“Lack of awareness about CVI is a large factor leading to it to be misdiagnosed or undiagnosed, which can mean years of frustration for children and parents who are unaware of an underlying vision issue and don’t receive help for it,” said report co-author, Lotfi B. Merabet, O.D., Ph.D., associate professor of ophthalmology, Massachusetts Eye and Ear and Harvard Medical School, Boston.

“Clarifying the factors for suspecting CVI should help build awareness and help eye care providers identify children for further assessment so they can benefit from rehabilitation and accommodation strategies as early as possible,” said report co-author, Melinda Y. Chang, M.D., assistant professor of clinical ophthalmology at the University of Southern California, Los Angeles.

Experts report that the five elements of CVI are:

• Brain Involvement: CVI encompasses a spectrum of visual impairments that involve an underlying brain abnormality affecting the development of visual pathways (the brain’s neural connections that process vision). In all people with CVI, these visual pathway abnormalities result in some degree of functional vision impairment, which interferes with how a person is able to use their vision for everyday activities.
• Visual dysfunction greater than expected based on eye exam: People with CVI may have a co-existing problem with their eyes. When the visual dysfunction is based primarily on a visual processing problem in the brain and cannot be explained by the ocular problem, CVI should be diagnosed.
• Types of visual deficits: CVI-related visual dysfunction can manifest as lower-order and higher-order visual deficits. Examples of lower-order deficits include impaired visual acuity (not seeing an eye chart clearly), reduced contrast sensitivity and reduced visual field (the scope of one’s vision). Higher-order deficits can include difficulty with face and object recognition, lessened ability to visually search for something or someone, difficulty with spatial orientation or complex motion perception, and seeing more than one object at a time.
• Distinguishing overlapping neurological disorders: While CVI can co-occur with other neurodevelopmental disorders, it is not primarily a disorder of language, learning, or social communication. Cerebral palsy is common among individuals with CVI, and autism and dyslexia can have overlapping manifestations with CVI. As a result, CVI is prone to misdiagnosis and underdiagnosis in children with other concurrent neurodevelopmental disorders.
• CVI is easily missed: The underlying neurological abnormality of a child’s developing brain may go unrecognized or undiagnosed until later in life when the individual is able to recognize and express their functional vision deficits. Screening for CVI should be considered in individuals who are at high risk of having had a neurological injury, such as infants born prematurely with periventricular leukomalacia, an abnormality of the brain’s ventricles found on imaging. However, current imaging technology is often not sufficient to diagnose CVI.

The CVI definition report is based on a workshop hosted by the NEI in partnership with the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the National Institute of Neurological Disorders and Stroke (NINDS).

In 2010, Jianxin Ma, a professor of agronomy, and his collaborators built the first reference genome for soybeans on the widely studied Williams 82 variety. Thousands of scientists and plant breeders have since used that genome in their own research on the genetic makeup underlying various characteristics, such as seed protein and oil content, plant architecture and productivity, and disease resistance and abiotic stress tolerance in soybeans.

Through the last decade, Ma, who is the Indiana Soybean Alliance Inc. Endowed Chair in Soybean Improvement, has been recognized internationally for his contribution to the soybean genome as well as for his continued research and innovation in the field. His most recent work, published in The Plant Cell, used advancements in genomic research to fill in gaps of the original soybean reference genome.

“The reference genome was like a dictionary when we announced it,” Ma said. “Each gene was like a single word. However, there was a piece of critical information lacking: transcription initiation sites for individual genes.”

Transcription initiation sites are locations in the DNA where a specialized transcription-factor protein can attach and then build an mRNA copy of the gene in front of it. That mRNA is read and translated at a cell’s ribosome to create more proteins, important for the chemical and physical function of every organism.

Knowing where the mRNA begins formation on the DNA strand is a significant part of understanding how genes are expressed. These initiation sites contain regulatory elements and provide information to the cell about when and where to transcribe each gene to make protein, and how frequently to do so at any point in time.

