rthm_health

RTHM’s Take: “This is a concerning study that shows Long COVID (and any COVID infection) may heighten the risk of ADRD, and in some cases accelerate disease progression. This study should sound a public health alarm that without effective treatments and better infection prevention, we may experience a worsening wave of neurodegenerative conditions and cognitive decline in the years to come.” “— Jennifer Curtin, MD, RTHM Co-Founder

Study Author Conclusions: “Results are consistent with the view that changes in pTau-181 inconsistent with normal ageing may be common among participants with N-PASC. Indeed, more than half of participants with N-PASC experienced a ≥20% increase in absolute levels of pTau-181 relative to pre-COVID-19 levels… Among participants with N-PASC who exhibited pTau-181 increases ≥20% relative to pre-COVID levels, 45.1% expressed pTau-181 levels above an established cutoff to identify ADRD (Alzheimer’s Disease and Related Dementias) “Intriguingly, in this study we found that evidence of increased pTau-181 was associated with increases in AB40/42 ratios consistent with a pTau-mediated ADRD. These findings support pTau-181 as a valuable longitudinal biomarker for N-PASC and highlight the potential need for early, tau-targeted interventions to mitigate progressive cognitive decline.” (Arrow pointing right) Small Citation

What This Suggests The authors connect findings to a broader hypothesis that COVID-related neuroinflammation/microglial activation could contribute to tau phosphorylation/spread, potentially accelerating latent vulnerability. Patients who develop N-PASC after COVID-19 might share certain clinicopathological features with Alzheimer's Disease, however the authors explicitly caution that replication with neuroimaging/brain measures is needed to know whether plasma pTau‑181 elevations reflect cerebral tauopathy in N‑PASC. The authors suggest pTau‑181 could potentially help prognosticate neurological Long COVID—especially for symptoms persisting beyond ~1.5 years—but emphasize the need for long-term follow-up to see whether pTau‑181 continues rising or predicts later cognitive impairment. (Arrow pointing right) Small Citation

Amyloid Signals Moved With pTau‑181 in a Subset Among people with N‑PASC, ≥20% pTau‑181 increases were linked to a much higher chance of a ≥20% increase in Aβ40/42 ratio and higher risk of a ≥20% rise in IAB. Authors frame this as potentially concerning because pTau‑181 + amyloid ratio changes are a pattern often discussed in Alzheimer’s disease biology—though this study does not diagnose dementia or measure brain pathology directly. Time Course Matters: pTau‑181 Elevation Bigger After 1.5 years of Symptoms Average pTau‑181 elevation was reported as ~14.6% within ≤1.5 years since infection, but ~56.5% among those assessed >1.5 years after symptom onset (suggesting a possible lag or progression). GFAP decreases were more pronounced earlier (≤1.5 years) than later.

Symptom cluster tracked with pTau‑181 rises A ≥20% pTau‑181 increase was associated with higher risk of: “Any central nervous system” symptoms (aRR ~1.31) Loss of taste/smell (aRR ~1.30) Anxiety/depression (aRR ~1.26) Brain fog (aRR ~1.22) Muscle weakness (aRR ~1.30 (Arrow pointing right) Small Citation

Before COVID: Evidence of Higher Amyloid Burden Helped Predict N‑PASC Individuals who developed N-PASC had higher Aβ40/42 ratios, NfL, and IAB values, before developing COVID-19. Interpretation offered by authors: this pattern could reflect pre-existing vulnerability (amyloid-related biology) that may make some individuals more susceptible to neurologic sequelae. Amyloidosis often requires a secondary neuropathology to elicit the most severe symptomatology Authors note that if these findings indicate that cerebral amyloidosis is present, even in its mildest forms, then the post-COVID-19 increase in pTau-181 may correspond to the onset of pathological Alzheimer's disease. (Arrow pointing right) Small Citation

Key Finding: After COVID, pTau‑181 rose sharply in N‑PASC, but not in controls Main longitudinal result: pTau‑181 increased ~59% after COVID-19 onset in the N‑PASC group, relative to matched controls. About 58.6% of N‑PASC participants had more than 20% increase in pTau‑181 from their own pre‑COVID levels. N-PASC was associated with changes in pTau-181 that exceeded cutoffs used in studies of ADRD (Alzheimer’s Disease and Related Dementias). In contrast, GFAP and NfL showed post‑COVID decreases in the N‑PASC group versus never‑COVID controls. (Paradoxical finding that could be from neuroimmune system repairing itself, or from neuroinflammation restricting glymphatic clearance.) Among participants infected with COVID-19, there was an increase in IAB (biomarker for Alzheimer's risk) when compared to never-infected controls (Arrow pointing right) Small Citation

