Miscellaneous Research Thread

Navigating Social Security disability benefits with Long COVID: A grounded theory study, 2026, Hair et al

Nicole Hair, Maushmi Patel, Ibitein Okeafor, Carly Urban, Nabil Natafgi

Background: Long COVID is an emerging public health challenge that impacts the health and financial security of millions. Individuals living with Long COVID may qualify for Social Security Administration (SSA) disability benefits; however, barriers limit access to these programs.

Methods: This qualitative study used Strauss and Corbin's grounded theory to examine how adults with Long COVID perceive and navigate SSA disability benefit programs, including factors shaping decisions to apply, delay, or discontinue applications. Data were collected through 17 interviews and 4 focus group discussions. Analysis was conducted using constant comparative methods until theoretical saturation was reached.

Population Studied: Participants included 35 US-based adults living with Long COVID, predominantly female (62.9%) and Black/African American (62.9%), representing 19 states. Eighteen participants reported applying to SSA programs; 15 had not applied, and two initiated but did not complete the application process.

Principal Findings: The central phenomenon, perceptions about SSA programs, reflects the conditions and processes shaping participants’ experiences.

Applicants described the process as complex and stressful, citing system-level biases, limited customer support, and insufficient information as key barriers. Uncertainty about eligibility, unclear procedures, long waiting times, and potential legal costs discouraged participation. Long COVID symptoms further compounded these challenges.

Applicants highlighted the importance of support from family, friends, providers, attorneys, advocates, and employers.

Conclusion: Administrative complexity and limited support within SSA disability programs present substantial barriers for individuals with Long COVID. Efforts to clarify eligibility criteria, streamline procedures, and strengthen support systems may improve access for individuals living with Long COVID.

Web | APHA 2026 Conference | Conference Abstract
 
Temporal Sequence of Onset: ME/CFS-like Fatigue and Functional Neurological Disorder (Gaber et al.)

Abstract said:

Background​

Fatigue is the most prevalent and one of the most disabling symptoms of Functional Neurological Disorder (FND), yet its causal relationship to the condition remains poorly understood. Emerging evidence suggests that chronic fatigue may precede rather than follow the onset of functional neurological symptoms. We hypothesised that a specific phenotype of chronic fatigue, resembling that seen in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), may act as a precipitating factor in FND.

Methods​

We conducted a retrospective review of clinical records from 89 patients assessed through an integrated ME/CFS and FND community service in Wigan, UK, between March 2022 and March 2025. Complete data were available for 76 patients. Fatigue prevalence, phenotype, and its temporal relationship to the onset of FND symptoms were extracted and analysed descriptively.

Results​

Fatigue was reported by 62 of 76 patients (81.5%). In 39 patients (51% of the cohort), fatigue predated the onset of FND symptoms by months to years and exhibited features resembling ME/CFS, including post-exertional malaise, cognitive dysfunction, pain, and immune-like symptoms unrelieved by rest. In all 39, fatigue onset followed one or more stressful life events. A further 23 patients (30%) reported fatigue emerging concurrently with or following FND onset, also with post-exertional exacerbation. The remaining 14 patients (18.5%) without significant fatigue tended to present with isolated focal symptoms and minimal fluctuation, or with primary psychiatric or pain co-morbidities.

Conclusions​

These findings suggest that ME/CFS-like fatigue may play a previously underappreciated precipitating and perpetuating role in a substantial subgroup of FND patients. One possible interpretation is that persistent fatigue and post-exertional symptom exacerbation may constrain the brain’s capacity to process and integrate information, potentially contributing to the emergence or persistence of functional neurological symptoms. These observations are preliminary and require prospective validation, but they raise important questions about FND phenotypic heterogeneity and the appropriateness of exercise-based interventions in fatigue-predominant presentations.
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Link | PDF (Advances in Rehabilitation Science and Practice, October 2026, open access)
 
In other words, it ain't FND.

The whole concept is simply irrelevant, and hence highly counterproductive.

While this is actually a noteworthy finding (that does not support an FND diagnosis), so also is that they twist what should be a clear diagnosis of ME/CFS into one for a prodromal phase for FND.
 
EBV hijacks the metabolic function of CD73 to resist the antitumor function of NK cells, 2026, Duan et al.

