Strength of Evidence to Support Decision-Making on the Use of Digital Mental Health Technologies in NICE Evaluations: Cross-Sectional Analysis of Studies

Background: Digital mental health technologies (DMHTs) are playing an increasing role in mental health services. The quality of evidence for DMHTs is variable, and there are concerns that evidence is not sufficient to support decision-making. Objective: This study used a cross-sectional analysis of evidence supporting DMHTs included in National Institute for Health and Care Excellence (NICE) evaluations to examine the strength of evidence available for decision-making. Methods: We identified all NICE evaluations relating to DMHTs by reviewing details of published NICE evaluations on the NICE website. From each of these evaluations, we identified included DMHTs and reviewed committee documentation to identify studies that provided supporting evidence for each of these technologies. We extracted information on a series of items relating to study quality and summarized the characteristics of evidence both at the level of individual studies and across the package of evidence from multiple studies supporting DMHTs. We also identified key evidence gaps in available evidence. Results: We included nine NICE evaluations relating to anxiety, depression, psychosis, insomnia, attention deficit hyperactivity disorder (ADHD), and tic disorders. These evaluations included 30 DMHTs and referenced 78 supporting studies. We identified common evidence gaps relating to effectiveness compared to relevant comparators, use of appropriate outcomes, including health-related quality of life, cost of delivery, and impact on resource use, and reporting of adverse events. Conclusions: Our study highlights that some DMHTs have been supported by high-quality studies and that evidence to support DMHTs is likely to be developed across a series of studies. However, there are often key evidence gaps that need to be addressed to provide a stronger case for adoption. Developers should ensure that they consider these gaps while planning evidence generation, and where possible, address them earlier in the product lifecycle.
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Medtech OEMs face a rare but closing window of opportunity

This is a manufacturing decision you can’t defer in 2026. Mark Freitas, Alvarez & Marsal Private-equity-backed CDMO platforms are aging into exits. OEMs who know what they want will move first. The 2022-2024 structural reset is over and the financing gap is narrowing. The sector has emerged from a period of value depression and as…

The post Medtech OEMs face a rare but closing window of opportunity appeared first on Medical Design and Outsourcing.

A Gamified Pain Management Intervention for Adults With Chronic Pain in Mainland China: Single-Arm Pre-Post Pilot Study With Machine Learning Predictive Modeling

Background: The widespread prevalence of chronic pain (CP) significantly impacts daily functioning worldwide. In mainland China, maintaining engagement in biopsychosocial interventions remains challenging. Gamification, designed based on self-determination theory, can enhance motivation, while machine learning (ML) algorithms can assist clinicians in dynamically optimizing pain management. Objective: This study aimed to (1) evaluate the preliminary effectiveness of a gamified pain management (GPM) program on CP and psychological outcomes and (2) identify key factors of significant pain improvements through the application of ML to guide intervention adjustments. Methods: A single-arm, pre-post study was conducted with 16 participants with CP in mainland China, recruited via social media using convenience sampling. Participants engaged in a 10-week web-based GPM intervention consisting of education, physical activities, and gamified elements, including points, avatars, and feedback. Primary outcomes were pain intensity and interference measured by the Brief Pain Inventory. Secondary outcomes included anxiety, depression, and quality of life. Analysis included paired tests, and ML models were trained to predict clinically meaningful pain reductions. Shapley additive explanations, least absolute shrinkage and selection operator regression, association rule mining, and Kaplan-Meier survival analysis were used to identify key predictors and optimal sessions and intervention durations across subgroups. Results: A total of 16 participants were engaged, with a mean age of 27.63 (SD 9.584) years. Results from paired tests reported significant improvements in pain intensity (decreased by 27.3%, 95% CI 1.061 to 3.064; =.001), pain interference (decreased by 27.3%, 95% CI 8.159-17.216; <.001), and psychological distress, including anxiety (=3.538, 95% CI 0.969 to 3.906; =.003) and depression (=4.559, 95% CI 2.230 to 6.145; <.001). The gradient boosting model demonstrated the highest predictive accuracy (area under the curve=0.89 and accuracy=0.82). Least absolute shrinkage and selection operator regression identified session 3 (β=−0.45, 95% CI −0.68 to −0.22; <.001) and session 5 (β=−0.32, 95% CI −0.59 to −0.05; =.02) as most predictive of clinical success, while association rule mining revealed effective session combinations for different patient subgroups. Time-to-event analyses indicated that individuals with low back pain and higher baseline severity required longer intervention durations for improvement (5 wk; =.03). Conclusions: This pilot study presents an innovative method that combines ML with dynamic engagement data from a GPM program during interventions, rather than relying on static baseline data in prior studies. The results show preliminary efficacy and identify specific optimal session combinations and personalized treatment durations for different pain subgroups. These exploratory findings contribute to the field by providing a data-driven method for adaptive, personalized digital health interventions that move beyond one-size-fits-all strategies, potentially enabling clinicians to modify content and dosage to improve engagement and outcomes if validated in larger sample trials. Trial Registration: Chinese Clinical Trial Registry ChiCTR2400094247; https://www.chictr.org.cn/showprojEN.html?proj=245138

