ca: 9oxGicd5KXNcthYM6yD23X9zcznQVnHjrAEN38fFpump tg: https://xitter.cf/t.co/qG4OIZelfS

Joined March 2026
BioLLM is the first independent dev / lab to take REAL human neurons and pair their behavior with non invasive BCI. I’ve controlled computers, robots, and pioneered a whole new category. Thanks to YOU! Our wonderful community 😃
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Exactly what we are doing with BioLLM! actual brain cells X AI
Yes, the most plausible form of naturalism for consciousness is biological naturalism. If they designed through artificial evolutionary processes something like an artificial living organism with a living brain (even silicon if that's possible), that would be a much more plausible strategy for creating strong AI than just improving LLMs.
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Most neurons are excitatory, but some do the opposite and dampen the activity of other neurons. In this visualization by our Electron Microscopy team, an axon (red) sneaks its way in between a satellite microglia (blue) and an inhibitory neuron (gray).
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The insula region of the brain makes the case for CL1 & its role in non invasive BCI. Even invasive technology can’t reach deep regions like this - our best hope is to model them by growing the cells outside the body.
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BioLLM retweeted
In the same mouse-brain dataset, GPT-Rosalind found a possible clue to why TSC2 mutations tend to cause more severe tuberous sclerosis than TSC1 mutations. The two genes work together to regulate mTOR. Yet in one group of cerebellar neurons, disrupting TSC2 changed the expression of dozens of genes, including genes involved in neuronal communication. Disrupting TSC1 had little effect on gene expression in the same cell type. Existing treatments already target mTOR. Do they reverse these changes, or is there more to TSC2’s role in these neurons?
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BioLLM retweeted
GPT-Rosalind surfaced a new lead for drug discovery: could restoring cholesterol transport protect neurons from degeneration? DCTN1 is a gene linked to Perry syndrome, a rare neurodegenerative disorder. In mouse-brain data, disrupting it increased expression of genes involved in making cholesterol. GPT-Rosalind suggested a possible explanation: cholesterol may not be reaching where neurons need it. That gives scientists a specific mechanism to test and, if confirmed, a direction for developing new treatments for neurodegenerative disorders. With @perturbai_tx and @scrippsresearch, a team of thousands of GPT-Rosalind agents worked in parallel, connecting gene-expression results from millions of mouse brain cells with scientific literature in just 32 minutes. We’re now expanding this collaboration to identify new drug targets. openai.com/index/scaling-ai-…
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Jeff Bezos in 1995 when his net worth was only $80k
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Wow! @OpenAI should check out @CorticalLabs CL1 as this might be the perfect device to really hone in on understanding neurodegenerative disease at a high resolution
Day 28 of the bio x ai arc Another huge day of headlines, with OpenAI announcing agentic generation of a new lead for drug discovery in neurodegenerative diseases. I keep seeing the question: so what's the bottleneck? I don't think the bottleneck framing is the correct approach. In the endgame, AI would supercharge every part of the process: 1. Pour over biological data 2. Come up with hypothesis 3. Experimentally validate hypothesis in wetlab 4. Design drug molecule in accordance with hypothesis 5. Test out different variants of said design 6. Print molecule and validate experimentally 7. Assess toxicity and developability in vitro 8. Further validation in vivo This announcement is a strong signal that AI is beginning to boost steps 1 and 2. Once 1 and 2 are boosted, we need to boost steps 3 through 8 to catch up. But big picture, if we are actually going to cure diseases, all 8 steps need to 100x. Therefore there is no single bottleneck right now. Every part of the chain needs to dramatically increase.
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We are once again LIVE on @Pumpfun with our robot 😃
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Hop on @Pumpfun we are streaming our neuron powered robot and doing some live development! solana:9oxGicd5KXNcthYM6yD23X9zcznQVnHjrAEN38fFpump
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In the coming weeks we will release a whole new iteration of BioLLM We have a completely auditable solution staged for release which uses Jacobian space (J Space) to encode / decode the models inner dialogue to real neurons and allow those same cells to steer inference 🤯
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This is the inference layer of BioLLM in action! 😂
Two brain cells having a chat
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This is powerful, and @CorticalLabs has been screaming it from the mountain tops since 2022 (Dishbrain Study)
I asked Opus what it thinks consciousness really is.
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BioLLM retweeted
BCI is a wrong target. Computers are no longer keyboard, mouse and screen, but AI agents working for you. The right target is a Brain AI interface. More below 👇
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AI neurons run on simple math. Real neurons are far weirder. A new open dataset fitted 1,000+ PyTorch-ready neuron models to real mouse and human cells. Does brain-like diversity make AI better? It's still an open question, but now it's testable. bit.ly/3WfGAwR
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Incredibly cool! We would love to consult with Google on a wet lab for neurons x robotics! 😃
We are bringing agents to the wet-lab bench at Google Research to navigate complex biological landscapes. Learn how we are grounding agents in physical lab robotics to run fast closed-loop molecular design cycles, ultimately discovering single-digit nanomolar protein binders for cancer targets →goo.gle/4B5mMMB
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The first AI robot to ring the bell on Nasdaq
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