Duan, Xiaobing; Hu, Jiali; Wan, Shuo; Luo, Qiong; Zhang, Yuncong; Feng, Guangyong; Luo, Miaoshan; Lin, Zhen; Yu, Pei; Jia, Hongyun; Li, Jinmei; Wang, Minhong; Wang, Zhongying; Chen, Mingxiao; Yang, Xinfeng; Lin, Meifang; Li, Siyu; Xiang, Tong; Zhou, Qiang; Zhang, Guihai

Abstract
CD73 is a metabolic immune checkpoint that regulates the homeostatic balance of adenosine levels in the tumor microenvironment (TME). However, the regulation of CD73 abnormal expression in Epstein-Barr virus (EBV)-associated malignancies remains unclear.

In this study, we demonstrate that CD73 is upregulated in EBV-associated malignancies and is negatively correlated with the anti-tumor activity of NK cells. Mechanistically, EBV latent protein LMP2A upregulates CD73 through the PI3K/AKT signaling pathway, and the metabolic product of CD73, adenosine, negatively regulates the anti-tumor function of NK cells through multiple signaling pathways.

Furthermore, targeted knockout of CD73, a small molecule inhibitor, or neutralizing antibody combined with the adoptive transfer of NK cells significantly improved the treatment efficacy for EBV-positive nasopharyngeal carcinoma (NPC). Importantly, we also found abnormal upregulation of CD73 in EBV-positive lymphoma, gastric cancer, and lung cancer.

In summary, our research identifies the mechanism of immune evasion of NK cell anti-tumor function in EBV-associated malignancies through the abnormal expression of CD73, and targeting CD73 combined with the adoptive transfer of NK cells may provide a new strategy for immunotherapy of EBV-related malignancies.

Web | DOI | PMC | PDF | npj Precision Oncology | Open Access
 
The role of the NLRP3 inflammasome in a CLN2 mouse model of neuroinflammation, 2026, Sánchez et al.
Sánchez, Kathryn E.; Elizalde, Samantha; Schwartz, Nancy B.; Domowicz, Miriam S.

Abstract
Neuronal ceroid lipofuscinoses, or Batten disease, comprises a group of inherited pediatric neurodegenerative disorders, and is characterized by the lysosomal accumulation of the fluorescent storage material lipofuscin.

The human classical late-infantile form of the disorder (CLN2) is caused by mutations in the CLN2 / Tripeptidyl peptidase 1 ( TPP1 ) gene. Comparable to human CLN2, a knockout of the Tpp1 gene ( Tpp1 -/- ) in the mouse leads to progressive vision loss, ataxia, motor atrophy, seizures, and premature death. While we previously showed using bulk RNA-seq analysis that reactive gliosis develops between 3 and 4 months in this animal model, the role of the inflammasome in CLN2 remains unexplored.

The inflammasome is a multiprotein complex formed through pattern recognition receptor engagement, which culminate in the cleavage and release of interleukin-1 beta. Here we report that while some inflammasome-associated genes are upregulated as early as 1-month in the Tpp1 -/- cerebellum, it is not until 3-months-old that all gene transcripts necessary for inflammasome assembly and function are upregulated, leading to IL1β release.

In Tpp1 -/- slice cultures, we demonstrated that MCC950, an inhibitor of inflammasome assembly, downregulates transcriptional expression of genes associated with reactive microglia and inflammasome function. Furthermore, prophylactic administration of MCC950 in drinking water of Tpp1 -/- animals for two months is sufficient to lower the expression of these same genes in the forebrain and cerebellum, suggesting that inflammasome inhibitors are promising therapeutics for CLN2 and neurodegeneration broadly. Graphical Abstract The role of the NLRP3 inflammasome in a CLN2 model of neuroinflammation.

The NLRP3 inflammasome is upregulated and assembled in Tpp1-/- microglia, leading to IL1β release. Treatment with an NLRP3 inflammasome inhibitor MCC950, in ex-vivo and in-vivo murine models of CLN2 neuroinflammation, results in the downregulation of inflammasome-associated genes.
Web | DOI | bioRxiv | Open Access
 
www.nature.com

Can GLP-1s heal the brain? Obesity drugs get a makeover for addiction and depression

Compounds inspired by the blockbuster weight-loss drugs are also being trialled for schizophrenia and Parkinson’s disease, among other conditions.
www.nature.com www.nature.com
Paywall

Can GLP-1s heal the brain? Obesity drugs get a makeover for addiction and depression​