Description of the Study: The authors studied a prospective cohort of essential workers with paired plasma samples (one collected before the pandemic and one after) to test whether neurological Long COVID (N‑PASC) tracks with changes in Alzheimer’s-linked blood biomarkers. Participants with N‑PASC (n=227) were matched 1:1 to controls (n=227) who either had COVID without N‑PASC (n=124) or had no COVID by follow-up (n=103) N‑PASC required ≥1 neurological symptom (e.g., loss of taste/smell, brain fog, dizziness/vertigo, tinnitus, headache, balance issues) emerging within 3 months of infection and persisting more than 3 months. N‑PASC was assessed on average ~2.7 years after symptom onset. They measured neurological biomarkers well-established to correlate with neurodegeneration: pTau‑181, GFAP, NfL, Aβ40, Aβ42; plus derived measures like Aβ40/42 ratio and an inverse mean amyloid burden (IAB) metric. (Arrow pointing right) Small Citation

New Study: Patients who develop Long COVID have increased amyloid biomarkers consistent with Alzheimer's Disease. Authors: Xiaohua Yang, Ashley Fontana, Sean A.P. Clouston, Benjamin J. Luft (Arrow pointing right) Small Citation

A study found that people with neurological Long COVID show blood biomarker changes linked to brain cell stress & Alzheimer’s biology. Tau and amyloid levels rose after infection and tracked with brain fog and cognitive symptoms, suggesting measurable neurological effects. doi.org/10.1016/j.eb...

Dr. Jennifer Curtin recently joined host Jill Brook in an episode of The POTScast to speak about RTHM’s innovative HIPAA-compliant AI platform, which equips people with infection-associated chronic conditions with practical guidance and tools.

🎙️Listen now-https://ow.ly/ji4Z50Y7T2f

RTHM is now accepting patients in Georgia and Ohio, expanding access to care for people managing Long COVID, ME/CFS, POTS, and other infection associated chronic conditions.

Explore RTHM Clinic → www.rthm.com/clinic

Study # 10 Title: Muscle tissue exposed to blood from ME/CFS & Long COVID patients leads to severe muscular and mitochondrial deterioration. Key Findings: Overall, skeletal muscle degeneration followed a multi-phasic progression from compensatory adaptation to structural and metabolic collapse driven by mitochondrial impairment and disrupted protein turnover. Author Conclusions “We propose that skeletal muscle tissue in ME/CFS and LC-19 progresses through a hypermetabolic state, leading to severe muscular and mitochondrial deterioration. This is the first study to suggest such transient metabolic adaptation.” doi.org/10.1088/1758-5090/adf66c

Blood vessels in the retinas of Long COVID patients show a significant reduction in density Description In the study, researchers used advanced imaging called optical coherence tomography angiography (OCT-A) to examine the retinas of Long COVID patients vs. healthy controls. 
 They found that patients with long COVID had a significant reduction in the density of small blood vessels in the back of the eye compared to healthy individuals, suggesting a reduction in the perfusion (blood flow) to the deep part of the retina. Author Conclusion: “In conclusion, our study identifies retinal perfusion changes in Neuro-PASC patients with a reduction in deep (DCP) capillary plexus and vessel length density (VLD), suggesting that the smallest capillary vessels are preferentially targeted.” Site Sourced: https://www.mdpi.com/2313-433X/11/2/62

AI model can identify ME/CFS patients with ~90% accuracy. A new artificial intelligence tool, BioMapAI, was developed by scientists at the Jackson Laboratory and Duke University School of Medicine, in collaboration with researchers at the Bateman Horne Center. The research team discovered that their AI tool could accurately estimate the severity of symptoms by analyzing immune cells and was able to predict gastrointestinal, emotional, and sleep problems by analyzing microbiome data. “Biologically, our study introduces a highly nuanced approach to link physiological changes in gut microbiome, plasma metabolome, and immune status, with host symptoms, moving beyond the initial causes of the disease… This study represents a substantial technical and biological advance over... other investigations of ME/CFS to date.” doi.org/10.1038/s41591-025-03788-3

Long COVID risk doubles in children after reinfection. Description A retrospective cohort study used data from 40 children's hospitals participating in the Researching COVID to Enhance Recovery (RECOVER) Initiative investigated reinfection in children and adolescents. This study was the first and largest investigation of its kind. The study included patients younger than 21 years with documented SARS-CoV-2 infection after Jan 1, 2022. The second SARS-CoV-2 infection was confirmed at least 60 days after the first infection. “Children and adolescents face a significantly higher risk of various PASC outcomes after reinfection with SARS-CoV-2… regardless of severity, and suggest that the risk of PASC might be cumulative with each successive infection” Author: doi.org/10.1016/S1473-3099(25)00476-1

