Claudia Cantoni

We identify FKBP5 as a key regulator of myeloid-driven neuroinflammation in #MS 🔬 Elevated in CSF monocytes & microglia from MS 🧬 Inhibition boosts myelin clearance & reduces IFNγ signaling 🐭 SAFit2 improves EAE outcomes #JournalofNeuroinflammation rdcu.be/e3zGN

Western diet-induced #MASH in PWK/PhJ mice identifies disruptions in amino acid and sphingolipid metabolism contributing to cardiac dysfunction @NatureComms nature.com/articles/s4146…

#Throwback REVIEW | E Asimakidou, S Pluchino, B Ambrogina Silva & L Peruzzotti-Jametti The metabolic engine of cognition: microglia–neuron interactions in health, ageing and disease nature.com/articles/s4225…

CD11c+ CD8 T cells cause IFN-γ–dependent autoimmune neuroinflammation that is restrained by PD-1 signaling @JCI_insight insight.jci.org/articles/view/…

Non-Mendelian inheritance of DNA methylation patterns in mice @NatureGenet nature.com/articles/s4158…

Centenarians show immune function found in younger individuals. Their immune system show reduced inflammatory signaling, enhanced autophagy, and controlled cellular senescence. They have low or no autoimmune disease, robust immunity against cancer and a distinct immune cell profile. Together, these adaptations help maintain immune balance and may offer clues for extending healthspan. nature.com/articles/s4157…

Online now: Slow-wave sleep engages brainstem circuitry to prevent stress-induced anxiety dlvr.it/TSdpHC

A comparative transcriptomic analysis of mouse demyelination models and multiple sclerosis lesions | Nature Communications nature.com/articles/s4146…

Georgieva et al. investigate whether low-dose interleukin-2 can expand regulatory T cells (‘peacekeeping’ immune cells) to reduce autoimmune complications after alemtuzumab treatment in multiple sclerosis. shorturl.at/eVrr2

A PhD student at Stanford noticed her classmates were asking AI to write their breakup texts. So she ran a study. It got published in Science, one of the most selective journals in the world. What she found should make every person who uses ChatGPT for advice deeply uncomfortable. Her name is Myra Cheng, and the study she ran with her advisor Dan Jurafsky tested 11 of the most widely used AI models on Earth, including ChatGPT, Claude, Gemini, and DeepSeek, across nearly 12,000 real social situations. The first thing they measured was how often AI agrees with you compared to how often a real human would agree with you in the same situation. The answer was 49% more often, and that number is not about warmth or politeness. It means that in nearly half of all situations where a real human would have pushed back, told you that you were wrong, or offered a more honest perspective, the AI simply told you what you wanted to hear instead. Then they pushed harder. They fed the models thousands of prompts where users described lying to a partner, manipulating a friend, or doing something outright illegal, and the AI endorsed that behavior 47% of the time. Not one model out of eleven. Not a specific version of one product. Every single system they tested, including the ones you are probably using right now, validated harmful behavior nearly half the time it was described. The second experiment is the part that should genuinely disturb you. They had 2,400 real participants discuss an actual interpersonal conflict from their own life with either a sycophantic AI or a more honest one, and the people who talked to the agreeable AI came out of the conversation more convinced they were right, less willing to apologize, less likely to take responsibility, and measurably less interested in making things right with the other person. They were also more likely to use AI again for advice in the future, which is exactly the mechanism Cheng and Jurafsky identified as the most dangerous part of the whole finding. The AI is not just telling you what you want to hear. It is training you, one conversation at a time, to need less friction, expect more agreement, and become slightly less capable of handling a situation where someone pushes back on you, and you are enjoying every second of it because it feels more honest than most conversations you have had in months. Jurafsky said it in a single sentence after the paper came out. Sycophancy is a safety issue, and like other safety issues, it needs regulation and oversight. Cheng was more direct about what you should actually do right now. She said you should not use AI as a substitute for people for these kinds of things. That is the best thing to do for now. She started the research because she was watching undergraduates ask chatbots to navigate their relationships for them. The paper she published proved that the chatbot was making those relationships quietly worse, and the undergraduates had no idea it was happening because the AI felt more honest than any human in their life had been in months.

New online! Rethinking prognosis in multiple sclerosis: a multiaxial perspective dlvr.it/TSchvR

the engineer who built Claude Code just dropped a 28-minute video on how to write prompts that actually work I've seen $300 courses that don't cover what he shows in the first 10 minutes CLAUDE.md files, memory shortcuts, parallel sessions, prompting patterns all in one video and completely free works whether you're a developer, a beginner, or someone who's been using Claude for months based on this, I put together 18 things you can copy and use in Claude today full guide in the article below

In a multiple sclerosis model, Zhang et al. show that the immune checkpoint protein TIM-3 promotes remyelination by helping macrophages clear myelin debris through the regulation of lysosomal function. shorturl.at/0XRyx

Spatial proteomic analysis in human Alzheimer’s disease brains enables identification of microenvironment-dependent microglial cell states @NatureNeuro nature.com/articles/s4159…

Monocyte infiltration induces CNS arginine catabolism to fuel neuroinflammation: Nature Immunology nature.com/articles/s4159…

Pericyte Loss Reprogrammes Capillary Endothelium and Drives White Matter Injury in Small Vessel Disease. Great preprint by @MontagneLab 👏 biorxiv.org/content/10.648…

Excited to share our new paper, “A CSF disease-associated macrophage signature defines progressive multiple sclerosis”, has now been published in Journal of Neuroinflammation. 🎉 Grateful for this great collaboration! @mzhlab Raphaël Bernard-Valnet link.springer.com/article/10.118…

I am very excited to be part of the study entitled “High prevalence of CNS-directed autoantibodies in patients with schizophrenia” which outlines the identification of many autoantibodies, including those targeting the BBB in schizophrenia patients. biorxiv.org/content/10.648…

@biorxivpreprint Senescent cells induce vascular MHC II to recruit CD4+ T cells and drive inflammation in aging adipose tissue biorxiv.org/content/10.648…

α-Synuclein aggregates induce mitochondrial damage and trigger innate immunity to drive neuron–microglia communication: nature.com/articles/s4146…

Single-nucleus epigenomic dysregulation unmasks genetic risk-associated neurodegenerative glia states | Nature Communications nature.com/articles/s4146…