approach increased complete tumor elimination rates to as high as 100 percent in mismatch repair-deficient colorectal cancer models and up to 73 percent in mismatch repair-proficient models. Anti-PD-1 monotherapy achieved no complete tumor responses in the models studied.
“This study highlights that overcoming immunotherapy resistance requires more than targeting a single pathway,” said co-senior author Robert M. Samstein, MD, PhD, associate professor of radiation oncology, and immunology and immunotherapy, at the Icahn School of Medicine. “By addressing both T cell dysfunction and the suppressive tumor environment, we can begin to design more effective combination strategies that have the potential to benefit a much broader group of patients.”
The findings build on prior evidence suggesting that T cell exhaustion and suppressive myeloid cells contribute to immune resistance. Earlier research had linked TCF-positive T cells to anti-PD-1 responses in melanoma and associated IL1B-positive monocytes and TREM2-positive macrophages with resistance in CRC and other tumor models.
Importantly, the study found that in mouse models where the initial tumors had been completely eliminated after checkpoint-targeted therapy were also protected against a second tumor inoculation, indicating that the combined approach generated sustained anti-tumor immunity that could reduce recurrence risk.
“This approach effectively reprograms the tumor microenvironment,” said first author Guillaume Mestrallet, PhD, a postdoctoral researcher at Mount Sinai. “By simultaneously reinvigorating T cells and targeting suppressive macrophages, we were able to restore immune coordination and generate powerful anti-tumor responses.”
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Autism Screening Proposed for Children with Epilepsy
Children with epilepsy are up to 10 times more likely than others to also have autism, according to research that exposes the scale of the association between the two conditions.
The findings, in more than 30,000 children, stress the importance of screening for developmental concerns among those with epilepsy, so support can be delivered as early as possible.
The study, Developmental Medicine & Child Neurology, revealed that girls with autism spectrum disorder (ASD) were more likely than boys to also have epilepsy.
Higher rates of intellectual disability were also seen in children with autism who additionally had epilepsy, and they were also diagnosed with the neurodiversity at an earlier age.
“Our findings emphasize the importance of screening for autism in this population to support earlier diagnosis and timely intervention, both of which are key to improving long-term outcomes,” said senior investigator Elaine Wirrell, MD, from the Mayo Clinic.
ASD and epilepsy are complex disorders of neuronal connectivity that frequently co-occur because of shared molecular and biological mechanisms.
While the increased risk of ASD in children with epilepsy is well documented, there are gaps in knowledge around its incidence and prevalence, and risk factors for their co-occurrence.
To investigate further, Wirrell and team studied the medical records of 30,490 children in Olmsted County, Minnesota, of whom 257 (0.84%) were diagnosed with epilepsy before the age of 19 years.
They found that children with epilepsy were more likely have ASD across all three research and clinical definitions compared with other children, with this likelihood increased between six and 10-fold.
The prevalence was a corresponding 21.4% versus 3.2% using broad research criteria, 14.0% versus 1.6% across stricter research criteria, and 7.9% versus 0.7% for a clinical diagnosis.
Among children with autism, those also with epilepsy were more likely to have a lower IQ on standardized testing than those in whom epilepsy was absent (56.5% versus 15.4%). Specifically, an IQ of less than 70 was observed in 57.4% of children with co-occurring epilepsy and autism compared with only 15.4% autism alone.
Those with autism and epilepsy were also more often female than those with autism alone (38.2% versus 25.8%), and were identified with autism at a younger age, at a mean of seven years and five months versus eight years and eight months).
“These insights underscore the critical need for comprehensive and early screening protocols to better address and manage the intersection of autism and epilepsy, ensuring timely interventions and tailored support for affected individuals,” the researchers concluded.
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Immune Mapping Links Sex-Specific Genetics to Autoimmune Disease
The largest study to date to examine immune differences between sexes at single-cell resolution has identified over 1,000 genetic switches that operate in distinct ways when comparing immune cells from men and women. Published today in The American Journal of Human Genetics, these findings could explain why women are much more likely to be affected by autoimmune conditions than men.
“Our findings show that the immune system needs to be studied with sex in mind,” says Seyhan Yazar, PhD, group leader of the precision immunology program at the Garvan Institute of Medical Research in Australia. “Even though we know men’s and women’s immune systems differ, many studies still overlook these differences, which can limit how well we understand disease, and in turn bias treatment options.”