In genetics, it has generally been accepted that each gene has one transcription initiation site, located downstream of a core promoter region and typically around a TATA box — a DNA sequence rich in thymine and adenine repeats. But Ma and his colleagues no longer think this is the case.

“There is a set of predicted transcription start sites for over 50,000 genes in soy, but based on our new study, less than 3% of those predicted transcription initiation sites actually are correct,” Ma said.

In 2020, the development of the Survey of TRanscription Initiation at Promoter Elements Sequencing (STRIPE-seq) technique offered Ma’s lab an effective, efficient, faster and more affordable way to identify transcription initiation sites across the entire soybean genome. It also provided information about the relative abundance of every mRNA copy, which gives clues as to how much a gene is expressed in different tissues and times.

With funding from the United States Department of Agriculture’s National Institute of Food and Agriculture (USDA-NIFA) and the National Science Foundation, Ma and his lab performed STRIPE-seq analyses on eight different tissues in soybean: leaves, stems, stem tips, roots, nodules, flowers, pods and developing seeds. Even though the plant’s DNA is consistent across these tissues, the expression of genes differs.

In their recent paper, the Ma lab identified transcription initiation sites for about 40,000 genes in soy. They discovered widespread alternative transcription initiation sites outside of the TATA box region and other sequences thought to be promoters. Some newly identified sites actually occur in the coding sequence of the gene that becomes an mRNA. Thus, transcription-factor proteins can bind to several different sections of the gene and begin making mRNA, each copy different from ones started at other sites. Each alternative transcription site could potentially create a different protein from the same gene.

One specialized subset of transcription initiation sites the group found was in root nodules, a structure on legumes’ roots that harbors interaction between the plant and Rhizobia bacteria. These soil-dwelling microbes fix nitrogen for specialized plants like legumes in return for sugars and protection. This symbiosis increases a plant’s survival in nitrogen-deficient soils without the use of nitrogen fertilizers.

“We found these particular transcription initiating sites in nodules, but not in the roots or any other tissues, suggesting they are for tissue-specific transcription and associated with nodule-specific function,” said Ma.

In order for DNA to fit within a cell’s nucleus, it is wound up around histone proteins to form a structure called “chromatin.” Depending on chemical markers placed on these histones, the chromatin can be wound tightly — preventing transcription factors from binding — or loosely, making it accessible for generating mRNA copies. Ma believes that these “epigenetic” changes are working hand-in-hand with the alternative transcription initiation sites in gene expression. Different transcription initiation sites can become available as a gene is tightened or loosened, and different proteins may be created.

“We have found nearly 7,000 genes that have the alternative transcription initiation within the coding sequences. These alternative transcription initiation sites tend to be tissue-specific and associated with histone modifications,” Ma said.

Evolutionarily, these alternative sites may have been beneficial to soybeans and other plants because they allowed for increased complexity and adaptability under a limited genome. Soybeans have experienced two whole-genome duplication events throughout their history, both several millions of years ago. Although some of the duplicated genes have since been lost, Ma thinks the duplication events may have given rise to altered or alternative transcription sites.

“After duplication, the majority of genes are still in pairs; however, they show different expression patterns, and many have functionally diverged to regulate different traits,” Ma said. “They start to transcribe from different sites, potentially contributing to their functional divergence.”

Currently, Ma is coordinating with USDA Agricultural Research Service scientists Rex Nelson and Jacqueline Campbell on making this research data accessible for others, just as he did with the original reference genome. The group is adding the data to SoyBase, a collaborative online database for soybean research.

Nelson, curator of SoyBase, explained, “having even a potential transcription start site will aid in the analysis of soybean gene promoter regions. This may shed light on the proteins that interact with promoters and induce transcription.”

Campbell, co-curator of the database, added that “the identification of transcription factors that bind promoter regions will allow researchers to identify gene regulatory interaction networks involved in the complex regulation of genes in agronomical important phenotypes.”