Autoimmune Disease-Related Inflammation Reduced with ENDOtollins Drug

A new study published in Nature Chemical Biology titled, “Munc13-4–STX7 inhibitors impair endosomal TLR activation and systemic inflammation,” scientists from Scripps Research have developed a new class of drug compounds, called ENDOtollins, that reduce harmful inflammation while maintaining the body’s ability to fight infections. The results offer new directions to treat autoimmune diseases, such as lupus, and rheumatoid and juvenile arthritis, which together affect more than 15 million Americans. 

“A key component of our approach is to begin by understanding the biological mechanisms at play,” said Sergio Catz, PhD, professor at Scripps Research and corresponding author of the study. “By accomplishing this first, we can more easily target the pathway driving inflammation without affecting other important processes.” 

Current autoimmune disease treatments, such as hydroxychloroquine, function by broadly blocking endosomes. While effective, this approach can lead to significant side effects, including gastrointestinal problems and, less commonly, vision damage, that cause patients to stop treatment. 

The authors focused on two proteins, Munc13-4 and syntaxin 7, that bind together to activate Toll-like receptors (TLRs), immune sensors that activate endosomes. This mechanism plays a key role in detecting foreign DNA and RNA from viruses and bacteria. In autoimmune diseases, TLRs become overactive and trigger chronic, damaging inflammation in the absence of a threat. 

The team screened roughly 32,000 compounds and identified molecules that specifically block the Munc13-4–syntaxin 7 interaction without disrupting other cellular functions. Given that Munc13-4 is found mainly in immune cells, the compounds offer a targeted approach to reduce inflammation. 

“Most treatments for autoimmune diseases manage symptoms; they don’t change the underlying course of the disease,” said Hugh Rosen, MD, PhD, professor at Scripps Research and co-author of the study. “What’s exciting about this approach is its potential to be disease-modifying: targeting the specific molecular machinery that drives inflammation, rather than broadly suppressing the immune system.” 

Notably, the study screened compounds in an intact cellular environment which contrasts from many drug screening approaches, which extract proteins from the cell. 

“By maintaining the proteins in their natural environment, we increase the likelihood that compounds we find will actually work in living cells,” said Jennifer Johnson, PhD, first author and senior staff scientist at Scripps Research. 

The most potent compound, ENDO12, reduced inflammation in animal models that were also given a TLR-activating molecule. Blood levels of inflammatory markers, including immune system activators IL-6 and IFN-γ, and the enzyme myeloperoxidase, dropped significantly in animals that were treated. 

ENDO12 treated animals demonstrated normal antiviral immune response when exposed to a virus. This selectivity addresses the concern that dampening inflammation with immunosuppressive drugs may leave patients vulnerable to infections. 

Looking ahead, the team will test ENDOtollins in models that more closely mimic human autoimmune diseases and evaluate the compounds’ chemistry for potential clinical use. 

Beyond autoimmune conditions, the researchers suggest ENDOtollins might help treat cytokine storms, the dangerous immune overreactions seen in patients with severe COVID-19 and as a side effect of CAR T cancer therapy. Both involve excessive IL-6 and runaway inflammation. 

