ex Aerospace Engineer, now ME/CFS & LC patient researcher and cofounder @amaticahealth https://t.co/BvmsOvch0p - email support@amaticahealth.com questions
Aug 19 • 16 tweets • 3 min read
🔬Interesting new brainstem and cerebellum study in Long COVID - new imaging findings from 2025
A new brain imaging study of Long COVID patients reveals major damage in key parts of the brain responsible for movement, balance, and automatic body functions like heart rate and sleep.
Let’s break it down. 🧵
The researchers scanned the brains of 44 Long COVID patients (15 bedridden) and 14 healthy people using high-resolution MRI.
They focused on a part of the brain called the brainstem, and the nearby cerebellar peduncles - which connect the cerebellum to the brain.
Aug 15 • 18 tweets • 3 min read
🔬New study shows SARS-CoV-2 causes direct damage to heart cell mitochondria - even months after recovery - helping potentially explain Long COVID heart symptoms like chest pain, palpitations & fatigue.
Been waiting to have time to read this paper. Let’s break it down. 🧵
Researchers studied 5 people who had COVID-19 weeks or months earlier. They all had new or unusual heart problems, like chest pain, irregular heartbeat, or even cardiac arrest.
Each patient had a heart biopsy (a sample of heart tissue examined under a microscope).
Aug 14 • 25 tweets • 4 min read
🔬Interesting new study: Researchers exposed lab-grown human muscle tissues to blood serum from people with ME/CFS and Long COVID.
After 48 muscles:
- Produced less force
- Fatigued faster
- Lost their ability to hold peak strength
Let’s breakdown the full paper 🧵
Cohort: 4 ME/CFS patients, 5 Long COVID patients, 4 healthy controls (all female).
Method: Researchers grew 3D muscle tissues from human cells, exposed them to patient serum for 48–144h, and tested strength, gene activity (using RNA-seq), structure, and metabolism.
Aug 12 • 16 tweets • 2 min read
Many new faces, so I thought I’d share my story and how @amaticahealth came to be.
I developed Long COVID in 2021 after a Delta infection, almost immediately experiencing neurological symptoms like vertigo and visual snow syndrome (VSS).
My condition worsened rapidly after my physician recommended intense exercise, leading to a major crash from which I never recovered.
Aug 11 • 26 tweets • 4 min read
🔬New @BhupeshPrusty paper breakdown - very cool paper:
The study finds that people with ME/CFS & Long COVID have antibodies in their blood that may directly interfere with mitochondria (how human cells create energy and regulate inflammation)
In simple language all findings 🧵
So some basic knowledge first:
Our immune systems make antibodies (also called IgG). These are proteins that help the body fight off infections.
In some people, antibodies don’t shut off properly and may begin to affect the body’s own cells. This is called autoimmunity.
Aug 9 • 9 tweets • 2 min read
🔬One of the main questions in Long COVID & ME/CFS
Autoimmunity vs Viral Persistence
- the virus never fully left, or
- the immune system started attacking the body
Our new @amaticahealth blood-RNA test may help insights into which is happening.
Let’s look at some markers 🧵
So some base information - what is the test?
The test is whole blood RNA Sequencing ~ 20,000 results per patient, with roughly 1500 pathways insights!
mRNA are messengers from our dna that help make proteins and this is what we test.
RABGAP1L is a protein that helps control how cells move and recycle materials. It turns off other proteins that guide tiny packages inside the cell. These packages carry waste, used-up parts, or germs to places where they can be broken down.
How it fights infection:
By turning Rab proteins off at the right time, RABGAP1L moves invading bacteria and viruses into compartments where they are broken down. Loss or reduction of RABGAP1L lets more influenza virus and Streptococcus pyogenes survive and replicate in cells.
Aug 6 • 22 tweets • 4 min read
🔬Simplified breakdown of the Decode ME results:
DecodeME identifies 8 gene regions linking immune response, mitochondrial energy control, and brain-cell signalling to ME/CFS
Genomic evidence the disease is biological.
Let’s breakdown everything in depth 🧵
Study Cohort:
15,579 people with doctor-diagnosed ME/CFS + 259,909 UK Biobank controls (no ME/CFS).
85 % were women, average age ≈ 52 y.
Jul 30 • 9 tweets • 2 min read
🔬Simplified Break down of the recent AI paper that was circulating by @DeryaTR_ & co
Researchers used AI + multi-omics to decode the biology of this misunderstood disease.
