Publisher Health

Eating cold-water fish and other sources of omega-3 fatty acids may preserve brain health and enhance cognition in middle age, new evidence indicates.
Having at least some omega-3s in red blood cells was associated with better brain structure and cognitive function among healthy study volunteers in their 40s and 50s, according to research published online Oct. 5 in Neurology®, the medical journal of the American Academy of Neurology. Faculty of The University of Texas Health Science Center at San Antonio (UT Health San Antonio) and other investigators of the Framingham Heart Study conducted the analysis.
“Studies have looked at this association in older populations. The new contribution here is that, even at younger ages, if you have a diet that includes some omega-3 fatty acids, you are already protecting your brain for most of the indicators of brain aging that we see at middle age,” said Claudia Satizabal, PhD, assistant professor of population health sciences with the Glenn Biggs Institute for Alzheimer’s and Neurodegenerative Diseases at UT Health San Antonio. Satizabal is the lead author of the study.
Volunteers’ average age was 46. The team looked at the relation of red blood cell omega-3 fatty acid concentrations with MRI and cognitive markers of brain aging. Researchers also studied the effect of omega-3 red blood cell concentrations in volunteers who carried APOE4, a genetic variation linked to higher risk of Alzheimer’s disease.
The study of 2,183 dementia- and stroke-free participants found that: Higher omega-3 index was associated with larger hippocampal volumes. The hippocampus, a structure in the brain, plays a major role in learning and memory. Consuming more omega-3s was associated with better abstract reasoning, or the ability to understand complex concepts using logical thinking. APOE4 carriers with a higher omega-3 index had less small-vessel disease. The APOE4 gene is associated with cardiovascular disease and vascular dementia.Researchers used a technique called gas chromatography to measure docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) concentrations from red blood cells. The omega-3 index was calculated as DHA plus EPA.
“Omega-3 fatty acids such as EPA and DHA are key micronutrients that enhance and protect the brain,” said study coauthor Debora Melo van Lent, PhD, postdoctoral research fellow at the Biggs Institute. “Our study is one of the first to observe this effect in a younger population. More studies in this age group are needed.”
The team divided participants into those who had very little omega-3 red blood cell concentration and those who had at least a little and more. “We saw the worst outcomes in the people who had the lowest consumption of omega-3s,” Satizabal said. “So, that is something interesting. Although the more omega-3 the more benefits for the brain, you just need to eat some to see benefits.”
Researchers don’t know how DHA and EPA protect the brain. One theory is that, because those fatty acids are needed in the membrane of neurons, when they are replaced with other types of fatty acids, that’s when neurons (nerve cells) become unstable. Another explanation may have to deal with the anti-inflammatory properties of DHA and EPA. “It’s complex. We don’t understand everything yet, but we show that, somehow, if you increase your consumption of omega-3s even by a little bit, you are protecting your brain,” Satizabal said.
It’s encouraging that DHA and EPA also protected APOE4 carriers’ brain health. “It’s genetics, so you can’t change it,” Melo van Lent said, referring to the vulnerability of this risk group. “So, if there is a modifiable risk factor that can outweigh genetic predisposition, that’s a big gain.”

Carnegie Mellon University researchers have pioneered the CMU Array — a new type of microelectrode array for brain computer interface platforms. It holds the potential to transform how doctors are able to treat neurological disorders.
3D printed at the nanoscale, the ultra-high-density microelectrode array (MEA) is fully customizable. This means that one day, patients suffering from epilepsy or limb function loss due to stroke could have personalized medical treatment optimized for their individual needs.
The collaboration combines the expertise of Rahul Panat, associate professor of mechanical engineering, and Eric Yttri, assistant professor of biological sciences. The team applied the newest microfabrication technique, Aerosol Jet 3D printing, to produce arrays that solved the major design barriers of other brain computer interface (BCI) arrays. The findings were published in Science Advances.
“Aerosol Jet 3D printing offered three major advantages,” Panat explained. “Users are able to customize their MEAs to fit particular needs; the MEAs can work in three dimensions in the brain; and the density of the MEA is increased and therefore more robust.”
MEA-based BCIs connect neurons in the brain with external electronics to monitor or stimulate brain activity. They are often used in applications like neuroprosthetic devices, artificial limbs, and visual implants to transport information from the brain to extremities that have lost functionality. BCIs also have potential applications in treating neurological diseases such as epilepsy, depression, and obsessive-compulsive disorder. However, existing devices have limitations.
There are two types of popular BCI devices. The oldest MEA is the Utah array, developed at the University of Utah and patented in 1993. This silicone-based array uses a field of tiny pins, or shanks, that can be inserted directly into the brain to detect electrical discharge from neurons at the tip of each pin.