Compounds inspired by the blockbuster weight-loss drugs are also being trialled for schizophrenia and Parkinson’s disease, among other conditions.
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Fast and inexpensive visualization of genome collection at scale, 2026, Kotte et al.
Kotte, Sujatha; Tiwari, Naina; Vaddadi, Kavya; Saipradeep, Vangala Govindakrishnan; Joseph, Thomas; Rao, Aditya; Srinivasan, Rajgopal; Sivadasan, Naveen
Abstract

Background​

Investigating genetic progression and lineage using sequence data is a fundamental focus within the realm of viral genome research. Given the substantial increase in publicly accessible genome sequences, tools designed for extensive data analytics, particularly insightful visualizations play an important role in elucidating the spatio-temporal evolution as well as the diversity of viral lineages.

Existing genome data analysis methods frequently rely on multiple sequence alignment (MSA) and phylogeny computations, making integration of new sequences computationally expensive. Such methods are often metadata agnostic and typically utilize a global distance metric between candidate sequences.

We present BOVIZ, a fast and inexpensive method for rich visualization of large-scale genome collections. BOVIZ leverages variant-level features from candidate sequences and employs a novel Bag-Of-Variants (BOV) method that transforms high-dimensional variant feature vectors into a 2D-space, effectively capturing sequence (dis)similarities. BOVIZ circumvents the need for expensive MSA and phylogeny analyses, enabling efficient integration of novel sequences and faster visualization of large-scale sequences on a standard desktop.

Furthermore, BOVIZ supports a variety of filters, including metadata filters and selection of genomic regions of interest for effectively capturing localized similarities and dissimilarities on-the-fly. We perform extensive benchmarking of BOVIZ with state-of-the-art visualization methods using the SARS-CoV-2 viral genome dataset.

Results​

BOVIZ consistently outperformed these methods in capturing inter-sequence similarity and diversity, offering superior visualization of spatio-temporal and clade-level evolution. It is able to effectively distinguish SARS-CoV-2 lineages into distinct clusters, visualize the evolution of specific sublineages like Omicron and their variant patterns, as well as visualize potential sub-cluster within the SARS-CoV-2 Delta variant.

Conclusion​

BOVIZ is an effective visualization tool for genome surveillance, complementing resource-intensive deep analytics by providing key insights about the underlying genome landscape in a fast and scalable manner.
Web | DOI | PDF | BMC Bioinformatics | Open Access
 
Healthcare trajectories diverge years before Huntington disease is recorded in claims: a nationwide French matched cohort study (2026, Journal of Neurology, Neurosurgery & Psychiatry)
BACKGROUND
Huntington disease (HD) develops years before it is formally recorded, yet whether this generates measurable healthcare demand, and when, is unknown. We aimed to determine when trajectories of incident HD diverge from matched controls.

METHODS
Retrospective matched cohort study using the French National Health Data System. Adults with incident HD (2018 to 2024; ≥2 hospital visits or ≥1 long-term registration for nternational Classification of Diseases, 10th Revision (ICD-10) G10 or F02.2; no HD code in the prior 9 years) were each matched to five controls on sex, age and deprivation. Recurrent events were modelled from 9 years before to 7 years after the first HD record.

RESULTS
Among 2659 cases and 13 295 controls, divergence preceded the first record by 6 to 8 years. Antipsychotic use rose earliest (8 years prior, HR 1.54, 95% CI 1.31 to 1.80). From 6 years prior, neurology (HR 1.53, 95% CI 1.06 to 2.22), psychiatry (HR 1.25, 95% CI 1.04 to 1.47) and speech therapy (HR 2.16, 95% CI 1.46 to 3.19) diverged. Before the record, neurology consultations occurred in 50.8% of cases versus 10.0% of controls, psychiatry consultations in 33.9% vs 10.0% and speech therapy in 8.5% vs 0.6%. After the record, divergence widened: neurology peaked at 3 years (HR 5.44, 95% CI 3.94 to 7.54) and antipsychotic use at 5 years (HR 3.63, 95% CI 3.06 to 4.30), while physiotherapy emerged only afterwards (4 years, HR 3.10, 95% CI 2.89 to 3.33).

CONCLUSIONS
HD generates substantial care years before diagnostic coding. Neuropsychiatric and communicative demand precedes motor-related rehabilitative care by several years, defining a measurable window for earlier referral.
 
