A.N./NeMO Nantes

Neuroscientist (PhD) in Team Neuroinflammation, Mechanisms & therapeutic Options.

[@BrainComms @braincomms]

Liou et al. found hospitalized COVID-19 patients had lower hippocampal volume, reduced plasma glial fibrillary acidic protein and poorer memory than age-matched controls, despite similar white matter hyperintensity burden.

Read at 👉 https://t.co/EP9O3B9RtQ

#neuroscience

[Danielle Beckman @DaniBeckman]

Crucial paper on #NeuroCovid just published! #LongCovid patients with neurocognitive symptoms showed increased antibodies against the nervous system that correlated with several neurological symptoms. Targeting these antibodies might offer therapeutic benefits for some patients

[A.N./NeMO Nantes @GroupNEMO]

CFNI meeting in Nantes. Thanks to our sponsors

[A.N./NeMO Nantes @GroupNEMO]

Great meeting from our CFNI club in Nantes today. This morning neurological diseases go « immune » 🔥 great talks, great advances.

[Manuel Ruiz @manruipa]

🔴⚠️This is exactly the pattern many of us have been pointing to for years.

HHV-6 appearing in Long COVID severity is not really surprising. In ME/CFS, higher salivary HHV-6/HHV-7 loads had already been associated with a worse clinical phenotype, and HHV-6 has been repeatedly reported across immune-mediated/autoimmune diseases such as multiple sclerosis, Hashimoto’s thyroiditis, systemic lupus erythematosus, autoimmune hepatitis and connective tissue diseases.

It seems the story is repeating itself… or perhaps it never really changed.

Another piece of the same pattern: persistent infection, immune exhaustion, loss of antiviral control, reactivation of latent herpesviruses and autoimmune/immunopathological contexts.

If a patient shows repeated reactivations of HHV-6 or other herpesviruses, this should be treated with antiviral therapy directed at the specific virus involved — not dismissed as incidental.

ME/CFS:
https://t.co/UqTBYOnjJh

Multiple sclerosis:
https://t.co/4Xkg0Qx4X8
https://t.co/UmU9fmWuBZ
https://t.co/L9WXkNDpNh
https://t.co/2163YLgtKK

Hashimoto’s thyroiditis / autoimmune thyroiditis:
https://t.co/87R5PKLPne

Systemic lupus erythematosus / lupus:
https://t.co/yDGbjiYQa1
https://t.co/spn501hd5W
https://t.co/7S8pw9E18h
https://t.co/Mypfv3y0uf

Autoimmune hepatitis:
https://t.co/0ssoU07M8H

HHV-6 / autoimmunity review:
https://t.co/l6S1ISSCoh

[Dan Elton @moreisdifferent]

An N95, taken off occasionally doesn't provide 100% protection. But even if you get sick while 😷, it's generally lower viral load, leading to milder illness. Each CV-19 illness causes persistent IQ loss that might be permanent. The degree of IQ loss is correlated with severity:

[Multiple Sclerosis News Today @MSNewsToday]

Irisin, a hormone released during exercise, reduced nerve cell loss and eased clinical symptoms in a mouse model of multiple sclerosis. https://t.co/X86QAQEKal #MultipleSclerosis #MSTreatment #MSResearch #MSNews

[Herbert Renz-Polster @RenzPolster]

I have only seen the poster & not read this yet but this could be a very weighty publication:
https://t.co/EuO0AOyKNM

[charlos @loscharlos]

Everyday there is new research demonstrating how extraorndarily bad it is to be indefinitely reinfected by this virus.

[@BrainComms @braincomms]

Leckey et al. report novel measures of neurofilament light chain kinetics in the human central nervous system using stable isotope labelling. Translation occurs within hours, but appearance in cerebrospinal fluid takes ∼100 days 👉 https://t.co/28ciywb47S

[@BrainComms @braincomms]

High-resolution retinal imaging reveals immune cell infiltrates in the inner retina of MS patients, particularly after optic neuritis. These cells may serve as early, non-invasive biomarkers of neuroinflammation 👉 https://t.co/bP9wwRknIP

#MS #OpticNeuritis #Biomarker

[@BrainComms @braincomms]

Ingvarsson et al. report that serological evidence of infection with human herpes virus 7 is associated with a higher risk of developing multiple sclerosis. They also report a synergistic interaction between human herpes virus 7 and Epstein–Barr virus 👉 https://t.co/BLwSNpyQa5

[Joe @LTSmash420]

⚠️ 🧠 😷 Les recherches récentes, notamment une étude marquante publiée en février 2026 dans Alzheimer’s & Dementia (le journal de l’Alzheimer’s Association), confirment que le SARS-CoV-2 ne se contente pas de "passer" par les poumons : il laisse une signature neurologique semblable aux premiers stades de maladies neurodégénératives.

Voici comment ce virus s'attaque à notre "tour de contrôle" et les découvertes récentes sur les ravages de la Covid Longue.

1. L'invasion : Comment le virus entre-t-il ?

Le virus utilise plusieurs "portes dérobées" pour atteindre le système nerveux central :
* La voie olfactive : C’est le chemin le plus court. Le virus infecte les cellules de soutien dans le nez, traverse la plaque criblée et atteint le bulbe olfactif, qui est directement relié aux zones du cerveau gérant la mémoire et les émotions (le système limbique).
* Le "Cheval de Troie" : Le virus peut infecter des cellules immunitaires (monocytes) qui traversent ensuite la barrière hémato-encéphalique (BHE), transportant le virus comme un passager clandestin.
* L'attaque des vaisseaux : Le virus cible les récepteurs ACE2 présents sur les cellules endothéliales des vaisseaux sanguins cérébraux, provoquant des micro-caillots et une inflammation des parois (vascularite).