While translating these findings into treatments for patients remains a long-term goal, Catz emphasizes that the mechanistic insights are valuable in their own right. ENDOtollins can serve as precision tools to probe other cellular processes regulated by endosomes and lysosomes, including pathways implicated in neurodegeneration and immune dysfunction.  

The post Autoimmune Disease-Related Inflammation Reduced with ENDOtollins Drug appeared first on GEN – Genetic Engineering and Biotechnology News.

Synaptic remodeling and the female depression exposome: a mini-review of neuroendocrine, epigenetic, and social determinants

Depression is a multifactorial, chronic disorder and represents a leading cause of disability, with women exhibiting nearly twice the lifetime prevalence compared to men. Growing evidence indicates that this disparity cannot be explained by hormonal or psychosocial factors, but rather by dynamic interactions between environmental exposures, neuroendocrine signaling, and epigenetic regulation across development. This mini-narrative review aimed to examine how sex-specific exposome components interact with epigenetic mechanisms and synaptic remodeling processes to influence vulnerability to Major Depressive Disorder in women. The reviewed evidence demonstrates that fluctuations in ovarian hormones modulate HPA axis responsivity, neuroinflammatory signaling, and glutamatergic transmission through epigenetic regulation of stress-responsive genes such as NR3C1, SLC6A4, and BDNF, consequently influencing synaptic remodeling within corticolimbic circuits. Environmental and social exposures, particularly early-life adversity and psychosocial stressors, further interact with microglial activation and chromatin remodeling to produce long-lasting alterations in hippocampal and prefrontal plasticity. Collectively, these findings support a model in which sex-dependent neuroendocrine sensitivity amplifies exposome-driven epigenetic programming across the lifespan. Future research directions emerging from this synthesis include longitudinal life-course studies integrating multi-omic biomarkers, quantitative exposome assessment, and neuroimaging approaches to identify modifiable environmental targets and advance precision, sex-informed preventive and therapeutic strategies in depression.

Stage-specific ERP correlates of audiovisual facial emotion processing across depressive tendencies

Emotional dysregulation can emerge as early as the initial stages of depression. This study aimed to examine event-related potential characteristics during the perception of negative, positive, and neutral facial expressions in healthy individuals across depressive tendencies. Twenty-six healthy participants underwent ERP measurements during emotion recognition using a facial emotion recognition task in visual and audiovisual modalities. The Emotion Regulation Questionnaire (ERQ), the Difficulties in Emotion Regulation Scale (DERS-16), and the Beck Depression Inventory II (BDI-II) assessed cognitive strategy, emotion regulation difficulties, and depression severity, respectively. Facial affect elicited larger amplitudes compared to neutral faces, from the N170 and early posterior negativity (EPN) in the temporo-occipital region to the late positive potential (LPP) in the centroparietal region. Under audiovisual conditions, P1 peak latency to negative stimuli in the temporal region exhibited significant negative correlations with DERS-16 and BDI-II scores. N170 peak latency to positive stimuli also demonstrated a significant negative correlation with BDI-II scores. Under visual conditions, EPN amplitude to negative stimuli in the occipital region exhibited a significant positive correlation with BDI-II scores. P1 and N170 latencies, or neural response speeds, and EPN amplitude, which represents emotional reaction strength, correlate with depressive tendencies in healthy individuals. These early components function as initial neural signals that may serve as electrophysiological markers of abnormal emotional processing within neuropsychological functions prior to clinical depression.

Esketamine ameliorates depression-like behavior in mice via modulation of the NRG1–ErbB4 pathway