Yazar’s team analyzed single-cell RNA sequencing data from over 1.25 million circulating immune cells from nearly 1,000 healthy individuals who participated in the OneK1K cohort. This Australian research program maps how individual immune cells respond to disease and pathogens to determine why some individuals respond to treatment but others don’t.
Results revealed distinct genetic and cellular profiles between both sexes. While men were found to have a higher proportion of monocytes, women showed higher levels of B cells and regulatory T cells. In men, genetic activity seemed to focus on basic cellular maintenance processes, but in women genetic activity heavily skewed towards the activation of inflammatory pathways.
“While this highly reactive immune profile gives females an advantage in fighting viral infections, it comes with a biological trade-off: a greater predisposition to autoimmune diseases,” says Sara Ballouz, PhD, senior lecturer at the University of New South Wales (UNSW). “On the other hand, male immune cells are less primed for inflammation, making men generally more susceptible to infections and non-reproductive cancers.”
Interestingly, most of the genetic switches found to be active in individuals of one sex but not the other were not found to be located in sex chromosomes. More than 1,000 sex-specific genetic switches were identified on autosomes, with many of them being directly linked to autoimmune conditions.
“This is the first time we have shown that these differences occur at the genetic control level, providing a new layer of insight into human immunity,” Ballouz says. “Having shown that female-biased genes are heavily enriched in inflammatory pathways, we now have another biological rationale for why the immune system can more easily mistakenly attack the body’s own tissues in women.”
The analysis found female-specific genetic variants that affected the expression of two genes linked to systemic lupus erythematosus (SLE), an autoimmune condition that is nine times more likely to affect women than men. Although conditions like SLE are multifactorial, uncovering the contribution of genetic variants to their development is an important step forward towards better understanding disease susceptibility between sexes.
“Our findings add strong evidence that female and male autoimmune diseases may not be the same, and the way we should treat them may not necessarily be the same,” says Yazar. “Currently, clinicians rely on a one-size-fits-all management approach for most autoimmune diseases—a more inclusive approach is needed.”
Currently, autoimmune conditions are often treated with broad immunosuppressants that reduce the activity of the entire immune system. Research is striving to move towards treatments that more precisely target each person’s unique needs, which is only possible through the identification of distinct genetic pathways driving autoimmune disease.
“If we want to realize the potential of precision medicine, we have to understand these fundamental biological variables,” says Joseph E. Powell, PhD, director of the translational genomics program at the Garvan Institute. “Treatments need to be tailored not just to the disease, but to how a patient’s immune system operates at a baseline genetic level.”
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Seaport’s IPO adventure, obesity pill battles, and Makary’s troubles
On this week’s episode of “The Readout LOUD,” we chat with Seaport Therapeutics CEO Daphne Zohar, fresh off the biotech’s successful IPO. Plus, Elaine, Allison, and Adam chat about this week’s notable news, including the obesity pill battle between Eli Lilly and Novo Nordisk, a Phase 3 study win for Cytokinetics, and FDA Commissioner Marty Makary’s White House troubles.
Oh, by the way, this is the 400th episode of your favorite biotech podcast.
Science is becoming less disruptive. Is an aging workforce to blame?
Physicist Albert Einstein, widely regarded as one of the most prolific scientists of the past century, conducted much of his transformative work at the beginning of his career, before spending years defending his theories against the burgeoning field of quantum mechanics.
A new study shows that Einstein is not alone, and that most researchers begin their careers conducting their more disruptive work — overturning conventional wisdom and forging paths of their own — but as they age, they tend to abandon that groundbreaking energy. Instead, many become adept at connecting previously unlinked ideas. The paper, published Thursday in Science, helps offer an explanation of a trend that has increasingly worried scholars of science policy and innovation: that the pace of discovery has slowed in recent years.
Official leading CDC’s cruise ship program retires
WASHINGTON — The top U.S. official responsible for public health on cruise ships is stepping down, according to an internal Centers for Disease Control and Prevention announcement obtained by STAT.
The retirement of Luis Rodríguez, who has been part of the Vessel Sanitation Program since 2010 and served as its chief since 2023, was announced internally at the CDC on Wednesday.