2. La découverte de 2026 : Le "gonflement" du plexus choroïde

L'étude de l'Université de New York (NYU), publiée dans le Alzheimer's Journal, a révélé un mécanisme clé jusque-là sous-estimé : le plexus choroïde.
Ce qu'ils ont trouvé :
* Augmentation de volume (10 %) : Les patients souffrant de Covid Longue présentent un plexus choroïde (la structure qui produit le liquide céphalo-rachidien et filtre les déchets) environ 10 % plus volumineux que les personnes saines.
* Fuite de la barrière : Ce gonflement indique une inflammation chronique sévère. Le plexus choroïde ne parvient plus à filtrer correctement les toxines, ce qui permet à des molécules inflammatoires du sang de "polluer" le cerveau.
* Signature Alzheimer : L'étude a corrélé ce gonflement avec la présence de biomarqueurs spécifiques dans le sang, comme la protéine pTau-217 et la GFAP (marqueur de lésion des cellules gliales), que l'on retrouve habituellement chez les patients au début d'Alzheimer.

3. Pourquoi le comportement change-t-il ?

L'infection directe et l'inflammation qui en découle altèrent la chimie du cerveau, provoquant des changements comportementaux parfois radicaux :
* Neuroinflammation persistante : Les cellules de défense du cerveau (la microglie) restent en état d'alerte maximale ("tempête de cytokines" locale), ce qui perturbe la communication entre les neurones.
* Atrophie limbique : Des scanners ont montré une réduction de la matière grise dans les zones liées à l'odorat et, par extension, aux émotions et à la mémoire.
* Déficit en neurotransmetteurs : L'inflammation réduit la disponibilité de la sérotonine et de la dopamine, ce qui explique l'émergence soudaine d'anxiété, de dépression sévère, d'apathie ou d'une irritabilité inhabituelle chez des personnes sans antécédents psychiatriques.

4. Les ravages de la Covid Longue : Le "Brouillard" et au-delà

Ce que nous appelons familièrement "brouillard cérébral" est en réalité une manifestation clinique de ces dommages structurels :

| Brouillard cérébral | Hypoperfusion (baisse du débit sanguin) et accumulation de déchets métaboliques.

| Pertes de mémoire | Dommages à l'hippocampe et accumulation de protéines Tau.

| Troubles exécutifs | Dysfonctionnement du cortex préfrontal (difficulté à planifier ou se concentrer).

| Fatigue neuro-cognitive | Le cerveau doit dépenser une énergie colossale pour effectuer des tâches simples à cause de la déconnexion neuronale.

En résumé

L'étude de 2026 montre que la Covid Longue n'est pas seulement une convalescence qui s'étire, mais un processus actif de "remodelage vasculaire" du cerveau.

[A.N./NeMO Nantes @GroupNEMO]

Previous PhD student from CRTI Inserm UMR1064. "Be curious. Be aware of your weaknesses. Stay grounded. Seek for help, mentors. Don't forget who you are." Bravo Annie...

[Nat Rev Neurology @NatRevNeurol]

📢NEW COLLECTION - NEUROIMMUNOLOGY

Nature Reviews Neurology is working with the International Society of Neuroimmunology (@ISNI_neuro) to include the best analysis and thought leadership on the breadth of neuroimmunology in this ongoing Collection!

https://t.co/I8KQ9sM377

[The Science of Parkinson's @ScienceofPD]

Using transgenic mice & #Parkinsons patient IPS cells, researchers report on a single point mutation in Transglutaminase 2 that abolishes only its cross-linking activity, rendering it incapable of causing α-Synuclein aggregation & neurodegeneration
https://t.co/EF6eiQc67F

[nature @Nature]

CAR T cells are laboratory-engineered immune cells that provide effective treatment for some cancers. Progress is being made towards creating these cells in vivo

https://t.co/Zht4rpioSK

[Aakash Gupta @aakashgupta]

Instead of Netflix, watch this conversation with the greatest living mathematician on the future of AI

[Smart Science @SmartScience]

BREAKING: Scientists have engineered a virus that invades and destroys glioblastoma one of the deadliest brain cancers while turning the immune system into a relentless tumor-killing force. This could be a historic shift in cancer treatment. 🧬🚨

[Shining Science @ShiningScience]

Researchers who discovered the master switch that prevents the human immune system from attacking itself.

And they just won the Nobel.

The 2025 Nobel Prize in Medicine has been awarded to Mary E. Brunkow, Fred Ramsdell, and Shimon Sakaguchi for their groundbreaking work on peripheral immune tolerance.

While the immune system is a powerful defense against external pathogens, it requires precise regulation to avoid damaging the body's own organs. Sakaguchi first identified a specialized group of 'regulatory T cells' that act as a biological brake on immune responses. This discovery was completed when Brunkow and Ramsdell identified the FOXP3 gene as the master switch governing these cells, a finding initially made while studying a rare and fatal autoimmune disorder in children.

By revealing how the body maintains this delicate internal balance, these laureates have provided the foundation for a new era of medical treatment. Their work explains the biological origins of autoimmune diseases and has led to the development of therapies that are currently being explored to treat chronic conditions, improve organ transplant success, and even reprogram the immune environment around tumors to fight cancer. These discoveries represent a fundamental shift in immunology, moving beyond simple defense to a sophisticated understanding of how the body governs its own cellular power.

source: Nobel Prize Outreach AB. (2025). The Nobel Prize in Physiology or Medicine 2025. Nobel Prize Press Release.