BackgroundEsketamine has a significant and rapid antidepressant effect. Although studies have shown that Neuregulin 1 (NRG1) and it’s signaling pathway are associated with depression, the possible regulatory relationship of esketamine on the NRG1-ErbB4 pathway is not yet clear.MethodsTo induce depressive-like behavior in mice, a Chronic Social Defeat Stress (CSDS) model was established. Behavioral indicators were then employed to assess depression in these mice, categorized into control, susceptible, and resilient groups. Following intraperitoneal injection of a subanesthetic dose of esketamine, behavioral tests were conducted at 30 minutes and 24 hours post-injection to observe any improvements in depressive-like behavior. Additionally, changes in immunofluorescence and protein expression levels of NRG1-ErbB4 and GAD67 in the prefrontal cortex were evaluated.ResultsCompared with the control group, the CSDS susceptible group mice showed decreases in social interaction ratio in the contact area, sucrose preference ratio, NRG1 immunofluorescence protein expression in the prefrontal cortex and NRG1 expression in tissue homogenate; showed significant increases in immobility time; the expression of NRG1 decreased;no significant change in GAD67 and ErbB4 expression level. in After 30 minutes of intraperitoneal injection of esketamine, the expression of NRG1 in the prefrontal cortex of susceptible mice increased significantly. no significant change in GAD67 and ErbB4 expression level. After 30 minutes and 24 hours of intraperitoneal injection of esketamine, the social interaction ratio of susceptible group improved compared to the control group, and the duration of forced swimming immobility was significantly shortened.ConclusionThe subanesthetic dose of esketamine may regulate the NRG1-ErbB4 signaling pathway and improve depressive like behavior in mice.

FcRn Inhibition in Autoimmune Disease

Eric Venker,
Eric Venker, MD, PharmD
CEO, Immunovant

Although immunoglobulin G (IgG) normally protects the body against pathogens, it can become problematic in many autoimmune diseases like lupus, rheumatoid arthritis, Graves’ disease, myasthenia gravis, and Sjögren’s disease.

“In these conditions, the immune system is creating defective IgGs—called autoantibodies—that are no longer fighting infections,” explained Eric Venker, MD, PharmD, CEO of Immunovant. “Instead, they are attacking a part of your normal functioning body and causing dysfunction.”

Leonard L. Dragone
Leonard L. Dragone, MD, PhD
Disease Area Leader
Johnson & Johnson Innovative Medicine.

Historically, autoimmune conditions have been challenging to treat because therapies like steroids rely on broad immune suppression, noted Leonard L. Dragone, MD, PhD, disease area leader of autoantibody and rheumatology at Johnson & Johnson Innovative Medicine. These non-specific approaches are often inconsistently effective and lead to adverse side effects.

“For many autoimmune diseases, there is a need for more targeted strategies that address disease-causing autoantibodies directly, rather than broadly suppressing the immune system,” emphasized Dragone. Beginning in 1998, the U.S. Food and Drug Administration (FDA) approved infliximab, a tumor necrosis factor (TNF)-α inhibitor, for the treatment of Crohn’s disease. This marked the first approval of a monoclonal antibody for the treatment of a chronic condition. Since then, targeted therapies for autoimmune diseases have expanded to address cytokine signaling pathways (TNF-α, IL-6, IL-17, IL-23), Janus kinase (JAK–STAT) signaling, and immune cell surface markers (CD20).

Another such targeted strategy involves an emerging drug class called FcRn blockers, which are now showing considerable promise in the treatment of certain autoimmune diseases.

FcRn blockers, which typically consist of monoclonal antibodies or antibody fragments, work by blocking the function of a protein receptor called FcRn (neonatal Fc receptor). This prevents IgG recycling, thereby reducing IgG levels in the body.

Immunovant
FcRn maintains levels of IgG in circulation by preventing IgG degradation in the lysosomes of cells. However, FcRn drugs block this pathway.

Venker compares FcRn inhibitors to cholesterol-lowering drugs such as statins. “LDL is the disease-causing agent that healthcare providers target to prevent many cardiovascular diseases. Likewise, in the case of FcRn blockade, we are aiming to lower IgG. We believe that deeper IgG reduction may provide improved results.”

As of early 2026, the FDA has approved three FcRn inhibitors for the treatment of myasthenia gravis, a chronic autoimmune disorder affecting up to 100,000 people in the U.S. Efgartigimod (approved in 2021), rozanolixizumab-noli (approved in 2023), and nipocalimab-aahu (approved in 2025) all work by reducing pathogenic IgGs associated with the disease.

Myasthenia gravis results
Myasthenia gravis results from harmful antibodies (anti-AChR or anti-MuSK) produced by the immune system that interfere with signaling in the neuromuscular junction.

