“Red meat is high in saturated fat and has been shown in previous studies to increase the risk of type 2 diabetes and heart disease, which are both linked to reduced brain health,” said study author Dong Wang, MD, ScD, of Brigham and Women’s Hospital in Boston. “Our study found processed red meat may increase the risk of cognitive decline and dementia, but the good news is that it also found that replacing it with healthier alternatives, like nuts, fish and poultry, may reduce a person’s risk.”

To examine the risk of dementia, researchers included a group of 133,771 people with an average age of 49 who did not have dementia at the start of the study. They were followed up to 43 years. Of this group, 11,173 people developed dementia.

Participants completed a food diary every two to four years, listing what they ate and how often.

Researchers defined processed red meat as bacon, hot dogs, sausages, salami, bologna and other processed meat products. They defined unprocessed red meat as beef, pork, lamb and hamburger. A serving of red meat is three ounces, about the size of a deck of cards.

Researchers calculated how much red meat participants ate on average per day.

For processed red meat, they divided participants into three groups. The low group ate an average of fewer than 0.10 servings per day; the medium group ate between 0.10 and 0.24 servings per day; and the high group, 0.25 or more servings per day.

After adjusting for factors such as age, sex and other risk factors for cognitive decline, researchers found that participants in the high group had a 13% higher risk of developing dementia compared to those in the low group.

For unprocessed red meat, researchers compared people who ate an average of less than one half serving per day to people who ate one or more servings per day and did not find a difference in dementia risk.

To measure subjective cognitive decline, researchers looked at a different group of 43,966 participants with an average age of 78. Subjective cognitive decline is when a person reports memory and thinking problems before any decline is large enough to show up on standard tests.

The subjective cognitive decline group took surveys rating their own memory and thinking skills twice during the study.

After adjusting for factors such as age, sex and other risk factors for cognitive decline, researchers found that participants who ate an average of 0.25 servings or more per day of processed red meat had a 14% higher risk of subjective cognitive decline compared to those who ate an average of fewer than 0.10 servings per day.

They also found people who ate one or more servings of unprocessed red meat per day had a 16% higher risk of subjective cognitive decline compared to people who ate less than a half serving per day.

To measure objective cognitive function, researchers looked at a different group of 17,458 female participants with an average age of 74. Objective cognitive function is how well your brain works to remember, think and solve problems.

This group took memory and thinking tests four times during the study.

After adjusting for factors such as age, sex and other risk factors for cognitive decline, researchers found that eating higher processed red meat was associated with faster brain aging in global cognition with 1.61 years with each additional serving per day and in verbal memory with 1.69 years with each additional serving per day.

Finally, researchers found that replacing one serving per day of processed red meat with one serving per day of nuts and legumes was associated with a 19% lower risk of dementia and 1.37 fewer years of cognitive aging. Making the same substitution for fish was associated with a 28% lower risk of dementia and replacing with chicken was associated with a 16% lower risk of dementia.

“Reducing how much red meat a person eats and replacing it with other protein sources and plant-based options could be included in dietary guidelines to promote cognitive health,” said Wang. “More research is needed to assess our findings in more diverse groups.”

A limitation of the study was that it primarily looked at white health care professionals, so the results might not be the same for other race, ethnic and non-binary sex and gender populations.

The study was supported by the National Institutes of Health.

Previous studies showed that a protein called PIN1 helps cancers initiate and progress, but its exact role in tumor development has remained unclear. Now, cancer biologists at the Salk Institute have discovered that PIN1 is a significant driver of bladder cancer and revealed that it works by triggering the synthesis of cholesterol — a membrane lipid essential for cancer cells to grow.

After mapping out the molecular pathway between PIN1 and cholesterol, the researchers developed an effective treatment regimen that largely halted tumor growth in their mouse model of cancer. The therapy consists of two drugs: a PIN1 inhibitor called sulfopin, an experimental drug not yet tested in humans, and simvastatin, a statin that is already used in humans for lowering cholesterol levels to reduce the risk of cardiovascular disease.

The findings were published in Cancer Discovery, a journal of the American Association for Cancer Research, on January 14, 2025.

“We’re excited to be the first to identify PIN1’s role in bladder cancer and to describe the mechanism it uses to drive tumor growth,” says senior author Tony Hunter, American Cancer Society professor and holder of the Renato Dulbecco Chair at Salk. “Given the high costs, morbidity, and mortality rates for bladder cancer, we’re especially thrilled to discover that targeting the cholesterol pathway with this therapeutic combination was so effective in suppressing bladder tumor growth in mice, and we hope to see this approach explored in a future clinical trial, once a PIN1 inhibitor is approved for clinical use.”

