Caredio Davide

PhD in Neuroscience @UZH alumn🧑🏻‍💻Neuroimmunology|Live-Microscopy| SpatialTranscript data-analysis & bioinformatics 🧫🧪 🇮🇹 🇵🇹 🇨🇭🇩🇪

[Pluchino lab - Regenerative Neuroimmunology @Pluchinolab]

Uncovering spatially resolved functional genomics with CRISPR screen sequencing: Cell https://t.co/StjfGexyui

[John Lukens @LukensJohnR]

Microglial mitochondria transfer to astrocytes via GPNMB-enriched extracellular vesicles alleviates cognitive deficits in tauopathy mice
@NatureNeuro

[Waggoner Lab @LabWaggoner]

In a prion disease mouse model that phagocytic Gpnmb⁺ microglial state reflects regional responses to cell death and lysosomal stress rather than direct sensing of amyloid fibrils
@NatureComms @AdrianoAguzzi @Elena_DeCecco 🇨🇭
https://t.co/VsBnBOPc4g

[Caredio Davide @dcare17]

@LukensJohnR Very interesting paper which very much aligns with our recent work on Gpnmb in neurodegenerative disorders (in our case prion disease) https://t.co/PTMN3jl9Uu

[Ruslan Rust @rust_ruslan]

🚨New preprint from our lab!🚨

You've heard of CAR-T cell therapy for cancer. But have you heard of CAR-NSC for stroke?

8+ years of work, this may be the most important work of our research so far!

Read more 👇

[Mohamad Amki @mohamad_elamki]

Did you know that if you remove a single endothelial cell from a brain capillary, neighboring endothelial cells have the capacity to rapidly extend to rebuild the vessel? Excited to share our new paper in Neuron. Congratulations to all co-authors. https://t.co/QsAtMH1598

[Caredio Davide @dcare17]

Importantly, when we removed Gpnmb from microglia, their ability to phagocytose apoptotic cells was significantly impaired, pointing to a critical role for Gpnmb in microglial clearance mechanisms during neurodegeneration.

[Caredio Davide @dcare17]

Such microglial state is characterized by enhanced lysosomal activity, lipid metabolism, senescence and ferroptosis markers.

[Caredio Davide @dcare17]

This microglial state was not present at earlier (but still late) timepoints. Stroke induced animal model proved that indeed cell death alone can trigger Gpnmb+ microglial state!

[Caredio Davide @dcare17]

Excited to share our new paper in @NatureComms ! 🧠🔥
https://t.co/PTMN3jl9Uu

Using spatiotemporal transcriptomics and functional validation, we identify a Gpnmb⁺ phagocytic microglial state associated with cell death during prion disease progression.
#Prions #STtranscriptomics

[Caredio Davide @dcare17]

Interestingly, we also observed Gpnmb⁺ microglia in white matter regions associated with demyelination, supporting the idea that this state may represent a broader phagocytic response to cellular damage.

[Caredio Davide @dcare17]

Gpnmb⁺ microglia were not broadly distributed across the brain, but instead localized specifically to regions undergoing severe cell death, suggesting that the surrounding tissue environment — rather than prion aggregates alone — plays a major role in shaping microglial states.

[Caredio Davide @dcare17]

Happy to see this work now published in PLOS Pathogens.

We identify TFAP2C as a functional interactor of hnRNPK and show how this axis regulates prion propagation via mTORC1 signaling.

Great team effort—congrats to Stefano Sellitto and all co-authors!

[Stefano Sellitto @SellittoStefano]

I’m excited to share that my first-author paper has just been published in PLOS Pathogens!

https://t.co/lOH5V9qmnp

[Stefano Sellitto @SellittoStefano]

I’m excited to share that my first-author paper has just been published in PLOS Pathogens!

https://t.co/lOH5V9qmnp

[IdoAmitLab @IdoAmitLab]

Excited to share two back-to-back studies with @jonykipnis @boskovic_p showing the promise of CAR T beyond cancer — in Alzheimer’s and stroke — inspired by the visionary work of Zelig Eshhar.