Exercise Increases Microclots In Long COVID. 46 people living with Long COVID with a low risk of experiencing post exertional malaise (PEM) completed two submaximal cardiopulmonary exercise tests (CPET), separated by 24 hours. They had blood drawn before starting the exercise test (CPET) and after, to look for microclots and cytokines. Author Conclusions; “This study provides.. a biological basis that might explain exercise-induced symptom exacerbation in people with Long COVID.. “ Small at the bottom: doi.org/10.21203/rs.3.rs-6717727/v1

Title at the Top: SARS-COV-2 infection in pregnant women is linked to developmental delays in toddlers This study aimed to evaluate the impact of maternal COVID infection on neurodevelopment of the child and investigate whether cytokine and chemokine profiles predict delays at 24 months. Author Conclusions “This study shows the long-term impact of maternal SARS-COV-2 infection on child development. Prenatal SARS-COV-2 infection in pregnant women is linked to developmental delays in toddlers, with cytokine and chemokine changes associated with neurodevelopmental outcomes at 24 months” Small at bottom: doi.org/10.1038/s41390-025-04192-w

Title at the top: Long COVID risk has not decreased over time As part of the National Institutes of Health (NIH)–funded Researching COVID to Enhance Recovery (RECOVER) Initiative, study authors leveraged electronic health record (EHR) data from three large clinical research networks to estimate Long COVID incidence over time. Author Conclusions: “We did not find evidence of Long COVID risk decreasing over time… Our findings indicate that preventing and mitigating Long COVID remains a public health priority.” Source: doi.org/10.1093/cid/ciaf046

Title at Top: 40% of Olympians experienced reduced sports performance for at least 4 months after COVID infection 37% reported symptoms lasting 
more than 4 weeks 25% had symptoms persisting for more than 8 weeks 20% were still symptomatic 16 weeks after initial infection. Author Conclusions “Our findings, which highlight the frequent occurrence of sport-limiting symptoms (e.g., fatigue) and performance impairments 16 weeks post-infection, underscore the need to revise current return-to-play (RTP) protocols for elite athletes.” Site: https://link.springer.com/article/10.1007/s12662-025-01024-1SOURCE

Title at Top: Infectious SARS-COV-2 particles detected in semen for up to 8 months after infections 45% had infectious viral particles confirmed via Vero cell culture. 55% had SARS-CoV-2 RNA detected in their semen (21 out of 38 patients). 91% detection in semen of patients with moderate acute COVID-19 severity. Author Conclusions: “This study confirms that SARS-CoV-2 can persist in the semen of patients who have recovered from COVID-19, indicating that the male genital tract may be a reservoir for the virus.” 

 Published 2024, observational cohort study (n=38)

Title at top: Long COVID may have surpassed Asthma as most common chronic condition in Children Among infants/toddlers (0-2 years) with SARS-CoV2 infection history, 40 of 278 (14%) were classified as having probable Long COVID. Among preschool-aged children (3-5 years), 61 of 399 (15%) were classified as having probable Long COVID. On average, infants and toddlers had symptoms that lingered for 10 months and preschool-aged children had symptoms that lingered nearly 17 months.

Title: 2025 End of Year Research Swipe to see the top research on Long COVID and ME/CFS ADD ARROW

A recap of key Long COVID and ME/CFS studies from 2025.

These findings continue to challenge outdated explanations and underscore the urgency of better care, better tools, and continued research.

Swipe through to see the studies shaping what comes next.

That’s a very reasonable question. Right now we don’t have clear timelines or guidance on this, which is why continued research is so important.

It can feel that way reading this, but this research doesn’t mean people are dangerous. It highlights biological changes that deserve care and investigation, not stigma.

That concern makes sense. The lab-grown muscle model helps isolate biological effects, but it doesn’t directly translate to real-world blood transfusion outcomes. It’s a step toward understanding mechanisms.

You’re right. Biomarkers are urgently needed. Research like this helps lay the groundwork for better screening, diagnosis, and clearer guidance going forward.

Being dismissed by doctors while losing work, stability, and support is devastating. None of this is your fault. It reflects systemic failure, not a lack of effort or strength on your part.

This is a common concern. There’s currently no evidence that ME/CFS or Long COVID is transmitted through blood, but studies like this help inform future research and safety guidance.

That anger and grief are completely understandable. Many people feel deeply let down by pandemic responses and the lack of support since. Losing a close friend on top of chronic illness is an enormous burden.

That’s a really thoughtful observation. Many people describe a loss of energy and capacity long before visible muscle loss, which is part of what makes this illness so hard to explain. Studies like this help explore what might be happening beneath the surface, even when changes aren’t obvious yet.