Ma is honored to give to the research community again. “The database serves as an important resource for both basic and applied research,” he said. “By making our data available there, we catalyze further research in understanding gene functions, regulatory mechanisms, gene networks and genetic variations associated with specific traits of interest. As we better understand how these alternative transcription sites affect particular traits, the hope is to see this lead to better soybean varieties.”

Cardiovascular disease and dementia are major public health challenges that cause a significant burden on both healthcare and society. A new study from Karolinska Institutet in Sweden shows that long-term use of common cardiovascular drugs is associated with lower risk of dementia later in life.

“We can see a clear link between long-term use — five years or more — of these drugs and reduced risk of dementia in older age,” says Mozhu Ding, assistant professor at the Institute of Environmental Medicine, Karolinska Institutet, and one of the lead authors of the paper.

The researchers used Swedish national registers. Around 88,000 people over the age of 70 who were diagnosed with dementia between 2011 and 2016 were included in the study, as well as 880,000 controls. Information on cardiovascular medicines was obtained from the Swedish Prescribed Drug Register.

The results show that long-term use of antihypertensive drugs, cholesterol-lowering drugs, diuretics and blood-thinning drugs is associated with between 4 and 25 percent lower risk of dementia. Combinations of the drugs had stronger protective effects than if they were used alone.

“Previous studies have focused on individual drugs and specific patient groups but in this study, we take a broader approach,” says Alexandra Wennberg, affiliated researcher at the Institute of Environmental Medicine and the other lead author of the paper.

The researchers also found that, on the contrary, the use of antiplatelet drugs may be linked to a higher risk of dementia. Antiplatelet drugs are medicines used to prevent strokes and stop platelets from clumping together. One possible explanation is that these drugs increase the risk of microbleeds in the brain, which are associated with cognitive decline.

The study is an important piece of the puzzle for finding new treatments for dementia, according to the researchers.

“We currently have no cure for dementia, so it’s important to find preventive measures,” says Alexandra Wennberg.

The researchers stress the importance of further studies, especially randomised controlled clinical trials, to better understand the mechanisms behind the findings. Among other things, they will continue to study how diet and lifestyle, in addition to drug treatment for cardiovascular disease, affect the risk of developing dementia.

The research was carried out by Karolinska Institutet and Lund University with research funding from Karolinska Institutet. Alexandra Wennberg has received funding from Janssen Phamaceutica NV for an unrelated project. No other potential conflicts of interest are disclosed.

This innovative framework has the potential to significantly improve approaches to personal development, as well as the clinical treatment of compulsive disorders (for example obsessive compulsivedisorder, addiction, and eating disorders).

The research was led by Dr Eike Buabang, Postdoctoral Research Fellow in the lab of Professor Claire Gillan in the School of Psychology and has been published as a paper, Leveraging cognitive neuroscience for making and breaking real-world habits, in the journal Trends in Cognitive Sciences.

Dr Buabang explains: “Habits play a central role in our daily lives, from making that first cup of coffee in the morning, to the route we take to work, and the routine we follow to prepare for bed. Our research reveals why these automatic behaviours are so powerful — and how we can harness our brain’s mechanisms to change them. We bring together decades of research from laboratory studies as well as research from real-world settings to get a picture of how habits work in the human brain.”

Our habits are shaped by two brain systems — one that triggers automatic responses to familiar cues and another that enables goal-directed control. So for example, scrolling through social media when you are bored is the result of automatic response system, and putting your phone away to focus on work is enabled by the goal-directed control brain system.

It is precisely the imbalance between these two brain systems that is key. The research found that such imbalance can lead to everyday action slips such as inadvertently entering an old password instead of the current one. In more extreme cases, Professor Gillan’s research has shown that it can even contribute to compulsive behaviours seen in conditions such as obsessive compulsivedisorder, substance use disorders, and eating disorders.

Habits happen when automatic responses outweigh our ability to consciously control them. Good and bad habits are two sides of the same coin — both arise when automatic responses overpower goal-directed control. By understanding this dynamic, we can start to use it to our own advantage, to both make and break habits.