[Feng Zhang @zhangf]

Excited to share our new work on immune aging! We explored whether the liver could serve as a temporary "factory" to produce immune factors that decline with aging, potentially helping to rejuvenate aged immunity. @mircoscopy.

[Chris Mason @mason_lab]

We have now reached a new level of spatial omics: translatomics! https://t.co/GXEtIhrpKd Fascinating new tech in new paper "Scalable spatial single-cell transcriptomics and translatomics in 3D thick tissue blocks" from @naturemethods

[Caredio Davide @dcare17]

Very elegant work from an amazing Italian scientist @SimonaParrinello!
Axonal injury → Wallerian degeneration → neuroinflammation → glioma growth. And it’s targetable.
#Glioma #Neuroinflammation #BrainCancer #Nature

Congratulations to all the author of this beautiful work!

[nature @Nature]

Nature research paper: Axonal injury is a targetable driver of glioblastoma progression

https://t.co/vASeNr4Wm2

[Le Cong@Stanford, AI+Bio+Gene-Editing @lecong]

🧬 BREAKING: Our CRISPR-GPT paper is out TODAY in Nature Biomedical Engineering @natBME !
🤯 We built an AI agent that turns ANYONE into a gene-editing expert in 1 DAY instead of months. An undergrad with ZERO experience achieved 90%+ editing efficiency on their FIRST attempt.
🧵 Here's how we're building expert AI agents for cutting-edge biotechnology:
🎯 The Problem: CRISPR is revolutionary but requires PhD-level expertise, it can take weeks to learn, adopt, and design, analyze a CRISPR experiment for R&D or making life-saving medicine. Even Pro scientists can make small mistakes (e.g. typos in guideRNA or cloning design) that cost months to find out, slowing us down.
💡 Our Solution: CRISPR-GPT - an AI co-pilot from @Stanford @Princeton @GoogleDeepMind that guides you through EVERY step via simple conversation
🔬 Real Results:
-Novice researcher: ~90% editing on 1st go
-Training time: Months → 1 day
-100% success rate in our trials
-Even experts save days/weeks on data analysis & troubleshooting
🤖 How it works: Our multi-agent system handles: CRISPR system and delivery method selection, guideRNA design, Protocol generation, Real-time troubleshooting, Data analysis, and beyond. All through natural language! No coding, no complex software.
📊 We benchmarked it extensively:
-288 evaluation scenarios/cases
-Outperformed GPT-4o on ALL gene editing tasks
-Trained on 11 years of expert discussions
-Covers knockout, base-editing, prime-editing & epigenetic editing
🌍 Why this matters:
-Every lab can now use CRISPR with an AI system distilling expert knowledge and skills.
-Every student can learn faster.
-Every researcher can tackle bigger challenges without worrying about small mistakes.
-Customized CRISPR design can be automated based on your need and the context of R&D workflow.
-Agentic AI ensure safety, privacy, and responsibility
-We're not just automating gene editing - we're using AI to power scientists to cure diseases.

🚀 Try it yourself! Beta access available at: https://t.co/CFQzrdVVPW
Paper: https://t.co/WOgmAjg1Ed
Code: https://t.co/UnPKrxyJuW
Benchmark (companion work, Genome-bench): https://t.co/LIooAXj2op

Co-first and key authors: @YuanhaoQ @KaixuanHuang1 @MingYin_0312
PIs: @lecong @MengdiWang10
Key collaborators: @Rbaltman @denny_zhou
The future of biology and science is conversational. The future is now. @natBME @NaturePortfolio

#CRISPR #AI #GeneEditing #Biotech #Science #AISafety

[Jun-Liszt Li @poppingjun]

In this study, we generated a Slco1c1-CreERmouse line (Slco1c1-KI-P2A-iCreERT2, briefly, Slco1c1-CreERKI). Our staining results validate its high specificity for labeling CNS endothelial cells, with rare expression in peripheral endothelial cells.

https://t.co/dfIk6wvLRT