Category: 8. Health

Alzheimer’s disease (AD) is a common, debilitating neurodegenerative disease affecting about 10 percent of people over the age of 65 and one third of people aged 85 and above. Besides environmental factors, the genes have a strong influence on whether or not a person develops AD during their lifetime. Through genome sequencing of DNA from large groups of healthy people and people with AD, some naturally occurring small changes in the DNA, known as genetic variants, were found to be more frequent in AD patients than in healthy people. As more and more of these AD-associated genetic “risk” variants are discovered, it is now possible to calculate a person’s individual polygenic risk score (PRS), meaning the likelihood of the person to develop AD, with high accuracy. Despite this progress, it is still largely unknown how genetic risk variants, or combinations thereof, cause AD in individual patients and more specifically, how risk variants impact the health and function of brain cells.

To address this, researchers in the UK Dementia Research Institute at Cardiff University, UK, have now generated the first large-scale stem cell bank from over 100 individuals selected for extremes of AD PRS, which had previously been determined by genome sequencing. The results of the work are published today in Stem Cell Reports. About two thirds of the donors had been diagnosed with AD and had a relatively high PRS while one third were cognitively healthy, age-matched individuals with a low PRS. Blood cells from these individuals were genetically engineered to turn them into induced pluripotent stem cells (iPSCs), which are immature cells capable of generating all cell types of the body. The new “iPSC Platform to Model Alzheimer’s disease Risk” (IPMAR) resource will be made available to researchers worldwide to facilitate studies on the impact of risk variants in iPSC-based cellular models of AD in the lab. Ultimately, the resource can be used to increase our understanding of genetic risk factors linked to AD, and may inform the design of new, individualized treatments or prevention strategies.

CINCINNATI, July 4, 2025 /PRNewswire/ — During the COVID-19 pandemic, scientists learned that the critical path to infection started with the SARS-CoV-2 virus invading the nasal tissues of its victims, then causing millions of deaths by spreading through the body and robbing the sickest people of their ability to breathe.

While the traditional way to administer protection has been to inject vaccines into the bloodstream, many experts called for developing a nasally delivered vaccine as a potentially more-effective approach. Now, encouraging results are in from the first human clinical trial to be conducted in the United States of a nasal COVID vaccine. Findings from the study led by an expert at Cincinnati Children’s were published July 4, 2025, in Science Advances.

“A single dose of this vaccine (CVXGA) was well tolerated. It generated a wide spectrum of specific immune responses including mucosal and systemic immune responses. Those who received the highest dose of the vaccine showed significantly lower rates of symptomatic COVID-19 infection,” says the study’s lead author, Paul Spearman, MD, a long-time leader in vaccine research and vice chair for clinical and translational research and education at Cincinnati Children’s.

The vaccine is made by the Georgia-based company CyanVac LLC, which also funded the clinical trial. Based on the promising data generated from this phase 1 trial, two larger clinical studies involving more people are underway (NCT05736835 and NCT06742281).

If these trials also prove successful, the CVXGA vaccine could join four other nasal COVID vaccines approved in other countries: two in China, one in Russia, and another in India.

Why is a nasal vaccine needed?

While the total number of deaths from COVID has declined far from the peak pandemic years, the virus has not disappeared. In fact, 663 Americans died of COVID in the 28 days ended June 15, 2025. Those deaths (which in one month exceeded the combined deaths of the three deadliest plane crashes since 2022) accounted for 67% of the 987 total deaths worldwide reported to the World Health Organization.

India (101 deaths) was the only other nation reporting more than 100 COVID deaths in this timeframe, and its population is more than four times larger than the US. The wealthy Western nation Sweden reported 22 deaths. 

Since the pandemic began, the virus has mutated several times. This has required adjusting the vaccine and suggests that annual re-vaccination may be needed to prevent another pandemic. A nasal vaccine could prove both more effective medically and more tolerable for young children and adults who may fear needles.

“There is a need for improved COVID vaccines that offer more complete and durable protection,” Spearman says. “A nasal vaccine has the potential to block SARS-CoV-2 at its mucosal entry site and to reduce transmission of the virus to others.”

How effective was the nasal vaccine?

The clinical trial included 72 people who received vaccinations, with ages ranging from 12 to 53. A total of 61 participants completed the entire trial. During the period of the trial from September 2021 to May 2023, various waves of SARS-CoV-2 variant infections emerged in the US.