The new framework describes several factors that can influence the balance between automatic responses and goal-directed control:

• Repetition and reinforcement are essential to making our habits stick. Repeating a behaviour builds strong associations between environmental cues and responses, while rewarding the behaviour makes it more likely to be repeated. In leveraging the same mechanism to break habits, we can replace old behaviours with new ones to create competing automatic responses.
• The environment also plays a key role in habit change. Adjusting your surroundings can help; making desired behaviours easier to access encourages good habits, while removing cues that trigger unwanted behaviour disrupts bad habits.
• Knowing how to engage your own goal-directed system can help strengthen and weaken habits. Disengaging from effortful control, such as listening to a podcast while exercising, accelerates habit formation. However, stress, time pressure, and fatigue can trigger a return to old patterns, so staying mindful and intentional is key when trying to break them.

Dr Buabang explains, “Our research provides a new ‘playbook’ for behaviour change by connecting brain science with practical, real-world applications. We include effective strategies like implementation intentions, so-called, if-then plans (“if situation X occurs, then I will do Y”), and also integrate clinical interventions such as exposure therapy, habit reversal therapy, contingency management, and brain stimulation. It is important that our framework not only captures existing interventions but also provides targets for the development of new ones.”

This research also opens new possibilities for personalising treatments based on how different people form and break habits, making interventions more effective. Professor Gillan explains “We are all different; depending on your neurobiology, it might make more sense to focus on avoiding cues than reducing stress or allowing yourself more time for your daily routine.” Beyond individual treatment, these insights could reshape public health strategies. Understanding the brain’s role in habit formation could help policymakers design more effective health campaigns, from encouraging regular exercise to reducing sugar consumption.

“By working with, rather than against, how our brains naturally form habits, we can create strategies that make healthier choices more automatic at both individual and societal levels.”

A single intranasal dose of EV25, a bispecific small molecule developed by Eradivir, acts faster than the current standard of care, eliminating the detectable virus within 24 hours. EV25 also has a window of efficacy of 96 hours postinfection, which is broader than the current standard of care.

A research paper titled “Targeted recruitment of immune effector cells for rapid eradication of influenza virus infections” has been published in the peer-reviewed Proceedings of the National Academy of Sciences.

EV25 was built on a platform created by Philip Low, the Presidential Scholar for Drug Discovery and the Ralph C. Corley Distinguished Professor of Chemistry in Purdue University’s College of Science. He is part of Purdue’s One Health initiative and on the faculty of the Purdue Institute for Drug Discovery and the Purdue Institute for Cancer Research. Low is Eradivir’s chief scientific officer and on its board of directors.

He disclosed the immunological innovations to the Purdue Innovates Office of Technology Commercialization, which has applied for patents to protect the intellectual property. OTC licensed the innovations to Eradivir for further development and commercialization.

Serious threats posed by influenza

Imrul Shahriar, a scientist at Eradivir, said the influenza virus remains a serious health threat for multiple reasons. One is that current FDA-approved drugs are only effective when administered early during an influenza infection, but they are less effective when administered in later stages of the disease.

“This emphasizes the need for a therapy that can treat more severe infection,” he said. “Familiarity with influenza may mollify public concerns about its risk, but infections still cause tens of millions of illnesses and medical visits annually in the United States, hundreds of thousands of hospitalizations, and tens of thousands of deaths.”

Other reasons influenza remains a serious health problem are:

• Only 50% of people in the U.S. get vaccinated, and the effectiveness of current vaccines ranges from only 19% to 60%.
• Current therapies are less effective against some strains of the flu as they mutate.
• Pandemic strains of the flu like the current H5N1 avian strain may mutate enough to be transmitted from animals to people and eventually from people to people. They are now being transmitted to dairy cattle that, in turn, are infecting people.

Developing and testing EV25

Shahriar, who recently earned his PhD in Low’s laboratory, said EV25 reduces viral loads of advanced-stage influenza in two ways.

“It binds and inhibits viral neuraminidase expressed on both free virus particles and virus-infected cells,” he said. “It also recruits naturally occurring antibodies to fight the virus.”