Bladder cancer is one of the most diagnosed cancers worldwide and the fourth most common cancer among men. It poses a serious threat to public health, as most cases result in either expensive, lifelong treatment, or rapid progression and mortality.

Hunter’s lab had originally discovered PIN1 in 1996 as a part of its work on phosphorylation, a process in which phosphate molecules are tacked onto proteins to change their structure and function. The lab showed that PIN1 is an enzyme that can recognize a protein when a phosphate is added to the amino acid serine while it’s next to the amino acid proline. PIN1 then changes that protein’s shape.

Phosphorylation of proteins at serine residues next to prolines is known to be a major signaling mechanism controlling cell proliferation and malignant transformation, and its dysregulation causes human cancers. PIN1 can target these phosphorylated areas and instigate structural and functional changes to the protein. Still, it’s been unclear exactly how this PIN1 activity contributes to tumor formation or which proteins PIN1 might be interacting with in bladder cancer cells.

In search of answers, the team compared normal human bladder cells with bladder cancercells, in culture dishes and implanted in mice.

First, they demonstrated that PIN1 expression was higher in bladder cancer cells — specifically in the specialized tissue layer that lines the inside of the urinary tract, called the urothelium. Then, they used genetic scissors to eliminate the PIN1 gene in the cancer cells. Without PIN1, they saw fewer cancerous cells develop, and those that did develop migrated less aggressively within and beyond the urothelium.

These findings indicated that PIN1 was contributing to the development of bladder cancer, but how?

The researchers returned to the cells that were missing PIN1 and looked to see if any other biological processes had been altered. Surprisingly, they found that one of the most affected pathways was the cholesterol synthesis pathway, mediated by a protein called SREBP2. Without PIN1, the bladder cells contained much lower levels of cholesterol.

“Cancer cells need a lot of cholesterol to accomplish their trademark excess growth,” says first author Xue Wang, a postdoctoral researcher in Hunter’s lab. “Our findings show that PIN1 plays an important role in cholesterol production, and removing it leads to lower cholesterol and therefore less out-of-control tumor growth.”

Through a series of experiments, the researchers confirmed that PIN1 was working with the SREBP2 protein to stimulate cholesterol production. Removing PIN1 effectively put a lid on the cancer’s fuel supply, but reinstating PIN1 reversed those anti-cancer effects. Without intervention, the high level of PIN1 in bladder cancer assists in tumor growth and metastasis.

How can we stop PIN1? One obvious answer is to inhibit the protein itself, but it’s also possible to inhibit an enzyme in the cholesterol pathway that PIN1 stimulates. One class of drugs, called statins, is already very widely used to control cholesterol levels. Statins work by blocking a protein in the cholesterol biosynthesis pathway called HMGCR. The idea was to attack the cholesterol pathway from two angles by combining simvastatin, a widely prescribed statin, to block HMGCR, and sulfopin to disable PIN1 and prevent its activation of SREBP2, thus drastically reducing the ability of the bladder cancer cells to make cholesterol.

When the researchers treated the mice with bladder cancer tumors with the PIN1 inhibitor sulfopin and the HMGCR inhibitor simvastatin, they found the combination suppressed cancer cell proliferation and tumor growth — importantly, the two worked better in tandem than as individual treatments.

“This is likely just one of many roles that PIN1 plays in cancers,” says Hunter. “What’s exciting about this discovery, though, is that statins are already in human use to prevent cardiovascular disease, and our work suggests an opportunity to use statins in combination with other drugs for bladder cancer therapy. And beyond this, we’ll continue to study whether PIN1 plays a similar role in other cancers, so our findings can hopefully improve lives regardless of cancer type.”

Not only did the team confirm PIN1’s role in bladder cancer progression, they also connected PIN1 to cholesterol biosynthesis and created viable treatment solutions to improve treatment outcomes.

Other authors include Yuan Sui and Jill Meisenhelder of Salk, Derrick Lee of UC San Diego, and Haibo Xu of Shenzhen University in China.

The work was supported by the National Institutes of Health (CCSG P30CA023100, CCSG CA014159, 5 R35 CA242443) and a Pioneer Fund Postdoctoral Scholar Award.

In a paper published recently in Nature Communications, the UC Irvine scientists describe their construction of complementary, internal, ion-gated, organic electrochemical transistors that are more amenable chemically, biologically and electronically to living tissues than rigid, silicon-based technologies. The medical device based on these transistors can function in sensitive parts of the body and conform to organ structures even as they grow.

“Advanced electronics have been in development for several decades now, so there is a large repository of available circuit designs. The problem is that most of these transistor and amplifier technologies are not compatible with our physiology,” said co-author Dion Khodagholy, Henry Samueli Faculty Excellence Professor in UC Irvine’s Department of Electrical Engineering and Computer Science. “For our innovation, we used organic polymer materials that are inherently closer to us biologically, and we designed it to interact with ions, because the language of the brain and body is ionic, not electronic.”