Participants were divided among four groups. One group received a low dose of the vaccine, which served as a control group. The other three higher dose groups included one group of adults that had never been infected or had not been vaccinated recently; a group of adults that had been recently vaccinated with a previous mRNA vaccine; and a group of teens that also had been vaccinated.

Overall, about 25% of recipients reported having a runny nose after the vaccine; 8% reported nausea. None had a fever.

The researchers found evidence that the vaccine was absorbed in the nasal tissues, and that it generated statistically significant antibody responses, as intended.

CVXGA1 produced a combined 51.9% mucosal antibody response rate across the three higher dose groups, compared to just 21.4% in the lower dose group.

The low-dose group (Group 1, enrolled from September 2021 to February 2022) had the highest overall COVID-19 infection rate: 73.3%. The other three groups had infection rates ranging from 11.1% to 22.2%. None of those found to be infected required hospital care.

The results suggest that the vaccine reduced the risk of infection by at least 67% compared to never being vaccinated before. However, definitive proof of efficacy will require larger trials designed specifically for this purpose.

What’s next?

By design, a phase 1 clinical trial involves low numbers of participants. However, the results were encouraging enough to recommend moving ahead with larger clinical trials.

The largest of the two ongoing trials (NCT06742281) seeks to enroll up to 10,016 participants by mid-2026 with the study completed by mid-2027.

SOURCE Cincinnati Children’s Hospital Medical Center

New research analyzing an online survey of 1,633 respondents found 15% recent use of doxycycline post- and pre-exposure prophylaxis (doxyPEP/PrEP) among men who have sex with men (MSM), transgender and gender diverse people in the Netherlands according to a recent study published by Eurosurveillance. These data highlight an increase in the informal use of doxyPEP/PrEP, with 65% of the participants intending to use it in the future. Currently, doxyPEP/PrEP is not recommended or actively promoted by healthcare professionals in the Netherlands. Informal use i.e. without a prescription by a healthcare professional, could contribute to antimicrobial resistance (AMR) and changes in the microbiome.

The use of doxyPEP has been shown to be an effective method in the prevention against sexually transmitted infections (STIs) in MSM, transgender and gender diverse persons. Clinical trials of doxyPEP have shown significant reductions in syphilis and chlamydia, with additional potential to reduce incidence of other bacterial STIs such as chlamydia and gonorrhea

However, the public health implications of the widespread use of doxyPEP are subject to current debate. The administration of doxyPEP to specific individuals could prevent a substantial number of STIs and lower antibiotic use, particularly among those who repeatedly have STIs.

Informal doxyPEP/PrEP use associated with HIV PrEP use, sexualized drug use and perception of safety

As highlighted by this paper and an accompanying editorial by Lyons et al., the prescription of doxyPEP to many sexually active individuals poses the risk of a substantial population-level increase in overall antibiotic consumption and an increase in AMR.

Teker et al. reviewed data from a cross-sectional study gathered from an online survey among MSM, transgender and gender diverse persons of 18 years of age or older. The survey focused on previous use of doxyPEP or doxyPrEP awareness and intention to use it. Participants were recruited through advertisements at the Centre for Sexual Health in Amsterdam, the Netherlands, as well as dating apps (Grindr), Instagram, Facebook, Facebook Messenger and targeted Instagram accounts.

In the study, 23% of participants reported having ever used doxyPEP/PrEP and 15% reported having used doxyPEP/PrEP in the six months prior to the survey. Respondents informing about recent use were more likely to report living with HIV or frequently using oral HIV PrEP in the six months before taking the survey. They were also more likely to report a history of bacterial STIs, having a higher number of sexual partners, and a higher frequency of engaging in chemsex and in group sex during that period.

Doxycycline was the most used antibiotic reported in this study, with 46% of the participants reporting using it recently as PEP, 29% of recent PEP users using it as PrEP and 25% using it as a combination of both. 

Overall, the intention to use doxyPEP/PrEP was very high among the study population, with more than half of the participants (65%) expressing intention to use. More than two thirds of respondents (72%) were willing to pay for doxyPEP/PrEP if it became formally available, indicating a potential demand for the drug among the study population and beyond. 