Now experts are calling for walkable communities, improved housing, and access to health care and better food, particularly in minority communities.Over the past 50 years, medical advances have led to a more sophisticated understanding of the causes of Type 2 diabetes and to an abundance of new tools for managing it. But better treatments have done little to stem the rise of the disease.One in seven American adults has Type 2 diabetes now, up from one in 20 in the 1970s. Many teenagers are developing what was once considered to be a disease of older people; 40 percent of young adults will be diagnosed with it at some point in their lives.Researchers who study Type 2 diabetes have reached a stark conclusion: There is no device, no drug powerful enough to counter the effects of poverty, pollution, stress, a broken food system, cities that are hard to navigate on foot and inequitable access to health care, particularly in minority communities.“Our entire society is perfectly designed to create Type 2 diabetes,” said Dr. Dean Schillinger, a professor of medicine at University of California, San Francisco. “We have to disrupt that.”Dr. Schillinger and nearly two dozen other experts laid out a road-map for doing so earlier this year in a comprehensive national report to Congress on diabetes, the first of its kind since 1975.It calls for reframing the epidemic as a social, economic and environmental problem, and offers a series of detailed fixes, ranging from improving access to healthy food and clean water to rethinking the designs of communities, housing and transportation networks.“It’s about massive federal subsidies that support producing ingredients that go into low-cost, energy-dense, ultra-processed and sugar-loaded foods, the unfettered marketing of junk food to children, suburban sprawl that demands driving over walking or biking — all the forces in the environment that some of us have the resources to buffer ourselves against, but people with low incomes don’t,” Dr. Schillinger said.“We feel impotent as doctors because we don’t have the tools to tackle the social conditions people are grappling with,” he added.The report, issued in January, calls for setting up a national policy office to roll out a far-reaching strategy to prevent and control diabetes. The document also pushes for a greater involvement of federal agencies, like those regulating housing and urban growth, that may seem to have little to do with health but could play a role in reducing the spread of the disease.The recommendations are intended to tackle the so-called social determinants of health, said Felicia Hill-Briggs, vice president for prevention at Northwell Health.What’s in the Inflation Reduction ActCard 1 of 8A substantive legislation.

A study led by Texas A&M AgriLife Research provides compelling evidence of the important role of hepatocyte adenosine kinase in the progression of nonalcoholic fatty liver disease, NAFLD.
The study, “Hepatocyte Adenosine Kinase Promotes Excessive Fat Deposition and Liver Inflammation,” appeared in September in the scientific journal Gastroenterology.
Hepatocytes are cells that play pivotal roles in liver function, including in metabolism, detoxification, protein synthesis and innate immunity.
An important player in the proper function of hepatocytes is an enzyme called adenosine kinase, ADK. However, the current study shows that ADK can also drive liver disease progression.
“We aimed to study whether hepatocyte ADK functions to promote excessive fat deposition and liver inflammation,” said Chaodong Wu, M.D., Ph.D., an AgriLife Research Faculty Fellow in the Texas A&M Department of Nutrition. Wu is also a Presidential Impact Fellow of Texas A&M University and the corresponding author for the study.
Wu said NAFLD is highly associated with obesity and progresses to an advanced stage when the liver develops overt inflammatory damage.