Shahriar said tests showed EV25 lowered secretions of pro-inflammatory markers and protected against virus-induced damage to lungs better than current therapies.

“As a result, we believe that combining an immunotherapy with a chemotherapy in a single pharmacological agent constitutes a promising new approach for treating the more challenging forms of influenza virus infection,” he said.

Next development steps

Recently EV25 was approved by the European and Belgian regulatory agencies to be used in a Phase 1 human trial that will conclude early next year. Shortly following the Phase 1 trial, a Phase 2a trial will be conducted to further establish the safety and begin to define the efficacy of EV25. Data from the Phase 2a will be available in July 2025.

Eradivir at OPTIONS XII

Jeffery Nielsen, vice president for research and development at Eradivir, presented information on two Eradivir drug compounds during OPTIONS XII, a global scientific conference focused on influenza held Sept. 29-Oct. 2 in Brisbane, Australia.

The poster presentation “Ligand-Targeted Immunotherapy for the Rapid Clearance of Influenza Infections” disclosed data about EV25. It won the Best in Clinical Science and Vaccinology award at the conference.

The oral presentation “Novel Ligand-Targeted Immunotherapy for the Treatment of Human Respiratory Syncytial Virus (RSV)” disclosed data about Eradivir’s small-molecule therapy to treat human RSV infections in all age groups.

Both EV25 and the RSV therapeutic are built on the BAiT platform, or Bispecific Antigenic immunoTherapy, developed at Purdue.

“It was tremendous that presentations about both therapeutics were accepted at OPTIONS XII, the premier conference on influenza and respiratory viruses,” Nielsen said. “EV25 is a game changer in how effective it is compared to existing therapeutics in preclinical models. The RSV drug is another game changer because it rapidly clears out infection in preclinical models; there are currently no therapies to treat a person who has been infected with RSV.”

A new study reveals that piangua populations are showing concerning signs of decline, largely due to overharvesting. Researchers used cutting-edge DNA analysis to examine these shellfish in two key locations along Colombia’s Pacific coast, providing the first detailed genetic profile of these important creatures.

The findings paint a worrying picture. “While piangua populations have been stable for over 100,000 years, recent decades of intensive harvesting have taken their toll,” explained Silvia Restrepo, president of the Boyce Thompson Institute and lead author of the study.

The numbers are striking. Piangua exports from Colombia skyrocketed from just 100 tons per year in 1980 to over 3,000 tons by 2004. In some areas, like Bahía Málaga, the population has plunged by 60%. This dramatic increase in harvesting has forced the piangua onto Colombia’s endangered species list.

“We discovered that the piangua are experiencing a significant loss of genetic diversity,” said Restrepo. “This is evidenced by a high level of inbreeding and a reduction in heterozygosity.”

Why is genetic diversity so important? Imagine the gene pool of a species as a deck of cards. Each card represents different genetic traits that help the species survive various challenges — disease resistance, temperature tolerance, or the ability to find food. When overharvesting reduces the population, it’s like removing cards from the deck. With fewer “cards” in play, the species becomes less equipped to handle new threats.

The study, recently published in Scientific Reports, also revealed something unexpected. Despite living in connected coastal waters, piangua populations in different areas maintain subtle genetic variations. This suggests that local populations might have special adaptations to their specific environments, making it even more crucial to protect them all.

This research has real-world implications for conservation. Equipped with this new genetic information, scientists, the Colombian government, and local communities can work together to develop better protection strategies. These might include creating protected areas, establishing sustainable harvesting quotas, or implementing restoration programs.

The study marks a significant milestone as the first genetic investigation of piangua in Colombia, complete with the first detailed mapping of its genome. This genetic blueprint will be an invaluable tool for future conservation efforts.

The message is clear for the communities along Colombia’s Pacific coast: without immediate action to protect these vital shellfish, they risk losing not just an important food source, but a crucial part of their cultural and economic heritage. The race is on to save the piangua while there is still time.

This research was funded by the Ministerio de Ciencia, Tecnología e Innovación (MinCiencias) of Colombia.