It was also found that doxyPEP/PrEP was primarily obtained from countries outside of the Netherlands or through prescriptions, with participants paying on average €30 for the drug.

Additional determinants for both informal use of doxyPEP/PrEP and high intention to use included using oral HIV PrEP or living with HIV, receiving advice from others to use doxyPEP/PrEP and perceiving doxyPEP/PrEP as an effective and safe method of STI prevention.

Potential antimicrobial resistance risks from lack of monitoring

The impact of prophylactic antibiotic use on AMR was highlighted in the study as there are uncertainties regarding the long-term adverse effects of doxyPEP/PrEP use. Teker et al. emphasize the potential harms of doxycycline effectiveness and AMR risks, as summarised in previous studies including in the United States. 

They also cite its potential effects on the gut microbiome, which need to be studied further. If doxyPEP is implemented in country-wide clinical guidance, it would be vital to monitor both individual and population-level resistance to doxycycline.

Lack of awareness on the extent of informal use of doxyPEP/PrEP makes it difficult to monitor and implement appropriate public health stewardship. This leads to difficulties in detecting overuse, misuseand adverse effects including AMR development and effects on microbiome composition.

A study has shown that neurons or nerve cells continue to form well into late adulthood in the brain’s hippocampus, which manages memory—a finding that presents compelling new evidence about the human brain’s adaptability.

Neurogenesis—a process whereby new neurons are created—is said to continue throughout one’s life, even as the rate is considered to slow down with age.

However, researchers from Karonlinska Institutet in Sweden said the extent and significance of neurogenesis is still debated with no clear evidence of cells that precede new neurons—or ‘neural progenitor cells’—actually existing and dividing in adults.

“We have now been able to identify these cells of origin, which confirms that there is an ongoing formation of neurons in the hippocampus of the adult brain,” Jonas Frisen, professor of stem cell research, Karolinska Institutet, who led the research published in the journal Science.

The team used carbon dating methods to analyse DNA from brain tissue, which made it possible to determine when the cells were formed. Tissue samples of people aged 0 to 78 were obtained from international biobanks, they said.

The results showed that cells that precede the forming of new neurons in adults are similar to those mice, pigs and monkeys, with differences in genes which are active.

The researchers also found large differences between individuals—some adult humans had many neural progenitor cells, others hardly any at all.

Frisen added that the study is an “important piece of the puzzle in understanding how the human brain works and changes during life”, with implications for developing regenerative treatments in neurodegenerative and psychiatric disorders.

A steady loss of neurons resulting in an impaired functioning and eventually cell death is said to drive neurodegenerative disorders, which affects the hippocampus, among other brain regions. Risks of the disorders are known to heighten with age.

For the study, the researchers used a method called ‘single-nucleus RNA sequencing’, which looks at activity of a gene in a cell’s nucleus.

This was combined with machine learning (a type of AI) to discern varied stages of how neurons develop, from stem cells to immature neurons, many of which were in the division phase, the team said.

“We analysed the human hippocampus from birth through adulthood by single-nucleus RNA sequencing. We identified all neural progenitor cell stages in early childhood,” they wrote.

“In adults, using antibodies against the proliferation marker Ki67 and machine learning algorithms, we found proliferating neural progenitor cells,” the authors wrote.

“The results support the idea that adult neurogenesis occurs in the human hippocampus and add valuable insights of scientific and medical interest,” the study said.

The Synaptic Physiology laboratory, led by Juan Lerma at the Institute for Neurosciences (IN), a joint center of the Spanish National Research Council (CSIC) and Miguel Hernández University (UMH) of Elche, has discovered that a specific group of neurons in the amygdala, a brain region involved in emotion regulation, plays a key role in the emergence of conditions such as anxiety, depression, and altered social behavior. This study, published in iScience, shows that restoring the neuronal excitability balance in a specific area of the amygdala is enough to reverse these behaviors in mice.

We already knew the amygdala was involved in anxiety and fear, but now we’ve identified a specific population of neurons whose imbalanced activity alone is sufficient to trigger pathological behaviors.”

Juan Lerma, Institute for Neurosciences (IN), a joint center of the Spanish National Research Council (CSIC)

His team utilized a genetically modified mouse model to overexpress the Grik4 gene, thereby increasing the number of GluK4-type glutamate receptors and raising neuronal excitability. These animals, developed by the same lab in 2015, show anxiety and social withdrawal behaviors very similar to those observed in individuals with disorders such as autism or schizophrenia.