In standard bioelectronics, complementary transistors have been composed of different materials to account for different polarities of signals, which, in addition to being unyielding and cumbersome, present the risk of toxicity when implanted in sensitive areas. The team of researchers from UC Irvine and Columbia University worked around this problem by creating its transistors in an asymmetric fashion that enables them to be operated using a single, biocompatible material.

“A transistor is like a simple valve that controls the flow of current. In our transistors, the physical process that controls this modulation is governed by the electrochemical doping and de-doping of the channel,” said first author Duncan Wisniewski, Columbia University Ph.D. candidate during the project who is now a visiting scholar in the UC Irvine Department of Electrical Engineering and Computer Science. “By designing devices with asymmetrical contacts, we can control the doping location in the channel and switch the focus from negative potential to positive potential. This design approach allows us to make a complementary device using a single material.”

He added that arraying transistors into a smaller, single-polymer material greatly simplifies the fabrication process, enabling large-scale manufacturing and opportunities to expand the technology beyond the original neurological application to almost any biopotential processes.

Khodagholy, who heads the UC Irvine Translational Neuroelectronics Laboratory, which recently moved to Irvine from Columbia University, said that his team’s work has the added benefit of scalability: “You can make different device sizes and still maintain this complementarity, and you can even change the material, which makes this innovation applicable in multiple situations.”

Another advantage highlighted in the Nature Communications paper is that the device can be implanted in a developing animal and withstand transitions in tissue structures as the organism grows, something that is not possible with hard, silicon-based implants.

“This characteristic will make the device particularly useful in pediatric applications,” said co-author Jennifer Gelinas, UC Irvine associate professor of anatomy and neurobiology as well as pediatrics, who’s also a physician at Children’s Hospital of Orange County.

“We demonstrated our ability to create robust complementary, integrated circuits that are capable of high-quality acquisition and processing of biological signals,” Khodagholy said. Complementary, internal, ion-gated, organic electrochemical transistors “will substantially broaden the application of bioelectronics to devices that have traditionally relied on bulky, nonbiocompatible components.”

Joining Khodagholy, Gelinas and Wisniewski on this project were Claudia Cea, Liang Ma, Alexander Ranschaert, Onni Rauhala and Zifang Zhao of Columbia University. The work was supported by the National Institutes of Health and the National Science Foundation.

Based on new research, we now know that college students gain the same amount of weight as older adults during the holiday season; however, they add new muscle not fat.

Obesity researcher Martin Binks, professor and chair of George Mason University’s Department of Nutrition and Food Studies, was surprised by the findings of this breakthrough research. “The differences between college students’ and older adults’ weight gain highlights the importance of understanding weight and health in the context of major life stages and transitions across the lifespan,” says Binks. “At this key transitional stage of life, the influence of the holiday season is uniquely different for college students than later in adulthood. It raises so many important scientific questions about what might be driving this.” Binks is interested in learning more about the reasons for this difference with future studies.

Binks has been a metabolic disease scientist and clinician for over 20 years. He has assisted thousands of patients with behavioral pharmacologic and surgical weight loss, health and wellness, and quality of life improvement. He has been chair of George Mason’s Department of Nutrition and Food Studies since August 2024. This publication is the result of a study that was conducted by undergraduate students who were guided by graduate students under Binks’ mentorship. “Mentoring students in conducting impactful research is at the heart of my lifelong passion and is integral to the vision of George Mason’s Nutrition and Food Studies department,” says Binks.

Obesity Science & Practice published “Holiday Weight Change in a US College Student Sample: A Prospective Observational Cohort Study” in January 2025. Additional authors include Hannah B Yoo (lead author), Casen Bigham, Sharmin Akter, Alexis Brown, Shruthi Durai, and Claire Brown from Texas Tech University; Tanisha Basu from the University of Cincinnati; Tiffany Tsai from Princeton University; and Sara Kiros from the University of Oregon.

In one such phenomenon, called quantum entanglement, pairs of photons become interconnected in such a way that the state of one photon instantly changes to match the state of its paired photon, no matter how far apart they are.

Nearly 80 years ago, Albert Einstein referred to this phenomenon as “spooky action at a distance.” Today, entanglement is the subject of research programs across the world — and it’s becoming a favored way to implement the most fundamental form of quantum information, the qubit.