“With FcRn blockers, it is exciting to know that there is now a targeted mechanism for patients around the world with autoimmune diseases caused by an IgG autoantibody,” said Venker.

Tackling Graves’ disease

In Graves’ disease, an IgG autoantibody called thyrotropin receptor antibody (TRAb), which targets the thyroid-stimulating hormone (TSH) receptor of the thyroid, is produced. The condition, which is the most common cause of hyperthyroidism, causes elevated heart rate, shakiness, irritability, muscle weakness, and weight loss.

“TRAb is an IgG antibody, but it is a badly behaving one that is basically hijacking the thyroid system,” noted Venker. “It doesn’t serve any purpose that is normal at all.”

Mark A. Lupo
Mark A. Lupo, MD
Founder and Medical Director
Thyroid & Endocrine Center of Florida

Unfortunately, the toolkit for treating Graves’ disease hasn’t changed much since 1950, when the FDA approved the drug methimazole, said Mark A. Lupo, MD, founder and medical director of the Thyroid & Endocrine Center of Florida.

Methimazole is an anti-thyroid drug that slows down the production of thyroid hormones. Although Graves’ patients benefit from anti-thyroid drugs, Lupo estimates a 50% relapse rate within two years of discontinuing these drugs.

Other options for treating Graves’ disease include surgical removal of the thyroid or the use of radioactive iodine to induce destruction of the thyroid gland. However, these approaches result in permanent hypothyroidism, and patients typically require lifelong thyroid hormone replacement after treatment.

Because TRAb is an IgG, FcRn drugs represent a potential autoimmune solution for Graves’ disease. Like all FcRn blockers, they may work by decreasing TRAb recycling and lowering TRAb levels.

Lupo highlights Immunovant’s recent proof-of-concept study of an FcRn inhibitor for Graves’ disease, the first such study for the condition. “Despite the small number of patients (around 25), the results from this study suggest a potential, durable remission six months off treatment,” said Lupo.

While study participants experienced an increase in total IgG levels following treatment, TRAb levels remained low over a six-month period. The thyroid also decreased in size. “To see TRAb levels down six months off the study drug caught the attention of the endocrine thyroid community,” noted Lupo.

“What was unexpected was that TRAb, the disease-causing antibody, stayed down for many months after stopping the investigational therapy,” added Venker.

“I think we are overdue for a new option in Graves’ disease that could help break some of these methimazole cycles and potentially address not the innocent thyroid gland but the underlying immune system issues,” concluded Lupo.

But are they safe?

Venker recalls that safety was an initial concern with FcRn inhibition. After all, these drugs work by reducing IgG, an essential part of the immune system. “Any time you are using an autoimmune drug that potentially suppresses your immune system, you have to think about going too far. Am I going to cause an infection or weaken the immune system?

“So far, this investigational drug has demonstrated a safety profile we expected, and appears positive,” noted Venker. “That makes sense mostly because FcRn blockade is pretty targeted.”

“Although there are no head-to-head comparative safety trials yet, most clinicians and principal investigators view FcRn blockers as relatively safe,” added Lupo. “There are FcRn blockers on the market, and they have demonstrated a good safety record in patients.” The most common side effect tends to involve injection site reactions with either intravenous or subcutaneous delivery.

Preventing fetal exposure

During pregnancy, maternal antibodies—called alloantibodies—can cross the placenta and attack the organs and tissues of the fetus, explained Dragone.

A distinguishing feature of Johnson & Johnson’s nipocalimab is its pH-independent binding to FcRn. This allows it to bind with high affinity in the placenta, a low-pH environment.

The drug is currently showing potential in the treatment of two alloimmune diseases of pregnancy: hemolytic disease of the fetus and newborn (HDFN) and fetal and neonatal alloimmune thrombocytopenia (FNAIT), said Dragone. These conditions can arise during alloimmunized pregnancies, when the pregnant person’s immune system forms alloantibodies against fetal red blood cells (HDFN) and/or fetal platelets (FNAIT). Importantly, published data on nipocalimab suggest minimal transfer of the drug to the fetus or infant. “Therapies like nipocalimab offer a blueprint for how precision medicine can expand to include pregnant people, a population that has historically been excluded from drug development,” noted Dragone. “Our approach with nipocalimab has the potential to change how we think about treating autoantibody-driven diseases in people of childbearing age.”

