Jack | amatica health Profile picture
Jul 15 8 tweets 3 min read Read on X
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.

🧵👇🏻 Image
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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.
Other studies:

- post‑COVID study showed AT1‑autoantibodies ↑ correlate with NfL ↑

frontiersin.org/journals/immun…
Direct Ang II - S100B data in Long COVID are limited

But S100B amplifies Ang II signalling via pathways like RAGE and S100B rises in acute neuro‑COVID.
Blocking Ang II in mice consistently lowers microglial activation, cytokines & cognitive defects.
Examples:

- AngII blockade cut lesion volume after TBI;

- AngII blockade reduced microglial IL‑1β & amyloid in AD mice l;

pubmed.ncbi.nlm.nih.gov/33178092/?utm_…

pmc.ncbi.nlm.nih.gov/articles/PMC64…
More research is needed, but could AngII be worth pursuing for a subgroup of ME & LC patients, potentially a target to lower neuroinflammation & injury?
To test your AngII, NEFL, and S100b - join our @amaticahealth batch 3 of the 31 marker panel.

amaticahealth.com/me-cfs-long-co…Image

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More from @JackHadfield14

Jul 11
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.
You can see the hold up as:

- The middle-step product sarcosine is high

- Later products dimethyl-glycine and choline are low

Hints that the system stalls somewhere in the middle.
Other clues show the brain rerouting energy:

compounds like creatine and trans-aconitate are higher than normal, suggesting a detour rather than a full-on fuel shortage.
Read 7 tweets
Jul 10
Breaking down the meaning behind some of the markers used in these clusters.

The main drivers of the cluster 3 neuro inflammatory group are NEFL & S100b.

What do elevated NEFL & S100b imply?

🧵 Image
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Elevated NEFL (neurofilament light chain) levels = sign of neuron damage, especially to axons.

It leaks into blood/CSF when brain or nerve cells are injured. Image
High NEFL isn’t disease-specific.

It shows up in MS, ALS, Alzheimer’s, stroke, trauma, and more. It reflects how much and how fast damage is occurring.
Read 9 tweets
Jun 24
3 Biological Neuroimmune Subtypes in Post-COVID & ME/CFS 🔬❕

We mapped our @amaticahealth post-COVID + ME patients into three distinct biological clusters using Neuroimmune markers

Cluster 1; mitochondrial stress
Cluster 2; Non inflammatory
Cluster 3; Neuro inflammatory

🧵 👇🏻 Image
How we did it:

• Serum & Plasma biomarker panel → neuro, immune, RAS & neuro mito markers

• Unsupervised Euclidean clustering → C1, C2, C3

Markers used for clustering:

- NEFL
- S100b
- PINK1
- DRP1
- BH4
- Serotonin
- Rock1
- Rock2 Image
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🔋Cluster 1 - Mitochondrial-Immune subtype

• PINK1 ↑↑ (mitochondrial recycling)
• ROCK1 ↓ (cytoskeleton/endothelial)
• ACE ↑, Ang-(1-7) ↓ → low protective RAS
• TWEAK & HIF-1α ↑ → inflam/hypoxia

Markers; No major neuro injury - some general inflam - mito stress high Image
Read 8 tweets
Jun 11
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. 🧵👇🏻 Image
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.
The death process is called necroptosis - a kind of self-destruct that bursts the cell open.

Somewhat like a popped balloon leaving bits of rubber behind.
Read 12 tweets
Jun 10
🔬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?

🧵👇🏻 Image
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. Image
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An interesting trend saw between these communities - was a reduction of serotonin in community 1:

What could explain this?

• Tryptophan diversion → kynurenine
• Poor gut tryptophan uptake
• Platelet hyper-activation & loss
• Fast-track breakdown via MAO-A/B

+ more 👇🏻 Image
Read 11 tweets
Jun 5
🧵 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.
Inflammatory markers like IL-6, TNF-alpha, and interferons stay elevated long after infection.

This persistent inflammation is linked to long-term disease - heart disease, diabetes, even neurodegeneration.
Read 10 tweets

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