OpenAI posted this on Tuesday. By Wednesday there was a $44,220 protocol on ResearchHub to test it in human iPSC neurons, reviewed and open to fund. The lead took 32 minutes. Testing it is still the slow part, and that's the part we're working on.
ALT Timeline: OpenAI's GPT-Rosalind DCTN1-cholesterol lead posted Oct 21; RFP and 10 candidate designs live on ResearchHub the same day; design #1 ($44,220, iPSC neurons, CRISPRi) reviewed and open for funding by Oct 22. Bar comparison: 2 days on ResearchHub vs about 270 days for an NIH R01 from submission to award.
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-…
OpenAI称，数千个AI代理用32分钟，分析了数百万个小鼠脑细胞的数据。
10月21日公布的研究由OpenAI、PerturbAI和Scripps合作。代理分头分析基因扰动、查文献，再汇总出机制假说。团队估计，同类人工分析和文献整理要数月到一年。
大实验能产出海量数据，人的阅读时间跟不上。把那些来不及细看的结果翻出来，研究者就多了一批可做实验的线索。数据已经花钱做出来了，放着没人细看，也是一种浪费。
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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GPT-Rosalind 讓近 2,000 個 AI Agent 平行協作，在短短 32 分鐘內，整合數百萬個腦細胞的基因數據與科學文獻，甚至提出膽固醇運輸可能與神經退化有關的新假設。
這代表 AI 正從被動分析工具，走向能主動發現線索、跨領域推理的科研夥伴。
但提出假設不等於證實機制。當 AI 能大量產生研究方向，未來的瓶頸，或許是人類能否跟上實驗驗證的速度。
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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⚡ 오픈AI GPT-Rosalind 에이전트 수천 개가 32분 만에 신경 질환 연구 단서를 냈습니다.
▪️ 희귀 질환 유전자 DCTN1
▪️ 콜레스테롤 운반 문제라는 가설
치료법이 아니라 실험할 가설입니다. 무엇부터 실험할지 고르는 시간이 줄어듭니다.
오늘은 또 뭘 시켜볼까요? 🤖
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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インターネットの次は生命倫理が壊れる番だよ😤
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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"AI will never help with drug discovery" did not last long.
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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Great
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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We used GPT Sol 6.1 to draft 10 preregistered proposals to test this hypothesis in the wet lab.
1. Funders: pool funds on the RFP
2. Scientists: upvote, comment, or review to strengthen the experimental design
3. Wet labs: comment if you want to run one
researchhub.com/rfp/33104/te…
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-…
به به عالیه ai کم کم به این سمت هم رسید
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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Most of the cholesterol in your blood test never reaches your brain. The brain makes its own and holds about a quarter of all the cholesterol in your body.
That matters because this post is not really about a blood number. It is about where brain cholesterol goes and what happens when that system breaks.
In a Scripps-led study, researchers switched off single genes in millions of mouse brain cells, and an OpenAI model helped interpret the results. When DCTN1 was switched off, neurons increased the genes they use to make cholesterol.
DCTN1 is the gene disrupted in Perry syndrome, a rare inherited brain disease with parkinsonism, and the model pointed to a simple explanation: cholesterol delivery inside those neurons may have failed, so the cells tried to make more.
That fits older brain biology. Astrocytes make cholesterol for neurons and deliver it through APOE. In people of European ancestry, one copy of APOE4 roughly triples the risk of Alzheimer’s disease, while two copies raise it about 15-fold.
The DCTN1 idea is still only a preprint, with no lab test yet. But if it holds up, the takeaway is clear: in the brain, cholesterol is not just about how much there is. It is about where it goes.
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-…
Thousands of AI agents.
32 minutes.
The timeline will get even more interesting here very soon. 👀
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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cool ～
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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holy sh*t.
openai just put thousands of AI agents on one rare brain disease.
they read millions of mouse brain cells against the science literature in 32 minutes and came back with a new drug lead.
forget model releases. this is what agents are actually for.
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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OpenAIのGPT-Rosalindが数千体で手分けし、数百万個のマウス脳細胞のデータと論文を32分でつないで、神経の病気の薬の手がかりを1つ出した。
ただ、出たのは「確かめる価値のある仮説」まで。どれを実験に回すかを選ぶ工程は人の手に残っている。
うちの仕事も同じで、議事録や問い合わせの下読みはAI社員に任せるが、どの案件を先に進めるかは任せない。そこを抜くと、積み上がった候補を社長が夜に1件ずつ読み直すことになる📋
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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omg they did the thing
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-…
🚨 آلاف الوكلاء من GPT-Rosalind حللوا بيانات ملايين خلايا المخ في 32 دقيقة فقط.. وخرجوا بخيط جديد لعلاج أمراض تنكس الأعصاب! 🤯
المشكلة: التجارب الحديثة تنتج بيانات أكثر بكثير مما يستطيع العلماء فحصه، وقدّر الفريق أن تحليلاً بشرياً مماثلاً مع مراجعة الأبحاث، تجربةً تلو الأخرى، كان سيستغرق من أشهر إلى سنة.
