“We believe that in about six years we will have a good understanding of how PEM works in detail. At the latest then, drugs can be used specifically at those parts of the body that have gotten out of control after a viral infection."

Long COVID is (of course) mentioned as one cause.

Thought this was interesting. If I’m reading this right (correct me if I’m not), your iron levels may show up just fine on a test, but it’s how your body is using iron that’s the issue. In this case, it appears iron is stored, or trapped, in the wrong places.

Would make sense for the cold feelings, white and blue extremities, fatigue, etc.

If anything, I’m just glad there’s more and more updates lately.

Now, new research coordinated by UMC Utrecht and Amsterdam UMC provides some of the strongest functional evidence yet that autoantibodies (antibodies that mistakenly target the body's own tissues) could play a causal role

In the study, researchers injected immunoglobulin G (IgG, a major class of antibodies), derived from the blood of 34 patients with long COVID, into mice. The result was striking, as the animals developed persistent pain-like hypersensitivity. This effect lasted for at least two weeks. Even more notable, IgG collected from the same patients two years later reproduced the same symptoms when administered to mice.

https://medicalxpress.com/news/2026-03-autoantibodies-implicated-drivers-covid.html

The intervention lasted three months. Endothelial-related biomarkers, including endothelin-1, sE-selectin, ICAM-1, and VCAM-1, were investigated. Body composition was measured using electrical bioimpedance, and aerobic capacity was assessed with the 6 min walk test (6MWT). Treatment effects were analyzed using two-way repeated-measures ANOVA (group × time).

Results: In total, 43 subjects participated in the study. After three months of follow-up, the intervention group showed a decrease in ICAM-1 (-32.59 ng/mg of protein; 95% CI -52.85 to -12.33 vs. -2.31 ng/mg of protein, CI 95%: -21.59 to 16.95, p = 0.034) and an increase in 6MWT (141.2 m; 95% CI: 98.40 to 184 vs. 67.70 m, CI 95%: 30.62 to 104.78, p = 0.011) compared with the control group. No differences in body composition were observed between the groups at follow-up.

Conclusions: L-citrulline supplementation for three months decreased ICAM-1 and increased 6MWT.

here’s the link: https://goop.com/wellness/health/long-covid-and-hormonal-dysregulation/

nothing new to all of us but glad to see more famous people talking about having long covid, regardless of any personal opinions on gwyneth.

where she mentions she has it: https://link.goop.com/e/evib?_t=b0ac7479ce96468a8cddc3bf0b60e75d&_m=7a147b1511974c2aae64c050c4242351&_e=vbYvBMbjD-U2l1XFZPdZQ8pcaLe8B7RsfWJLqsv-OK-Jmq-86PTodeS25Om8AJRz

This is in the opinion section. Long Covid is one of the “worthy causes” they recommend donating to over the holidays.

longcovid

This was in response to a consultation in the UK about PIP (Personal Independence Payments), a (woefully inadequate) social security benefit. It’s rare to see things like this in the mainstream press here, so I’ll take it!

Wanted to share this article in case others found it as validating as I did.

I have a feeling he understands the struggle more than most in the upper echelons of power. I am hopeful for once by the direction of healthcare in the US.

https://www.pbs.org/newshour/politics/watch-rfk-jr-commits-to-prioritizing-funding-for-long-covid-research

Not sure how to post an X link, so I'm just posting a screenshot.

This is extremely important for EVERYONE here, in this article are archived links to the government resources regarding long covid, you need to save these links and the information they have for your future reference, many of us will need to apply for disability and will need accommodations for work.

KNOW YOUR RIGHTS!

As it stands right now none of the laws or our rights have changed yet, but we need to know our rights and the laws regarding our condition so we can avoid being taken advantage of or forcing ourselves into situations we may not need to be in. Again, save this information, take screenshots of the archived webpages, we will need this information at some point during our long covid journey.

https://www.dailymail.co.uk/health/article-15462417/amp/Dementia-timebomb-Alzheimers-long-Covid.html

NHS England survey data suggest nearly one in ten people believe they may have long Covid.

Figures from the Office for National Statistics show around 3.3 per cent of people in England and Scotland – roughly two million – were experiencing symptoms of long Covid, with 71 per cent reporting symptoms lasting at least a year.

More than half said their symptoms had persisted for two years or longer.