The researchers normalized the gene’s expression specifically in neurons of the basolateral amygdala, which restored communication with another group of inhibitory neurons in the centrolateral amygdala known as ‘regular firing neurons’. “That simple adjustment was enough to reverse anxiety-related and social deficit behaviors, which is remarkable”, says Álvaro García, first author of the study.

The animals were evaluated using electrophysiological techniques and behavioral tests that measure anxiety, depression, and social interaction in rodents, based on their preference for exploring open spaces or their interest in unfamiliar mice. Then, using genetic engineering and modified viruses, the scientists selectively corrected the alteration in the basolateral amygdala and observed changes in both neuronal activity and the animals’ behavior.

They also applied the same procedure to wild-type mice that displayed intrinsic anxiety, and it was also effective in reducing their anxiety. “This validates our findings and gives us confidence that the mechanism we identified is not exclusive to a specific genetic model, but may represent a general principle for how these emotions are regulated in the brain”, Lerma adds.

Some behavioral deficits, such as object recognition memory, were not resolved, suggesting that other brain areas, such as the hippocampus, may also be involved in these disorders and remain uncorrected. The study opens the door to new therapeutic possibilities: “Targeting these specific neural circuits could become an effective and more localized strategy to treat affective disorders”, the researcher concludes.

This work was possible thanks to funding from the Spanish State Research Agency (AEI) – Spanish Ministry of Science, Innovation and Universities, the Severo Ochoa Excellence Program for Research Centers at the Institute for Neurosciences CSIC-UMH, the European Regional Development Fund (ERDF), and the Generalitat Valenciana through the PROMETEO and CIPROM programs.

Although the last 50 years have seen a decrease in heart disease deaths, chronic disease mortality has concurrently risen in a trade-off from more patients surviving events such as heart attacks.

According to a recent study, heart disease accounted for 41% of all deaths in the US in 1970; by 2022, it accounted for 24% of all deaths. The proportion of deaths caused by acute myocardial infarctions (AMI) dropped by almost 90% during this period. However, chronic heart diseases, such as heart failure, hypertensive heart disease, and arrhythmias, are rising substantially in the American population.1

“People are now surviving these acute events, so they have the opportunity to develop these other heart conditions,” said Sara King, MD, a medical resident of Stanford University of Medicine and lead author of the study.1

Investigators collected data from the National Vital Statistics System Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research database, examining adults ≥ 25 years of age in the US from 1970 to 2022. Investigated outcomes included absolute number and age-adjusted mortality of total heart disease, ischemic heart disease, and other subtypes.2

During the indicated time, the US population > 25 years of age increased from 108.9 million to 229 million. Life expectancy likewise increased from 70.9 years to 77.5 years. The National Vital Statistics System recorded a total of 119,152,492 deaths, with 37,276,835 (31%) attributed to heart disease. In 1970, 733,273 heart disease deaths were recorded, of which 666,257 (91%) were ischemic and 67,016 (9%) were from other diseases. In 2022, investigators found 701,443 heart disease deaths, of which 371,360 (53%) were ischemic and 330,083 (47%) were from other heart diseases.2

Age-adjusted mortality for AMI also decreased by 89%, from 354 per 100,000 in 1970 to 40 per 100,000 in 2022. Average annual percentage change (AAPC) for AMI was -4.2% (95% CI, -4.3 to -4.1) from 1970 to 2022. Age-adjusted mortality for chronic ischemic heart disease fell by 71%, from 343 per 100,000 to 98 per 100,000. AAPC for chronic ischemic heart disease was -2.5% (95% CI, -2.6 to -2.4).2

Notably, investigators also saw age-adjusted mortality for other heart disease subtypes increase by 81%, from 68 per 100,000 to 123 per 100,000. AAPC for other heart disease subtypes was 1.2% (95% CI, 1.1 to 1.2). Heart failure, hypertensive heart disease, and arrhythmia had the greatest mortality increases, with age-adjusted mortality rising from 13 to 32 per 100,000 (146% increase), 16 to 33 per 100,000 (106% increase), and 2 to 11 per 100,000 (450% increase).2