🔥 ماذا اكتشفوا؟
• الجين DCTN1 مرتبط بـ Perry syndrome، وهو مرض نادر لتنكس الأعصاب بأعراض تشبه Parkinson
• في بيانات مخ الفئران، تعطيل هذا الجين رفع نشاط الجينات المسؤولة عن تصنيع الكوليسترول
• تفسير GPT-Rosalind المقترح: الكوليسترول ربما لا يصل إلى حيث تحتاجه الخلايا العصبية
• والسؤال الذي يفتحه للمختبر: هل استعادة التوزيع الطبيعي للكوليسترول قد تحمي الخلايا العصبية؟
📌 كيف عمل النظام؟
• OpenAI مع PerturbAI و Scripps Research قسّموا التحليل على آلاف الوكلاء بالتوازي
• كل وكيل يفحص تعطيل جين واحد، ويحلل استجابة الخلايا، ويبحث في الأبحاث المنشورة، ثم يقترح تفسيراً
• عند أكبر حجم عمل: الوكلاء الموزعون استشهدوا بأكثر من 700 مرجع، مقابل 11 فقط لوكيل واحد
• في مقارنات عمياء، فضّل الخبراء تقارير الوكلاء الموزعين بنسبة 75%
💡 وليس اكتشافاً واحداً: الوكلاء رصدوا أيضاً فرقاً غير متوقع بين الجينين Tsc1 و Tsc2 في المخيخ، قد يرتبط بمرض tuberous sclerosis.
الخلاصة: هذه ليست أدوية جاهزة، بل فرضيات قابلة للاختبار.. لكن الـ AI بدأ يحوّل جبال البيانات المهملة إلى التجربة التالية التي تستحق أن تُجرى.
احفظ التغريدة، والرابط في أول رد 🧵👇
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-…
生物+AI😀😀😀
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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it got me thinking, what we gon' do when humans ain't the smartest ones on earth no more?
we’ve been through this kind of existential crisis before.
first, we discovered that earth wasn’t the center of the universe. then Darwin told us we weren’t some special creation of god, we’re just another species that evolved like every other animal.
imagine how people felt back then. things they believed made humans special suddenly weren’t true anymore. and now it’s happening again. intelligence, the thing we’ve always believed makes humans special, might no longer belong to us.
a lot of people questioning the meaning of what they’re doing. mathematicians wondering what’s the point of solving problems if AI can do it better. researchers wondering if their life’s work will still matter.
but looking at history, humans have always gone through a period of denial and existential crisis, and then found new meaning. life didn’t become meaningless after Copernicus or Darwin.
same thing will happen again.
if AI can do all “bits” work better than us, what should we do then?
i actually think the next 10-20 years will open up some of the most exciting things humans have ever done.
there are 3 directions i keep thinking about.
1. virtual worlds
entire game worlds generated by world models, where humans and AI can live, explore, build things and have experiences together. an entirely new form of entertainment, maybe it can even connected to our real world.
(yes, i think entertainment will definitely be the most important thing in most people's life)
2. make the physical world better
as Peter Thiel has pointed out, we’ve spent decades putting so much talent and capital into bits rather than atoms.
software was easier to build, scale and monetize, while changing the physical world was incredibly hard.
i think this could reverse. when intelligence becomes cheap, discovering new technologies won’t be the bottleneck anymore. actually bringing those technologies into the physical world will be.
(I recently read about Travis Kalanick’s Atoms, I find its quite fascinating)
there’s so much we still haven’t built in the real world.
3. space exploration
just like the age of exploration, humans will always have new frontiers to explore. new places to go, new worlds to discover, new adventures to have.
TLDR;
The economic value of humans in knowledge work will decline a lot.
and it's fine.
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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에이전트 하나에 다 맡기는 것과 잘게 쪼개서 수천 개에 나눠 맡기는 것. 어젯밤 OpenAI가 테스트했어요.
1) GPT-Rosalind 에이전트 1,946개가 생쥐 뇌 CRISPR 아틀라스를 32분 만에 분석. 유전자 하나당 에이전트 하나
2) 같은 모델, 같은 일인데 에이전트 1개는 논문 11편 인용, 쪼개서 돌린 쪽은 700편 이상. 블라인드 박사급 평가자 75%가 쪼갠 쪽 보고서를 골랐어요
3) 아틀라스 논문을 안 본 상태로.... 어쩌구 저쩌구인데.
그냥 결론 작은 단위로 에이전트 나눠서 하세요. 훨신 성능이 좋습니다.
깊은 내용은 아래에서..
#AI에이전트 #자동화 #업무자동화 #인공지능 #OpenAI #멀티에이전트 #워크플로 #생산성 #AI활용 #테크뉴스 #바이오AI #노코드 #AIAgents #Automation #MultiAgent #AINews
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-…
Agent 活一多就偷懒
这回 OpenAI 自己测出来了
几千个 GPT-Rosalind 一起上
分析几百万个小鼠脑细胞的数据
32 分钟干完
再看对照组
只用一个 Agent 的时候
活越多它查的文献越少
最后只引了 11 篇
几千个一起上的引了 700 多篇
你们跑长任务的时候
碰到过这种情况吗
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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