Currently, the most efficient way to create photon pairs requires sending lightwaves through a crystal large enough to see without a microscope. In a paper published today in Nature Photonics, a team led by Columbia Engineering researchers and collaborators, describe a new method for creating these photon pairs that achieves higher performance on a much smaller device using less energy. P. James Schuck, associate professor of mechanical engineering at Columbia Engineering, helped lead the research team.

These findings represent a significant step forward in the field of nonlinear optics, which is concerned with using technologies to change the properties of light for applications including lasers, telecommunications, and laboratory equipment.

“This work represents the embodiment of the long-sought goal of bridging macroscopic and microscopic nonlinear and quantum optics,” says Schuck, who co-directs Columbia’s MS in Quantum Science and Technology. “It provides the foundation for scalable, highly efficient on-chip integrable devices such as tunable microscopic entangled-photon-pair generators.”

How it works

Measuring just 3.4 micrometers thick, the new device points to a future where this important component of many quantum systems can fit onto a silicon chip. This change would enable significant gains in the energy efficiency and overall technical capabilities of quantum devices.

To create the device, the researchers used thin crystals of a so-called van der Waals semiconducting transition metal called molybdenum disulfide. Then they layered six of these crystal pieces into a stack, with each piece rotated 180 degrees relative to the crystal slabs above and below. As light travels through this stack, a phenomenon called quasi-phase-matching manipulates properties of the light, enabling the creation of paired photons.

This paper represents the first time that quasi-phase-matching in any van der Waals material has been used to generate photon pairs at wavelengths that are useful for telecommunications. The technique is significantly more efficient than previous methods and far less prone to error.

“We believe this breakthrough will establish van der Waals materials as the core of next-generation nonlinear and quantum photonic architectures, with them being ideal candidates for enabling all future on-chip technologies and replacing current bulk and periodically poled crystals,” Schuck says.

“These innovations will have an immediate impact in diverse areas including satellite-based distribution and mobile phone quantum communication.”

How it happened

Schuck and his team built on their previous work to develop the new device. In 2022, the group demonstrated that materials like molybdenum disulfide possess useful properties for nonlinear optics — but performance was limited by the tendency of light waves to interfere with one another while traveling through this material.

The team turned to a technique called periodic poling to counteract this problem, which is known as phase matching. By alternating the direction of the slabs in the stack, the device manipulates light in a way that enables photon pair generation at miniscule length scales.

“Once we understood how amazing this material was, we knew we had to pursue the periodic poling, which could allow for the highly efficient generation of photon pairs,” Schuck says.

This work occurred within Programmable Quantum Materials, a Department of Energy energy frontier research center (EFRC) at Columbia, as part of a larger effort to understand and exploit quantum materials. This work was possible due to contributions from the Baso, Delor, and Dean labs. Postdoctoral researcher Chiara Trovatello led the effort.

“Many of the materials in our day-to-day lives are flammable, and offering a solution to protect from fire benignly is difficult,” said Maya D. Montemayor, a graduate student in the Department of Chemistry at Texas A&M and the publication’s lead author. “This technology can be optimized to quickly, easily, and safely flame retard many flammable materials, offering vast protection in everyday life, saving money and lives of the general population.”

Current studies developing flame retardant coatings deposited via polyelectrolyte complexation require two or more steps, increasing the time and cost to coat a material effectively.

In contrast, this study recently published in ACS Applied Polymer Materials hopes to achieve the same results using only one step. The researchers address this issue by incorporating a volatile base, a molecule that evaporates under ambient conditions. Using ammonia as the volatile base, the base evaporates to reduce the pH and induce complexation (a chemical reaction that forms a stable complex) on the cotton’s surface. Until now, this technique has been proposed but never used to prepare a flame-retardant treatment.

This research can be utilized to deposit polyelectrolyte-based flame-retardant coatings in a scalable and efficient manner. Other positive attributes of the technology include that it is aqueous (water-based) and non-toxic, unlike many other flame-retardant treatments.

The researchers will continue evaluating this technology in partnership with companies in hopes of using their findings to protect wood, fabric, foam and other textiles.

“This cutting-edge research offers Texas A&M recognition as one of the leaders of this technology and the opportunity for further development with external companies,” said Dr. Jaime Grunlan, Leland T. Jordan ’29 Chair Professor in the J. Mike Walker ’66 Department of Mechanical Engineering at Texas A&M. “The scope of this research positively impacts our community by improving our safety in an environmentally benign manner. TEES is licensing this and similar technologies to companies for various applications.”

Other contributors to the findings include Texas A&M graduate students Danixa Rodriguez-Melendez, Dallin L. Smith, Natalie A. Vest and Bethany Palen, and Texas A&M undergraduate students Edward Chang and Alexandra V. Moran.

Funding for this research is administered by the Texas A&M Engineering Experiment Station (TEES), the official research agency for Texas A&M Engineering.