Researchers led by Rahel Marti at the University of Basel in Switzerland report that viewing, feeling, and touching real dogs leads to increasingly higher levels of activity in the prefrontal cortex of the brain. Published in PLOS ONE on October 5, the study shows that this effect persists after the dogs are no longer present, but is reduced when real dogs are replaced with stuffed animals. The findings have implications for animal-assisted clinical therapy.
Because interacting with animals, particularly dogs, is known to help people cope with stress and depression, researchers think that a better understanding of the associated brain activity could help clinicians design improved systems for animal-assisted therapy. The prefrontal cortex might be particularly relevant because it helps regulate and process social and emotional interactions.
In the study, activity in the prefrontal cortex of the brain was non-invasively measured with infrared neuroimaging technology as 19 men and women each viewed a dog, reclined with the same dog against their legs, or petted the dog. Each of these conditions was also performed with Leo, a stuffed lion with fur that was filled with a water bottle to match the temperature and weight of the dogs.
Results showed that prefrontal brain activity was greater when participants interacted with the real dogs, and that this difference was largest for petting, which was the most interactive condition. Another key difference was that prefrontal brain activity increased each time people interacted with the real dog. This was not observed with successive interactions with the stuffed lion, indicating that the response might be related to familiarity or social bonding.
Future studies will be needed to examine the issue of familiarity in detail and whether petting animals can trigger a similar boost of prefrontal brain activity in patients with socioemotional deficits.
The authors add: “The present study demonstrates that prefrontal brain activity in healthy subjects increased with a rise in interactional closeness with a dog or a plush animal, but especially in contact with the dog the activation is stronger. This indicates that interactions with a dog might activate more attentional processes and elicit stronger emotional arousal than comparable nonliving stimuli.”
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An epigenetics drug currently being used for the treatment of blood cancers and rare sarcomas can stop the growth of bladder cancer by activating the immune system, reports a new Northwestern Medicine study done in mice.
It’s the first time a drug used in hematologic malignancies and rare sarcomas has been used to treat one of the most common solid tumors. The drug, tazemetostat, was originally developed to treat lymphoma.
“We’ve discovered for the first time that the drug actually works by activating the immune system, not just by inhibiting the tumor,” said lead study author Dr. Joshua Meeks, an associate professor of urology and of biochemistry and molecular genetics at Northwestern University Feinberg School of Medicine and a Northwestern Medicine physician/scientist.
The study will be published Oct. 5 in Science Advances.
“We think the specific mutations that may make the drug successful are found in almost 70% of bladder cancers,” said Meeks, also a member of the Robert H. Lurie Comprehensive Cancer Center of Northwestern University.
Bladder cancer affects more than 700,000 individuals in the U.S. It is the sixth most common cancer overall and the fourth most common among men. More than 80,000 people in the U.S. are diagnosed yearly with bladder cancer.

Synthetic biology strives to achieve robust control of biological processes in order to create designer organisms for a variety of industrial, diagnostic, and therapeutic applications. Researchers at the iNANO center of Aarhus University have developed RNA origami sponges and CRISPR-based regulators for advanced genetic control of enzymatic pathways in microorganisms to improve production of valuable biochemicals.
Developing tools for precise control of biological processes has been one of the main pillars of the now mature field of synthetic biology. These scientific tools borrow principles from a multitude of research fields which when combined enable unique applications that are potentially transformative for the modern society. Translating modern RNA nanotechnology innovations in the biological context possesses immense potential due compatibility with folding and expression in cells, but also imposes unique challenges such as tight performance conditions and inherent instability of RNA molecules.
However, a recent structural RNA design approach developed in the Andersen lab, termed ‘RNA origami’, is trying to tackle this. This approach attempts to generate complex human-made RNA-based devices that are stable in cells, interact with other biomolecules, including other RNA and proteins, and enable unique applications, particularly in the context of gene regulation. Demonstrated by two distinct approaches recently published, RNA origami is presented as a sophisticated RNA design platform that when applied in the cellular context, generates unique molecules for synthetic biology-based regulation.
RNA sponges regulate enzyme production in bacteria
In the first approach, the RNA origami was used to achieve precise control of protein production levels when expressed in bacteria. Self-inhibiting protein expression cassettes were made by installing a strong binding site for the expressed protein in its own gene. Afterwards, RNA origami decorated with the same protein-binding sites was expressed in large excess. In this way, the RNA origami serves as a protein-sponge that sequesters proteins in the cell and allows expression of the self-inhibited protein. This general concept was shown to enable regulation of several proteins simultaneously and turn on enzymatic pathways for improved product yields.
CRISPR-based regulators for yeast chemical factories
In the second approach, RNA origami was combined with CRISPR, one of the most popular modern molecular biology techniques, to regulate gene expression in yeast. The RNA origamis were integrated in the small RNAs that guide CRISPR-Cas9 to target specific sequences in the DNA genome. The RNA origami scaffolds were decorated with protein-binding sites capable of recruiting transcription factors. By targeting the RNA scaffolds to promoter regions, the transcription factors activated gene expression. It was shown that the expression strength can be tuned by the orientation of the scaffold and the amount of transcription factors recruited. Finally, it was demonstrated that multi-enzyme pathways could be controlled for high-yield production of the anti-cancer drug violacein.
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Duke University researchers have developed an RNA-based editing tool that targets individual cells, rather than genes. It is capable of precisely targeting any type of cell and selectively adding any protein of interest.
Researchers said the tool could enable modifying very specific cells and cell functions to manage disease.
Using an RNA-based probe, a team led by neurobiologist Z. Josh Huang, Ph.D. and postdoctoral researcher Yongjun Qian, Ph.D. demonstrated they can introduce into cells fluorescent tags to label specific types of brain tissue; a light-sensitive on/off switch to silence or activate neurons of their choosing; and even a self-destruct enzyme to precisely expunge some cells but not others. The work appears Oct. 5 in Nature.
Their selective cell monitoring and control system relies on the ADAR enzyme, which is found in every animal’s cells. While these are early days for CellREADR (Cell access through RNA sensing by Endogenous ADAR), the possible applications appear to be endless, Huang said, as is its potential to work across the animal kingdom.
“We’re excited because this provides a simplified, scalable and generalizable technology to monitor and manipulate all cell types in any animal,” Huang said. “We could actually modify specific types of cell function to manage diseases, regardless of their initial genetic predisposition,” he said. “That’s not possible with current therapies or medicine.”
CellREADR is a customizable string of RNA made up of three main sections: a sensor, a stop sign, and a set of blueprints.