Similar approach to what we will be doing @amaticahealth
So what did they find? 🧵
The team followed 249 people over 4 years - 153 with ME/CFS, 96 controls.
They collected gut microbiome, blood metabolites, immune cell profiles, lab tests, and symptom reports at each visit.
Then trained a deep neural net (BioMapAI) to map it all.
Jul 15 • 8 tweets • 3 min read
One of the most interesting trends in our recent @amaticahealth neuro-immune ME/CFS & Long COVID subgrouping data:
A Renin‑Angiotensin - neuro inflammation/injury axis signal.
And we aren’t the only people who have found this.
🧵👇🏻
Cluster 3 individuals with high brain‑injury markers - S100B (astroglia) & NfL (axons) - also had higher plasma angiotensin II (Ang II).
Ang II is a vaso‑active peptide that *drives* endothelial + neuro‑inflammation via AT1‑ROS pathways.
Jul 11 • 7 tweets • 1 min read
Interesting paper - simple breakdown 🔬
At rest, the ME/CFS fluid had extra serine (a protein building block) and less of a folate-type vitamin called 5-MTHF.
That hints the brain’s ‘recycle & repair’ chemistry is off-balance.
So there was a lot of talk recently about a paper discussing COVID-19 micro-clotting.
I thought I’d break it down in simple language.
The paper looked at why tiny blood vessels get blocked in severe COVID-19. They discovered, it is not the usual clots we hear about. 🧵👇🏻
Inside capillaries, the “wall” is a layer of endothelial cells. When these cells die suddenly, they leave rough patches that blood cells can stick to.
Jun 10 • 11 tweets • 3 min read
🔬Low serotonin in ME/CFS & Long COVID - what could explain it?
Within our community 1 energy metabolism group, a trend to low serotonin was seen, what could explain this?
🧵👇🏻
Brief reminder:
We split our ME/CFS and Long COVID cohort into communities based on how closely related their metabolism markers were.
We ended up with 2 main groups.
Community 1 having mitochondrial stress markers high - the others, not as much.
Jun 5 • 10 tweets • 2 min read
🧵 COVID Isn’t Over - Even If You Feel Fine Post Infection
Even mild cases with no immediate long lasting symptoms can cause lasting immune changes.
After the 1918 flu, Parkinsonian illness spiked. Decades later, H1N1 was linked to dementia and Parkinson’s.
COVID-19 likely will have similar outcomes.
Studies show even mild infections can leave the immune system inflamed and fatigued months later.
The damage is often silent - but significant and ongoing.
Jun 4 • 10 tweets • 5 min read
🧵In our metabolic subgrouping, two distinct clusters appeared showing the variability of ME/CFS and Long COVID.
Two different biomarker profiles, each able to lead to similar pathological issues.
These differences can be what drives drug response differences in patients.
1/
In our data, two clear groups show up
• Group 1: high markers of hypoxia and mitochondrial stress
• Group 2: normal mitochondria, but high vascular stress and low nitric oxide production hints
May 30 • 7 tweets • 3 min read
🧵We clustered our patients based on metabolic / O₂-sensing / mitochondrial markers.
Two distinct subgroups appeared, showing potential differences in underlying metabolic function.
We also looked at which other markers separated them.
Here’s what we found 👇
@amaticahealth
The metabolic/mito markers we used:
Your mitochondria normally run the TCA/Krebs cycle.
Under threat, immune cells take a detour: IRG1 converts cis-aconitate → itaconate.
That detour = the itaconate shunt.
May 13 • 9 tweets • 2 min read
With my recent results from the @amaticahealth panel, I’ve had a lot of people mention specific theories I may fit into, so I thought I’d break them down!
• Itaconate Shunt Theory (Davis & Phair Theory)
What is it and what does it mean?
🧵👇🏻
Infections make you feel exhausted.
This occurs because your immune cells may be diverting energy through a “detour” known as the itaconate shunt, aiming to starve pathogens but temporarily reducing your energy supply.
Apr 11 • 11 tweets • 3 min read
New Research Post 🔬❕
47.1% of ME/CFS & Long COVID patients had elevated ANG II compared to all controls.
Correlation between ANG II and NEFL (P<0.0001), potentially linking ANGII levels with neuroinflammation
🧵👇🏻
Ang II is part of the renin–angiotensin–aldosterone system (RAAS). It raises blood pressure, tells your body to retain salt & water, and boosts thirst.
It’s essential for survival — but too much of it can be detrimental