Additionally, the rise in non-ischemic heart disease deaths reflects a rise in risk factors including obesity, diabetes, hypertension, and physical inactivity, according to King and colleagues. Roughly 50% of adults have diabetes or pre-diabetes, and 40% have obesity.1

While investigators noted the reduction in heart disease mortality over the last 50 years may be indicative of success in medical and public health interventions, they also indicated the emerging challenges presented by chronic ischemic heart disease and similar conditions. They suggest several possible explanations for the shift; interventional methods to reduce mortality from AMI, improvement in cardiac imaging, and the development of beta blockers, renal-angiotensin-aldosterone system inhibitors, and others.2

“We have so many tools in our toolbox now, but still, there’s a lot more that can be developed and improved,” King said. “I hope the numbers just keep getting better.”1

References

1. Standford Medicine. As fewer Americans die from heart attacks, more succumb to chronic heart disease. Eurekalert! June 25, 2025. Accessed July 2, 2025. https://www.eurekalert.org/news-releases/1088540

2. King SJ, Wangdak Yuthok TY, Bacong AM, et al. Heart disease mortality in the United States, 1970 to 2022. Journal of the American Heart Association. 2025;14(13). doi:10.1161/jaha.124.038644

Journal: JSES Reviews, Reports & Techniques

Title: Mechanisms and Trends of Pediatric Clavicular Fractures in the United States: A 10-Year Epidemiologic Analysis of National Injury Data

Authors: Charu Jain, MD candidate at the Icahn School of Medicine at Mount Sinai

Sheena Ranade, MD, Associate Professor of Orthopedics (Pediatric Orthopedic Surgery) at the Icahn School of Medicine at Mount Sinai

Bottom line: Clavicular fractures are common injuries among children, usually due to sports-related trauma or accidental falls. The purpose of this study was to assess the epidemiology of clavicular fractures among children in the United States between 2014 and 2023.

Why this study is unique: This study is the first of its kind to analyze 10 years of national emergency department data on pediatric clavicle fractures in the United States.

Why the study is important: Understanding how and where children sustain clavicular fractures helps guide injury prevention, especially in sports and at home. The rise in hospital admissions over the course of this study underscores a need to examine why these injuries may be getting more severe.

How the research was conducted: Data were extracted from the National Electronic Injury Surveillance System (NEISS), a publicly available database representing approximately 100 emergency departments in the United States. NEISS was queried for all shoulder fractures in patients 0-18 years old. These fractures were then filtered for clavicle fractures. Queries were restricted to fractures from January 1, 2014, to December 31, 2023.

Results: The findings show that while overall rates for pediatric clavicular fractures remained stable over the course of the study, there was a statistically significant increase in hospital admissions due to those injuries during that same period. This suggests an increase in severity of those injuries necessitating admission.

What this study means for doctors: The data suggest that pediatric clavicular fractures may be becoming more severe, which calls for better injury prevention and management strategies for doctors, parents, and patients. For physicians, this requires careful assessment and more intensive treatment or monitoring as needed. This study provides valuable insight into where pediatric clavicle fractures are treated-whether in emergency departments, outpatient clinics, or primary care-which can help guide resource allocation for health systems and improve care pathways for patients. Since many clavicle fractures in children heal well without surgery, understanding treatment settings can support better patient management, reduce unnecessary ED visits, and optimize follow-up care.

What this study means for patients: For patients and their parents, the findings emphasize that while many clavicular fractures may heal, some may require closer care or even hospitalization. The findings also emphasize the need for rigorous safety protocols during play and sports to reduce injury risk.

What the next steps are for this work: Next steps include using this data to investigate whether clavicular fracture cases presenting to the ED are more severe or more likely to require surgery compared to those seen in outpatient settings. We also aim to identify how many cases go untreated and explore whether specific injury patterns or treatment settings correlate with better long-term outcomes. This will help refine clinical decision-making and improve care strategies for pediatric clavicular fractures.

Quotes:

“Our review of recent national data on pediatric clavicle fractures demonstrates that among younger children, there has been an increase in bed-related falls causing clavicular fractures,” says Dr. Ranade. “Just as there has been a strong emphasis on safe sleep for infants, this study shows that attention should be placed in safe sleeping environments for toddler aged children to prevent falls out of bed.”