FcRn blockers bind to FcRn receptors
Nipocalimab (IMAAVY®) and other FcRn blockers bind to FcRn receptors and reduce levels of both normal and harmful IgG antibodies.

The FDA has granted a fast track designation to nipocalimab for both FNAIT and HDFN, and Phase III studies are underway to further investigate the drug in both diseases.

Expanding indications

“There are probably 20 trials out there for FcRn blockers, and many are likely to work,” noted Venker. “There are a ton of potential new indications under investigation, including rare diseases that have been ignored historically.”

He notes that Immunovant’s pipeline alone includes potential indications in endocrinology (Graves’ disease), rheumatology (rheumatoid arthritis, Sjögren’s disease, and cutaneous lupus erythematosus), and neurology (myasthenia gravis and chronic inflammatory demyelinating polyneuropathy).

Venker stresses that no FDA-approved solutions exist for Sjögren’s disease, which affects as many as four million Americans. The condition causes severe dry eyes and mouth, fatigue, and joint and muscle pain. Immunovant and Johnson & Johnson are conducting clinical trials to evaluate FcRn blockers for the disease.

Hani Houshyar
Hani Houshyar, PhD
Strategy Team Lead
argenx

Meanwhile, argenx’s FcRn inhibitor efgartigimod has been used in 19,000 people worldwide for myasthenia gravis and other autoimmune conditions, said Hani Houshyar, PhD, FcRn asset strategy lead for argenx.

“However, we believe myasthenia gravis is just the beginning,” she said. As of 2026, the company has active clinical trials to test the drug’s effectiveness in additional autoimmune diseases with high unmet medical need, like myositis, Sjögren’s disease, ocular myasthenia gravis, systemic sclerosis, Graves’ disease, and autoimmune encephalitis.

UCB’s rozanolixizumab was the first FcRn blocker to be approved for the treatment of generalized myasthenia gravis in adults who are positive for anti-AChR or anti-MuSK antibodies, who together account for approximately 90% of cases, said Omar Sinno, MD, UCB’s U.S. medical strategy lead of rare disease. So far, the drug has been approved in the U.S., Canada, the EU, Australia, Switzerland, China, Turkey, and Korea.

Omar Sinno
Omar Sinno, MD
Medical Strategy Lead, UCB

Rozanolixizumab is administered via a convenient subcutaneous infusion rather than intravenously. The company’s long-term studies demonstrate robust IgG reductions (up to 75%) with sustained benefit across multiple treatment cycles. UCB is also investigating rozanolixizumab as a potential treatment for a rare autoimmune condition called myelin oligodendrocyte glycoprotein antibody-associated disease.

Finally, Johnson & Johnson’s nipocalimab is in mid-to-late-stage studies for Sjögren’s disease, lupus, warm autoimmune hemolytic anemia, and chronic inflammatory demyelinating polyneuropathy.

Drugs in development

Viridian Therapeutics is currently investigating two FcRn inhibitors, VRDN-006 and VRDN-008, said Steve Mahoney, president and CEO. Both candidates are designed as subcutaneous products that can be conveniently self-administered by the patient.

Steve Mahoney
Steve Mahoney
President and CEO
Viridian Therapeutics

VRDN-006 is an Fc fragment in Phase I trials, while VRDN-008 is made up of an Fc fragment and an albumin-binding domain designed to prolong IgG suppression. Mahoney notes that VRDN-008 showed a longer half-life and more sustained IgG reduction than efgartigimod in a high-dose, head-to-head study in non-human primates.

Clinical trial results of VRDN-008 in healthy volunteers are expected later in 2026. “What we believe differentiates VRDN-008 from other FcRn inhibitors is a longer half-life, which has the potential to support less frequent dosing for patients to enhance convenience,” said Mahoney.

Although three FcRn blockers are currently FDA-approved to treat myasthenia gravis in the U.S., Venker notes that Immunovant is continuing to investigate the condition with the company’s follow-on FcRn candidate, imeroprubart (IMVT-1402).