Yeah it's very clear that there are similar signals for a lot of illnesses. Here they seem especially inappropriate, but that's just common, I guess. It's something that makes poor recording of intermediate signals a real problem. There is likely more similar data out there in those cases that just never got recorded, or was misinterpreted.

People's lives don't change when they get a diagnosis of X. Those lives often change much earlier than that, diagnosis is just a step, one that apparently changes a focus on incorrect treatment approaches to the possibility of correct ones. There is a lot to learn here, and it's fortunate that AI is about to change everything, because it's not the kind of lessons that humans tend to do well at.
 
I am very sure that a prodromal sub-clinical phase is a thing (for many conditions, not all).

Also that it is a missed thing for far too long in far too many cases, greatly reducing the effectiveness and benefit of earlier treatment and/or management.

Might even be the biggest black hole in medicine.
 
HD is in a bit of a unique situation in terms of the diagnostic process because it’s hereditary. If you have it, there’s a 50 % chance to pass it on to your children.

There’s a simple and accurate test for the genetic mutation, but only 10-15 % of the people that are known to be at risk from their parents or grandparents actually take it. That’s understandable because there are no treatments, it’s a horrible horrible disease, and you’ve probably seen how it affects family members, so most people prefer to live with the hope of not being affected instead of having 50 % odds of getting a death sentence.

As soon as there are effective disease-modifying treatments of some kind, most people at risk will probably chose to get tested sooner, especially because there are measurable changes to the brain before the first symptoms.

HD involves a lot of psychiatric changes so that’s an appropriate profession to be involved with those patients, but how they are treated is probably different from patients where you assume there’s no damage to the brain. It’s not that unusual for people around them to believe they are using something, for example.

E: Someone sent me the paper - thanks!
 
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Sean said:
I am very sure that a prodromal sub-clinical phase is a thing (for many conditions, not all).

Also that it is a missed thing for far too long in far too many cases, greatly reducing the effectiveness and benefit of earlier treatment and/or management.

Might even be the biggest black hole in medicine.
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And aligns with the lack of back-propagation, of looking at past records to figure out who, what and why things went wrong when such errors are identified. Much of this is due to lack of capacity, though. Not all of it, but until electronic records it was not feasible to do any of this. That excuse has run out a few years ago, though.

The main obstacle will be confidentiality, though. AI systems working through those records to find those chains of events will massively improve the quality of health care and reduce errors, but it's a dual-edged sword, bit how top-end AI models can now find vulnerabilities in software, but whether the goal is to exploit or fix them is a whole different layer of concerns.
 
rvallee said:
And aligns with the lack of back-propagation, of looking at past records to figure out who, what and why things went wrong when such errors are identified. Much of this is due to lack of capacity, though. Not all of it, but until electronic records it was not feasible to do any of this. That excuse has run out a few years ago, though.

The main obstacle will be confidentiality, though. AI systems working through those records to find those chains of events will massively improve the quality of health care and reduce errors, but it's a dual-edged sword, bit how top-end AI models can now find vulnerabilities in software, but whether the goal is to exploit or fix them is a whole different layer of concerns.
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I'm not so sure. When the local hospital got a new electronic health journal, it created havoc in many systems as a "temporary diagnostic code" was mandatory in the new electronic journal, but this code just hung around and was not removed further down the line when automatic data collection to various other systems took place.

From research on bad practice in community care, we also know things are not coded where they are supposed to to avoid it to be counted. So instead of writing in the correct place that a patient did not get the care they were supposed to, where it would be counted as something didn't go to plan that day, it is kept in a note passed to the next carer that no one else sees. Data can be made to disappear quite easily sometimes.
 
Midnattsol said:
From research on bad practice in community care, we also know things are not coded where they are supposed to to avoid it to be counted. So instead of writing in the correct place that a patient did not get the care they were supposed to, where it would be counted as something didn't go to plan that day, it is kept in a note passed to the next carer that no one else sees. Data can be made to disappear quite easily sometimes.
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Legitimizing neglect - a qualitative study among nursing home staff in Norway
 
A study which includes negative experience of Buddhist meditation.