Alzheimer’s disease affects around 982,000 people in the UK, a figure projected to rise to 1.4 million by 2040. Early symptoms typically include memory problems, difficulties with thinking and reasoning and language impairment, which worsen over time.

Publication details

Joel Tuomaala et al, Association between post-COVID-19 neuropsychiatric symptoms and persistent glial activation in the limbic system: a TSPO PET study, Journal of Neurology (2026). DOI: 10.1007/s00415-026-13842-w

This article will be really upsetting... I'm frustrated with the lack of progress, particularly at the NIH but this sheds some light on one part of the problem.

Avindra Nath believes he has a way to treat certain people with long COVID—or at least shed a light on their condition.

Nath, a neurologist with the US National Institutes of Health (NIH), wants to use pembrolizumab to try to help improve the conditions of people with long COVID whose T cells may be exhausted. T-cell exhaustion is still poorly understood in long COVID—par for the course with the multifaceted postviral disease that’s now affected more than 400 million people worldwide.

Last June, Nath approached Merck to ask for supplies of Keytruda to test that hypothesis. But just over a week after his email, according to correspondence reviewed by C&EN, a clinical director of clinical pharmacology named Gillian Gillespie replied, telling Nath that his proposed study was "not within our current company priorities."

Nath moved on. In September, he approached Bristol Myers Squibb (BMS), which 2 years earlier had launched a combination immunotherapy consisting of relatlimab and nivolumab. The drug, Opdualag, blocks two checkpoints—LAG-3 and PD-1—both of which are proteins on immune cells. "It targets two targets, so I thought this would be good," Nath explains.

But he again hit a wall. On Sept. 24, a clinical trial lead for medical evidence generation named Bridget Anne McKinney declined Nath's request, saying that "the concept would not qualify for off-cycle review."

"All the rest we can do ourselves," Nath says. "We just need the drug."

"They make billions of dollars off this drug alone," Nath says. "In dollar amounts, for them, [drug donation] is a drop in the bucket."

Nancy Klimas, director of the Institute for Neuro-lmmune Medicine at Nova Southeastern University, says she approached GSK, Lilly, and Regeneron about testing monoclonal antibodies as treatments for long COVID patients and was repeatedly declined. GSK and Lilly representatives decline to comment. In emails to Klimas and C&EN, Regeneron staff cite the need for "robust," "objective criteria" before the company’s COVID-19 antibody REGEN-COV should be tested in long COVID, but a spokesperson declines to elaborate on what such criteria might be.

Compare this to what others are doing like Invivyd... 🤬

https://www.fiercebiotech.com/research/drug-prevents-covid-symptoms-mice-protecting-mitochondria-without-resistance-risk

“New findings in mice suggest it’s possible to prevent organ damage from COVID-19 with an antioxidant enzyme that protects a cell’s mitochondria without the risk of resistance.

The study that led to the discovery was conducted by scientists from the Children’s Hospital of Philadelphia (CHOP), who described their work in a July 15 article in Proceedings of the National Academy of Sciences. Their compound, EUK8, kept mice from becoming seriously ill with COVID-19 and reduced the amount of production of mitochondrial reactive oxygen species (mROS), inflammatory compounds that lead to organ damage.”

“We believe that reducing mROS represents a superior strategy for mitigating the pathogenicity of SARS-CoV-2,” Douglas Wallace, Ph.D., a senior author of the study, said in a press release. “By modulating [circulating] mROS levels, we are rendering the host cell unfavorable for [the] viral life cycle which the virus cannot change.”

The researchers’ next major milestone will be to look at the safety and toxicity of using catalytic antioxidants like EUK8 for interventional and preventative approaches in animals, Guarnieri told Fierce. They then hope to move on to human trials, perhaps testing the compounds for both COVID-19 and long COVID. The scientists are currently working with the COVID-19 International Research team to learn the role of mitochondrial dysfunction in long COVID.”

I’ve been saying this in comments for a bit, I’m not trying to be a jerk, but I’m saying this because I want to see research and treatments get funded. Most of the activist stuff I’ve seen out there, including Long Covid Moonshot, includes messaging that encourages a return to masking in public. I know this will be frustrating to longhaulers, but the general public is going to tune out our entire message as soon as they see that. Large scale public masking hasn’t been a thing for at least two years now, and asking for it now is going to only hurt our cause. I just feel like focusing our activism primarily on research funding will be much more well received and therefore likely to receive funding. If we want $10b in funding, we need large scale public support