“Understanding common mechanisms like sports injuries and falls from beds can help guide targeted prevention strategies and parent education,” says Ms. Jain. “I would like to thank the Mount Sinai Department of Orthopedics for their support, our co-authors for their contributions, and Dr. Ranade for her guidance and mentorship throughout this project.”

Can research into a rare, accelerated aging disease and “zombie cells” teach us something about the normal aging process?

Did you know that a small molecule called NAD⁺ plays a critical role in our ageing process? A deficiency of this molecule may cause you to age much faster than normal. Imagine your cells stopping energy production or your DNA struggling to repair itself. This is the harsh reality of aging, as well as the experience of individuals with Werner syndrome, a rare and severe genetic disorder that leads to premature aging.

Now, in groundbreaking studies, researchers have found that NAD⁺ supplementation could be a potential treatment for these accelerated aging diseases. The study on NAD+ deficiency in Werner syndrome was published in the leading aging journal Aging-US.

The reality of Werner syndrome

“Werner syndrome is an adult-onset progeria where individuals age more rapidly. By their 20s and 30s, the patients start to show greying and loss of hair, wrinkles, and appear much older than their actual age,” explains Dr. Sofie Lautrup, a postdoctoral researcher at the Department of clinical molecular biology at the University of Oslo and Akershus University Hospital. Patients with Werner syndrome experience typical age-related diseases and life-threatening complications as early as in their 30s-40s, accompanied by significant changes in cellular metabolism, which means that the cells no longer behave normally.

“Our research has found that one reason for this is that they have lower levels of NAD⁺ in their mitochondria, the body’s cellular powerhouse,” Lautrup shares.

Dr. Lautrup and her colleagues have analysed cells from patients with Werner syndrome in the lab. Their research reveals, for the first time, that these individuals have decreased NAD⁺ levels in their mitochondria compared to healthy individuals. This supports their previous findings on dysregulated NAD⁺ metabolism and mitochondrial function in premature aging.

The promise of NAD⁺, a vital molecule in life

The researchers investigated whether supplementing NAD⁺ could restore normal cellular function and achieved remarkable results. “We found that supplying NAD⁺ can stimulate stem cell growth and inhibit the premature ageing process in stem and skin cells from patients,” Lautrup elaborates. This suggests that NAD⁺ supplementation could be a potential treatment for Werner syndrome patients. But could NAD⁺ also significantly impact normal aging?

So, what exactly is NAD⁺, and why is it essential for our bodies? NAD⁺ is a molecule found in all living cells, which plays a vital role in numerous cellular functions. “We need NAD⁺ to produce energy in our cells. It contributes to cellular health and metabolism by eliminating damaged mitochondria and plays several other critical roles in our cells,” explains Lautrup, adding, “Without NAD⁺, we literally cannot live.”

Thus, despite its small size, NAD⁺ has a monumental effect on the body, acting as an invisible force driving key metabolic processes.

Using Werner Syndrome to understand aging

As natural aging occurs, our NAD⁺ levels substantially decline. Previously, Lautrup and her team observed that patients with Werner syndrome also have significantly lower NAD⁺ levels in their blood. This condition accelerates the aging process, making it a useful model for researchers to gain insights into ageing itself.

Zombie cells: neither dead nor alive

A crucial function of our bodies is cell division, which we need to grow and repair damaged tissue. As we age, this ability diminishes, resulting in a state called senescence. Werner syndrome is caused by mutations in a gene essential for DNA maintenance and repair, and therefore cell division.

“One major hallmark of Werner syndrome is lack of proliferation and premature senescence. This means that cells without the WERNER protein divide poorly. Even though patients are relatively young, their cells stop dividing,” Lautrup explains.

Therefore, Werner syndrome patients show loss of stem cell proliferative capacity, which has detrimental consequences to the patients. “One could explain senescence cells as a type of zombie cells. They are neither dead nor alive, unable to perform their normal functions.”

Researchers suspect that the low level of NAD⁺ in these patients contributes to the early onset of this zombie state.

Reversing aging with NAD⁺

In their studies, the researchers examined both stem cells and skin cells from Werner syndrome patients in the lab, comparing them with cells from healthy controls. “We wondered whether NAD⁺ could reinstall proliferation in patient-derived cells,” Lautrup says.