The varieties of contemplative experience: A mixed-methods study of meditation-related challenges in Western Buddhists

Lindahl, Jared R.; Fisher, Nathan E.; Cooper, David J.; Rosen, Rochelle K.; Britton, Willoughby B.
Buddhist-derived meditation practices are currently being employed as a popular form of health promotion. While meditation programs draw inspiration from Buddhist textual sources for the benefits of meditation, these sources also acknowledge a wide range of other effects beyond health-related outcomes. The Varieties of Contemplative Experience study investigates meditation-related experiences that are typically underreported, particularly experiences that are described as challenging, difficult, distressing, functionally impairing, and/or requiring additional support. A mixed-methods approach featured qualitative interviews with Western Buddhist meditation practitioners and experts in Theravāda, Zen, and Tibetan traditions. Interview questions probed meditation experiences and influencing factors, including interpretations and management strategies. A follow-up survey provided quantitative assessments of causality, impairment and other demographic and practice-related variables. The content-driven thematic analysis of interviews yielded a taxonomy of 59 meditation-related experiences across 7 domains: cognitive, perceptual, affective, somatic, conative, sense of self, and social. Even in cases where the phenomenology was similar across participants, interpretations of and responses to the experiences differed considerably. The associated valence ranged from very positive to very negative, and the associated level of distress and functional impairment ranged from minimal and transient to severe and enduring. In order to determine what factors may influence the valence, impact, and response to any given experience, the study also identified 26 categories of influencing factors across 4 domains: practitioner-level factors, practice-level factors, relationships, and health behaviors. By identifying a broader range of experiences associated with meditation, along with the factors that contribute to the presence and management of experiences reported as challenging, difficult, distressing or functionally impairing, this study aims to increase our understanding of the effects of contemplative practices and to provide resources for mediators, clinicians, meditation researchers, and meditation teachers.

Web | DOI | PMC | PDF | PLOS ONE

Project page

Skeptical Inquirer article
 
"Transforming growth Factor-β1 as a longitudinal Indicator of treatment outcome in Obsessive-Compulsive disorder"

Background​

While the immune system’s role in obsessive–compulsive disorder (OCD) pathogenesis has been increasingly recognized, cytokine studies have yielded inconsistent findings. This study assessed serum cytokine levels in patients with OCD and a control group at baseline and after 12 weeks of fluoxetine or group cognitive-behavioral therapy (GCBT), investigated associations with clinical parameters, and examined whether cytokine trajectories differed by treatment response.

Methods​

The study included seventy patients with OCD enrolled in a 12-week clinical trial and eighty-eight control participants. Clinical and immune assessments were conducted at baseline (T1) and 12 weeks later (T2); patients with OCD received either fluoxetine or GCBT. Treatment response was measured using the Yale-Brown Obsessive Compulsive Scale (Y-BOCS). Serum concentrations of IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-8, IL-10, TNF-α, TGF-β1, and IFN-γ were measured, and longitudinal cytokine trajectories were analyzed using linear mixed-effects models.

Results​

No significant differences in cytokine concentrations were observed between patients with OCD and control participants at either baseline or 12-week follow-up, nor did longitudinal change in TGF-β1 differ significantly between groups (time × group interaction: p = 0.126). Among patients with OCD, transforming growth factor-β1 (TGF-β1) increased significantly over the 12-week treatment period (marginal time effect: p = 0.0033). Estimated marginal contrasts showed that the increase in TGF-β1 from T1 to T2 was significantly greater in non-responders than in responders (estimate =  − 0.435, SE = 0.141, p = 0.0039; FDR q = 0.039).

Conclusions​

Longitudinal changes in TGF-β1 were associated with treatment response in OCD, with greater increases observed among patients who did not achieve clinical improvement. These findings suggest that TGF-β1 may be more informative as a longitudinal correlate of treatment response than as a diagnostic marker of OCD. Replication in larger prospective cohorts is needed to clarify its biological significance and potential clinical utility.

Link
 
I had heard that New Scientist has fallen in quality but geez. This is supposed to be based on a study, but the article is paywalled and ain't nobody got time for that.

Can a positive mindset protect us from the sniffles?
If you’re trying to avoid the worst of cold and flu season, looking after your mind can help shape your immune system, finds columnist David Robson
www.newscientist.com

Can a positive mindset protect us from the sniffles? | New Scientist

If you’re trying to avoid the worst of cold and flu season, looking after your mind can help shape your immune system, finds columnist David Robson
www.newscientist.com www.newscientist.com
 
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