Retinal vasculature is like a window into the brain because the eyes and the brain share the same system.

In this study changes were detected that weren’t too different from MS in LC patients.

In PCS, three layers were significantly thinner. pRNFL (nerve fibre layer around the optic disc), GCIP (ganglion cells plus their synaptic layer), TMV (total macular volume). And the worse the symptoms, the thinner the tissue!
Neuroretinal tissue is being lost - and it scales with how sick the person is.

This exact pattern - pRNFL and GCIP thinning - is an established marker of axonal and neuronal loss in multiple sclerosis, where OCT is used as a proxy for what’s happening in the brain

>A naturally occurring molecule released during exercise may hold the key to strengthening muscles without physical activity. In experiments, mice given BAIBA developed larger muscles, improved muscle function, greater fatigue resistance and better exercise performance than untreated mice.
by u/mvea in science

It would be very interesting for people with ME/CFS if you could get the physiological benefits of exercise without actually doing it. I hope this research advances fast!

"This study suggests that a proportion of patients with ME/CFS have elevated CSF opening pressures and may experience symptom relief following CSF subtraction. Our data indicate that some anatomical structures in the craniocervical area may be related to CSF pressure, although interpretation is challenging and merits further investigation."

New brain MRI study which induced hypoxia (too little oxygen) to compare reactions in the brain of patients to controls.

Interestingly lactate levels were already elevated at baseline in patients. Under hypoxia conditions controls started to produce more lactate to match while ME patients levels stayed at the elevated levels they were already at.

Roughly lactate is a byproduct of the less efficient way our system produces energy when oxygen is lacking (though its role in the brain is more complex than just that).

The group around Putrino has successfully completed their first mitochondrial transplant in a patient with vision loss after a brain bleed with the help of other experts in the field.

This should pave the way to trialing mitochondrial transplants in Long Covid and ME which Putrino already has plans on trialing.

“Also, there are so many conditions that can benefit from this work - including other forms of brain injury and neurodegeneration, but also #LongCOVID, #MECFS and other complex chronic illness where energy limitation is a problem. We will be aiming to get an active research arm off the ground on this ASAP.”

Source: https://bsky.app/profile/putrinolab.bsky.social/post/3msqs6xrgkc2i

Abstract

Long COVID (LC) - a chronic condition characterized by persistent, debilitating symptoms following SARS-CoV-2 infection - has emerged as a major public health challenge. Although many interrelated mechanisms have been proposed as drivers of LC, the root causes have yet to be identified, posing significant challenges for therapeutic development. While many blood-based studies have been conducted, they have not yielded conclusive mechanistic insights into LC pathogenesis.

Attention has therefore turned toward direct tissue investigation, with the gastrointestinal (GI) tract becoming a major focus due to evidence that virus or viral components can persist at this site for months to years following an episode of COVID-19. Here, we performed a high-dimensional characterization of colorectal tissue and peripheral blood in a highly characterized cohort of 44 people with LC and 13 recovered controls. We profiled SARS-CoV-2 persistence, host immune responses, and tissue inflammation using bulk and single-cell RNA sequencing, nCounter RNA probe hybridization, quantitative PCR, metagenomic next-generation sequencing, plasma proteomics, high-dimensional spectral flow cytometry, in situ-hybridization/immunohistochemistry, and single-cell digital spatial omics.

Our results support a model in which LC is driven by long-term immune dysregulation and perturbations of the regulatory gut immune environment which imply ongoing viral persistence, although direct viral detection was only observed in a subset of participants. Specifically, we identify a tissue-based transcriptional environment in which SARS-CoV-2 activates innate myeloid immune signaling, driving chronic inflammation while simultaneously downregulating pathways responsible for immune-mediated clearance of infected cells, including antigen presentation, phagocytosis, cytotoxic immune cell trafficking, and granzyme production.

Importantly, signatures in peripheral blood are considerably weaker than those observed in tissue. Together, these findings provide a direct biological rationale for therapeutic strategies in LC aimed at enhancing or redirecting cytotoxic immune function to overcome immune dysregulation and clear persistent viral reservoirs.

Realistically, how many years away are we?

In the German CoCo-Fakt study at Cologne and Ausberg, patients who later developed Long Covid reported doing more and more intense physical activity prior to infection than controls who had COVID-19 but no long term symptoms.

The researchers expected the opposite.

The paper concludes:

"Unexpectedly, participants with long-term symptoms reported a longer PA [physical activity] duration in the four weeks before quarantine than those without long-term symptoms, albeit with a trivial effect size."

This study was summarised using Gemini AI.