In Immunovant’s proof-of-concept study for Graves’ disease, TRAb stayed low even six months after the investigational treatment was discontinued. But how long will this effect last? “We don’t know that yet because our randomized trials with IMVT-1402 are ongoing,” Venker said. “However, Graves’ disease has given us the first hint that FcRn drugs may be able to put certain autoimmune conditions into permanent remission.”

Viridian’s VRDN-006 illustration
Viridian’s VRDN-006 (top) is an Fc fragment, whereas VRDN-008 (bottom) is made up of an Fc fragment and an albumin-binding domain designed to prolong IgG suppression.

“A key question for autoimmune disease, the holy grail, so to speak, is whether we can reset the immune system so the person can function normally without medication for the rest of their lives,” he added.

Finally, argenx is developing ARGX-213, a next-generation FcRn inhibitor engineered to extend half-life and sustain IgG reduction.

“Looking ahead, FcRn inhibition represents an increasingly important approach across IgG-driven disease,” noted Sinno. “By selectively reducing pathogenic IgG, these agents enable more targeted autoimmune care. And as clinical experience with FcRn inhibition grows, treatment paradigms may shift toward earlier intervention.”

 

Tiffany Yesavage, PhD is a freelance writer from Denver, Colorado.

The post FcRn Inhibition in Autoimmune Disease appeared first on Inside Precision Medicine.

<![CDATA[A relationship between inflammatory skin disease and depression revealed in new research.]]>

The Unspoken Toll: Why Exam Pressure Must Be Part of the Youth Mental Health Discussion

A Conversation with Tatum Redmond and Amanda van der Vyver-Anderson from Community Keepers, South Africa


By Mai El Shoush, Partnerships Campaign Manager, Stavros Niarchos Foundation (SNF) Global Center for Child and Adolescent Mental Health at the Child Mind Institute


Community Keepers is an award-winning organization based in Stellenbosch, South Africa, which works to improve the social and emotional well-being of learners and their caregivers. The SNF Global Center at the Child Mind Institute works with the organization to further advance the comprehensive mission of transforming schools into safe spaces where student well-being is prioritized alongside academic achievement. This includes strengthening the workforce to expand evidence-based support and brief interventions through low-intensity psychological therapy approaches.

While addressing the workforce gaps, the partnership has yielded valuable insight into the essential competencies front line workers require to effectively support young people experiencing mental health challenges. Together with other NGOs, Community Keepers has also been instrumental in strengthening the process of developing context-sensitive and culturally appropriate training materials scheduled for pilot implementation in South Africa later this year – representing an important step towards strengthening mental health care systems for underserved communities. The partnership also extends beyond training development, as the SNF Global Center at the Child Mind Institute continues to collaborate closely with Community Keepers on an upcoming randomized control trial (RCT). The scientific evaluation will assess both the feasibility of establishing a virtual clinic for young people and the effectiveness of remotely delivered cognitive behavioral therapy (CBT) interventions via video consultations. The research is intended to expand access to equitable and quality mental health care for young people across South Africa. Tatum Redmond has been a care facilitator in one of the Community Keepers’ high school-based offices, while Amanda van der Vyver-Anderson is an educational psychologist and heads the training and development of Mental Health First Aiders for internal and external staff.

Amanda van der Vyver-Anderson

How important is it to approach issues such as academic pressure within the wider conversation around youth mental health in South Africa, and beyond?

It is critical to integrate discussions of exam stress into the broader dialogue surrounding youth mental health, both here in South Africa and internationally. We see countless students under immense pressure to not only pass, but also secure their future prospects and meet family expectations. This is unfortunately often dismissed as “just school” or a “normal” experience. However, it impacts a substantial number of young people, often more severely than we acknowledge. And the level of support available is not equitable across the board. Addressing this is crucial because of the detrimental effects on core cognitive functions — and ultimately, academic performance — as well as the significant toll on mental health. This can manifest as anxiety, burnout, and even depression.

In what ways can exam-related stress connect to broader mental health challenges?

While a certain level of stress can serve as a beneficial motivator, severe distress can lead to cognitive shutdown. This specifically impacts the executive functions — planning, organizing, prioritizing, working memory, focus, and concentration — that are fundamental to preparing for exams. This shutdown can then create a detrimental, ongoing cycle of heightened stress about exams or the future, coupled with a decline in the ability to take effective action.