A new screening test app could help advance the early detection of Parkinson’s disease and severe COVID-19, improving the management of these illnesses.
Developed by a research team of engineers and neurologists led by RMIT University in Melbourne, the test can produce accurate results using just people’s voice recordings.
Millions of people worldwide have Parkinson’s, which is a degenerative brain condition that can be challenging to diagnose as symptoms vary among people. Common symptoms include slow movement, tremor, rigidity and imbalance.
Currently, Parkinson’s is diagnosed through an evaluation by a neurologist that can take up to 90 minutes.
Powered by artificial intelligence, the smartphone app records a person’s voice and takes just 10 seconds to reveal whether they may to have Parkinson’s disease and should be referred to a neurologist.
Lead researcher Professor Dinesh Kumar, from RMIT’s School of Engineering, said the easy-to-use screening test made it ideal to use in a national screening program.

As COVID-19 wreaks havoc across the globe, one characteristic of the infection has not gone unnoticed. The disease is heterogeneous in nature with symptoms and severity of the condition spanning a wide range. The medical community now believes this is attributed to variations in the human hosts’ biology and has little to do with the virus per se. Shedding some light on this conundrum are Associate Professor SUMI Tomonari from Okayama University, Research Institute for Interdisciplinary Science (RIIS) and Associate Professor Kouji Harada from Toyohashi University of Technology, the Center for IT-based Education (CITE). The duo recently reported their findings on imbalances in the host immune system that facilitate persistent or severe forms of the disease in some patients.
The researchers commenced their study by computer simulations with models based on a host’s immune system and its natural response to SARS-CoV-2 exposure. Mathematical equations for the dynamics of cells infected by SARS-CoV-2 were plugged in to predict their behavior. Now, the immune system has messenger cells known as dendritic cells (DCs). These cells report information (in the form of antigens) about the invaders to the warriors, or T cells, of the immune system. The model showed that at the onset of infection, DCs from infected tissues were activated and then antibodies to neutralize SARS-CoV-2 gradually started building.
To investigate long-term COVID-19, the behavior of DCs 7 months after infection was evaluated by the computer simulation. the baseline model simulation revealed that DCs drastically decreased during the peak of infection and slowly built up again. However, they tended to remain below pre-infection levels. These observations were similar to those seen in clinical patient samples. It seemed like low DC levels were associated with tenacious long-term infection.
The subsequent step was to understand if DC function contributed to disease severity. It was found that a deficiency of the antigen-reporting function of DCs and lowered levels of chemicals known as interferons released by them were related to severe symptoms. A decrease in both these functions resulted in higher amounts of virus in the blood (viral load). What’s more, the researchers also found two factors that affected the virus’s ability to replicate in the host, namely, antigen-reporting DCs and the presence of antibodies against the virus. Anomalies in these functions could hamper viral clearance, enabling it to stay in the body longer than expected, whereas a high ability of these immune functions suppresses viral replication and yields prompt viral clearance.
Components of immune signalling that directly affect the outcome of COVID-19 infection were revealed in this study. ” Our mathematical model predicted the persistent DC reduction and showed that certain patients with severe and even mild symptoms could not effectively eliminate the virus and could potentially develop long COVID,” concludes the duo. A better understanding of these immune responses could help shape the prognosis of and therapeutic interventions against COVID-19.
Background
Dendritic cells and the immune system: Dendritic cells (DCs) are part of the body’s innate immune system and are present in areas that come in close contact with pathogens such as the skin, respiratory tract, and gastrointestinal tract. When these tissues are infected, the DCs collate information about the pathogen and display it. DCs are now activated and transform into antigen-presenting cells (APCs). APCs then migrate to the lymph nodes where T cells reside to report this information. The T cells then migrate to and kill the invading pathogens. DCs also play a role in inflammation, a protective mechanism of the body, by releasing interferons. Interferons are chemical messengers that warn neighboring cells of a viral infection.
It is known that although the numbers of DCs do not change with age, their function is impaired. Since older patients have a higher proclivity for developing severe COVID-19, the patterns of DC function in severe infection were thus investigated by the computer simulation experiments.
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