The study investigates how the SARS-CoV-2 accessory protein ORF7a manipulates host cell metabolism to create an environment that favors viral replication and immune evasion. Normally, healthy cells rely heavily on mitochondria to efficiently produce energy through a process called oxidative phosphorylation. However, the researchers discovered that the ORF7a protein essentially short-circuits this system, forcing the cell to rely on a less efficient, glucose-heavy energy pathway called glycolysis.

Cellular Changes Induced by ORF7a

Key Mechanisms of Mitochondrial Sabotage

The researchers identified two primary ways that ORF7a breaks the cell's mitochondrial engine:

• The PDK4 Roadblock: ORF7a causes a massive increase in the enzyme PDK4. PDK4 then phosphorylates and turns off the Pyruvate Dehydrogenase Complex (PDHC). This effectively acts as a roadblock, stopping pyruvate (the cell's standard fuel) from entering the mitochondria to be burned for energy.
• Direct Complex I Impairment: Independent of the PDK4 roadblock, ORF7a selectively cripples "Complex I," a crucial piece of the mitochondrial electron transport chain. It also stops these respiratory complexes from assembling together properly.
• Irreversible Damage: When scientists treated the cells with a drug called dichloroacetate (DCA) to remove the PDK4 roadblock, mitochondrial energy production still failed to recover. This proved that the damage to Complex I is a separate, profound disruption caused by the virus.
• Oxidative Stress: Because the mitochondria are malfunctioning, they leak reactive oxygen species (ROS), and the cell's natural antioxidant buffers (like glutathione) are depleted, leading to severe cellular stress.

Key Takeaway

The SARS-CoV-2 ORF7a protein cripples the host cell's mitochondria via a "two-pronged attack"—blocking fuel entry by activating PDK4 and destroying the engine itself by impairing Complex I. This forces the cell into an inflexible, stressed, glucose-burning state that likely fuels the severe inflammation and metabolic complications seen in COVID-19 patients.

Link to 2026 study

I would like to get genetic testing done to look at mthfr, mitochondrial issues, etc.

I'm completely overwhelmed with the options. Is there a company who is more medically aimed? Or one that's the most comprehensive? I know I'll have to put whatever one into one of those other sites, but don't want to waste money on a company that isn't the best choice.

Any recommendations would be greatly appreciated!

The newest international research on fibromyalgia.

https://www.nature.com/articles/s41591-026-04492-6

One of the main Results they found is: Associations with 26 variants establish genetic underpinnings of fibromyalgia

And: BREAKTHROUGH IN RESEARCH Fibromyalgia is a physical pain disease! Fibromyalgia is a physical pain disease that originates in the central nervous system. This is shown by new, international research. FSF welcomes all research that can help shed more light on possible causes of the development of fibromyalgia, so that we can learn more about the disease. We have taken a decisive step with a new and comprehensive international research project, which was published at the end of July 2026 in the renowned international journal Nature Medicine. The researchers identify 26 areas in the genome that can influence the development of fibromyalgia. A genetic predisposition to fibromyalgia is well described, but the study has now identified a genetic signature that relates specifically to the brain and nervous system. The researchers have not found the actual cause of the disease, but their results place fibromyalgia firmly among other physical diseases.

This summary was made using Gemini AI.

The study is by Alain Moreau et al.

This study, published in August 2026 in the International Journal of Molecular Sciences, explores the biological reasons why Long COVID affects people so differently—specifically focusing on cognitive decline (often called "brain fog") after physical or mental effort. The researchers investigated whether a person's haptoglobin (Hp) phenotype—a genetic variation of a specific blood protein—could predict how severe their post-exertional symptoms would be.

How They Did It

The researchers compared 44 individuals with Long COVID to 20 control patients who had quickly and fully recovered from a COVID-19 infection. They analyzed the participants' genetics, blood metabolites, and physiological data both before and after a 90-minute post-exertional stress challenge.

Key Findings

The study revealed that a person's haptoglobin genetics strongly predicted their reaction to the stress test:

• The Hp2 Variant (Hp2-2 and Hp2 allele carriers): People with this genetic variant experienced worse overall fatigue, poorer physical function, and more severe symptoms after exertion. Immediately following the stress test, they showed a significant drop in cognitive performance. They also had lower levels of energy-related blood metabolites (like citric acid), which correlated directly with their poorer brain function.
• The Hp1-1 Variant: Individuals with this specific variant demonstrated "cognitive resilience". Their brain function did not decline after the stress test, and they had much better long-term cognitive trajectories. Their brains were also significantly better at extracting oxygen during the challenge compared to the Hp2 group.

The Takeaway

In short, your haptoglobin genetics might help explain why you might experience severe brain fog and crashes after exertion with Long COVID, while someone else might not. If validated in larger groups, a simple blood test to check your haptoglobin type could be used as a biological marker to classify Long COVID severity and eventually tailor personalized treatments based on your genetic profile.

Link to 2026 study