It’s vital to recognize that exam stress does not merely stay in the exam room — it can be a gateway to larger mental health challenges. Constant stress regarding school performance, marks, or the fear of failure can escalate into conditions like anxiety, chronic overwhelm, or depression. Students may experience sleep disruption, poor nutrition, and feelings of inadequacy. And these symptoms often persist long after the test is over. Compounding this is the reluctance of most students to seek help because they believe their feelings are normal or fear appearing weak. Yet, if left unaddressed, sustained pressure along with these symptoms can profoundly affect their psychological well-being.

Tatum Redmond

What role do community-focused organizations such as Community Keepers play in linking academic stress to systematic youth mental health support and improvement?

Organizations like Community Keepers play a truly pivotal role — not merely as emergency responders but as an integrated support system within educational institutions as well. Crucially, they move beyond immediate crisis response by collaborating with schools to develop long-term support and to provide safe spaces to engage in dialogue. They offer genuine attention and care when learners are struggling with school demands, exams, and family pressures.

The approach is not just “addressing stress today” but asking, “How can we create an enduring environment where young people feel safe, supported, and connected?” Doing this requires collaboration with the learners themselves, educators and school staff, as well as parents, caregivers, and community leaders.

What factors make schools uniquely positioned to be safe and supportive spaces?
Schools are exceptionally well-positioned to serve as safe and supportive spaces for students for several key reasons:

  • Learners spend a substantial portion of their day at school, making it a primary setting where adults can observe signs of distress, anxiety, or coping difficulties.
  • Schools have the opportunity to house critical personnel — teachers, counselors, and external partners like Community Keepers — who are on hand to offer support or a listening ear.
  • The curriculum can extend beyond academic skills and learning. It can include mental health and emotional literacy, stress management, and peer support.
  • When a school actively fosters an environment of safety, respect, and validation, it fundamentally alters how learners navigate pressure, stress, or complex personal problems. Having a guaranteed safe space at school is deeply stabilizing for the mind.

How can the goal of securing mental health support as a pillar of education be reached?
Achieving the goal of establishing mental health support as a solid, non-negotiable pillar of education requires several strategic commitments:

  • Schools must actively allocate resources for it, ensuring adequate numbers of support staff, rather than relying on minimal provision. Teachers need training to recognize signs of distress and respond helpfully and appropriately.
  • Mental health literacy must be integrated into the curriculum. Instead of only focusing on academic subjects, topics like stress management, emotional intelligence, and maintaining healthy relationships should be covered.
  • The government must demonstrate a serious commitment, including mental health support in education budgets, developing clear policies, and ensuring rigorous follow-through.

How have your practices and initiatives in promoting and supporting schools as safe spaces made meaningful change?
We’ve observed tangible change in the learners’ attitudes; those who feel comfortable expressing their emotions are generally happier and more resilient because they have established a safe, non-judgmental space where trust is built.

What role can teachers and school leadership play as partners in creating an evidence-based supportive learning environment? Where are the gaps in building capacity and how can they be better supported?
Educators and school leadership are essential partners in establishing an environment that successfully supports learner mental health and cultivates a culture of well-being. They can do so by:

  • Prioritizing both the physical space and curriculum time necessary for learners to engage with support services.
  • Serving as role models who embody and encourage emotional regulation and actively normalize help-seeking behaviour.
  • Remaining deeply cognisant of factors that contribute to learner distress so as to not inadvertently exacerbate it.

Investing in staff wellness and support, capacity building, and policy reform is not merely beneficial, but a foundational requirement to capacitate educators effectively. This allows them to sustainably support the mental health of their entire school community.

The SNF Global Center’s work in South Africa is carried out through the Child and Adolescent Mental Health Initiative (CAMHI South Africa). We are proud to expand the partnership with Community Keepers and value their collaboration towards co-creating scalable, school-centered mental health approaches that authentically respond to the diverse lived-experiences of young people.

The post The Unspoken Toll: Why Exam Pressure Must Be Part of the Youth Mental Health Discussion appeared first on Child Mind Institute.