Within just 24 hours of receiving a precursor molecule that converts to NAD⁺, multiple proliferation-related pathways were upregulated and senescence related pathways were downregulated.

“We found that NAD⁺ treatment can clearly reverse these features of the disease. The cells looked more like healthy cells,” Lautrup states. “NAD⁺ reduced the number of zombie cells and slowed down the ongoing senescence in the patients’ cells.”

A glimmer of hope from fruit flies

Previously, Lautrup and her colleagues conducted experiments with roundworms and fruit flies (drosophila melanogaster) modelling Werner syndrome.

They administered a molecule that converts into NAD⁺ within the cells. The results showed that NAD⁺ treatment successfully stimulated stem cell proliferation in the fruit flies, leading to improved mitochondrial function. Even with Werner syndrome, these organisms lived longer than expected.

“This finding in fruit flies made us wonder if NAD⁺ could restore cell division in the cells of actual patients,” she adds.

Paving the way for new treatments

Lautrup’s research has triggered clinical studies currently underway in Japan, focusing on Werner syndrome and NAD⁺.

“We eagerly await the results,” she shares. “We hope that this study, combined with our previous work on Werner syndrome and NAD⁺, will pave the way for new treatments not only for Werner syndrome but potentially for other aging-related diseases.”

Can we slow down the aging process?

If researchers can restore cellular NAD⁺ levels, the goal is to slow the ageing process. “We use Werner syndrome as a model for normal ageing. We’re continually hopeful that our research will provide insights for studies on typical ageing; however, we still do not know if NAD⁺ can help slow down natural ageing in humans,” Lautrup concludes.

As this research progresses, the scientific community remains hopeful that understanding the role of NAD⁺ and addressing the phenomenon of zombie cells may open new avenues for promoting longevity and better health in aging populations.

The paper builds on a collaborative project between both University of Oslo, Chinese University of Hong Kong, Shiba University in Japan, Bergen University and more supported among others by NordForsk (a Japan-Norway-Sweden collaboration).

According to UCLA, researchers led by Jun Chen, an associate professor of bioengineering at the UCLA Samueli School of Engineering, have developed a smart, self-powered, 3D printed magnetoelastic pen that could help detect early signs of Parkinson’s disease by analyzing a person’s handwriting.

Every year, tens of thousands of people with signs of Parkinson’s disease go unnoticed until the incurable neurodegenerative condition has already progressed. Motor symptoms, such as tremors or rigidity, often emerge only after significant neurological damage has occurred. By the time patients are diagnosed, more than half of their dopamine-producing neurons may already be lost. This kind of diagnostic delay can limit treatment options and slow progress on early-stage interventions. While there are existing tests to detect biomarkers of Parkinson’s, including cell loss in the brain and inflammatory markers in blood, they typically require access to specialists and costly equipment at major medical centers, which may be out of reach for many.

The highly sensitive diagnostic pen, described in a UCLA-led study published in Nature Chemical Engineering, features a soft, silicon magnetoelastic tip and ferrofluid ink – a special liquid containing tiny magnetic particles. When the pen’s tip is pressed against a surface or moved in the air, the pen converts both on-surface and in-air writing motions into high-fidelity, quantifiable signals through a coil of conductive yarn wrapped around the pen’s barrel. Although not intended for writing, the pen is self-powered, leveraging changes in the magnetic properties of its tip and the dynamic flow of the ferrofluid ink to generate data.

To test the pen’s diagnostic potential, the team conducted a pilot study with 16 participants, three of whom had Parkinson’s disease. The pen recorded detailed handwriting signals, which were then analyzed by a neural network trained to detect motor patterns associated with the disease. The model was able to distinguish participants with Parkinson’s from healthy individuals with an average accuracy of 96.22%.

“Detection of subtle motor symptoms unnoticeable to the naked eye is critical for early intervention in Parkinson’s disease,” said Chen, who is the study’s corresponding author. “Our diagnostic pen presents an affordable, reliable, and accessible tool that is sensitive enough to pick up subtle movements and can be used across large populations and in resource-limited areas.”

The researchers anticipate that this pen could transform early detection of Parkinson’s and other neurodegenerative conditions. Rather than waiting for symptoms to become disruptive, primary care physicians or geriatric specialists could administer a quick handwriting test during routine visits and use the data to inform earlier referrals or treatment.