We often think of the brain in our head as the sole commander of our body, but your heart actually has its own mini nervous system embedded directly within its tissues — often referred to by neuroscientists as the heart’s “little brain.”
How the Heart’s “Little Brain” Works.
A subset of cardiac neurons keep the heart from malfunctioning in stressed mice.
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A curated summary of Terence Tao’s current thinking on AI, with practical guidance and links to source material. Positions are distilled from ~70 Mastodon posts, some sixteen interviews and talks, six long-form essays and lectures, ~55 of his own blog comments, and a direct interview; not everything he has said appears here, by design — omission is editorial. Voice is third person; scope is confined to what is obviously about AI.
Latest: his ICM 2026 public lecture “Mathematics in the age of AI” (July 24, 2026) gathers much of this into one argument — the slides are linked here now, and its content will be folded into this summary once the recording is available.
How this page was made. This summary was compiled and drafted by an AI assistant (Claude) from Terence Tao’s public writing, talks, and interviews, then reviewed and corrected by him; the companion interview was conducted by that assistant, with his answers reproduced verbatim (lightly edited). It is a living document, revised as his views develop. Like the rest of tao-web, it is maintained with AI assistance.
A UNIGE study shows that even a slight overproduction of tubulin, a protein essential for cell structure, is enough to disrupt tissue organization, highlighting the need for tight regulation of protein levels.
For cells to function properly, they must produce the right amount of each protein. It is a delicate balance: both too little and too much can compromise essential cellular functions. A team from the University of Geneva (UNIGE) has now shown that even a modest excess of tubulin – the protein that assembles into microtubules, the cell’s internal scaffolding – is enough to disrupt tissue architecture and reduce cell viability. Published in Nature Communications, the study demonstrates that the quantity of a protein is just as important as its function.
Microtubules, built from tubulin, form the cell’s internal skeleton. They help cells maintain their shape, transport molecules, divide, and remain firmly attached to neighboring cells. Rather than being rigid structures, microtubules are constantly assembled and disassembled to adapt to the cell’s changing needs. This dynamic behavior depends directly on the amount of tubulin available.
Fifteen years ago, I spent an hour with the man who gave us the word.
Vernor Vinge coined “technological singularity.” In his 1993 paper for NASA, he put a clock on it: within thirty years we would have the technological means to create superhuman intelligence. Shortly after, he wrote, the human era would end.
That deadline came and went. Vinge died in March 2024, past his own due date, which means he never got to grade his own paper. The rest of us are holding the pencil now.
The title of our conversation was his line, not mine:
We can surpass the wildest dreams of optimism.
From most people, that would be marketing. From a hard #ScienceFiction writer who spent thirty years teaching math and computer science, it was a hypothesis with conditions attached, and he was just as specific about what happens when the conditions are not met.
Now, researchers at Duke University School of Medicine say restoring healthy mitochondria could offer a completely new way to treat that pain.
In a study published in Nature, the team used both human tissue and mouse models to test whether replenishing mitochondria could help damaged nerve cells recover. The treatment significantly reduced pain linked to diabetic neuropathy and chemotherapy-related nerve damage. In some cases, the relief lasted for up to 48 hours.
Rather than simply blocking pain signals, the researchers believe the approach may address one of the underlying causes of chronic nerve pain by restoring the energy supply nerve cells need to function properly.
The plague has killed more people than World War II. The bacterium Yersinia pestis (Yp), which causes plague, has triggered three major pandemics throughout history, leaving behind a casualty toll of more than 200 million people. Although the plague no longer causes pandemics on the scale seen in history, it still occurs in many parts of the world today. Vaccination remains our best defense against the disease, but approved options remain scarce.
In a new study, scientists tested two live-attenuated plague vaccines, LMA and LMP—weakened forms of the plague bacterium that cannot cause disease—both alone and in combination with the virus-based vaccine Ad5-YFV.
They genetically engineered the mice to completely lack a signaling protein called interferon-gamma, which plays a crucial role in activating immune cells. Despite lacking a key immune protein, the vaccines protected 80% to 100% of mice exposed to highly lethal doses of the pneumonic plague-causing Yp CO92 strain, while triggering strong antibody and immune responses in all vaccinated animals.
Most everyday moments are quickly forgotten, while others stay with us for a lifetime. How the brain determines which memories are retained and which are lost remains an open question.
A neuroscience team at the University of Tübingen, led by Professor Andrea Burgalossi of the Institute of Neurobiology and the Werner Reichardt Center for Integrative Neuroscience (CIN), has found that spontaneous fluctuations in the brain’s internal state influence how ready the memory system is to store new information. The new study has been published in Nature Communications.
The researchers used mice to investigate the neural mechanisms of memory formation, focusing on the hippocampus, a region of the brain known to be essential to the formation of episodic memories. The hippocampus of mammals, including mice and humans, contains neurons called place cells that represent experiences in the brain.