To try everything Brilliant has to offer—free—for a full 30 days, visit https://brilliant.org/ArtemKirsanov/. You’ll also get 20% off an annual premium subscription.
===== My name is Artem, I’m a neuroscience PhD student at Harvard University. 🌎 Website and Social links: https://kirsanov.ai/ 📥 \.
To learn more, please visit the YouTube Help Center: https://www.youtube.com/help
Your brain is running on twenty watts right now. The power of a dim lightbulb. And yet it contains the entire eight-hundred-million-year history of life’s most improbable experiment — the experiment of intelligence itself. In this episode, we follow that experiment from its very beginning: from the first bacterium that navigated a chemical gradient in the ancient ocean, through the nerve nets of jellyfish, the distributed arms of the octopus, the tool-making crow, the grieving elephant, the dreaming mammalian brain — all the way to the only creature that has ever turned its intelligence on the question of where intelligence came from. This is not a story about the human brain. It is a story about what matter does when evolution pressures it long enough and hard enough. It is the deepest origin story you have.
/ @theevolutionoflife2026 Subscribe to the channel and join us — there is much more of this story still to tell.
Problem-solving using novel solutions without explicit training is often considered a hallmark of cognitive flexibility. We investigated whether bumble bees (Bombus terrestris) could solve a novel object manipulation task spontaneously. Bees trained to associate a blue ring (“flower”) on the floor with a reward successfully moved a ball underneath a flower relocated to the ceiling to reach the flower. In control experiments in which the flower was out of sight when ball movement began and remained hidden during transport, bees still succeeded in the task. These results suggest that these were goal-directed actions rather than reinforcement-based associations driven by perceptual feedback. Our findings provide evidence that bumble bees can exhibit spontaneous problem-solving, challenging the notion that such advanced cognitive abilities are exclusive to large-brained vertebrates.
To determine whether canonical GLP-1R signaling is required for liraglutide to remodel the gut microbiota, we performed 16S rRNA sequencing on fecal samples from CUS-exposed wild-type (WT) and Glp1r−/− mice treated with or without liraglutide. Analyses of alpha-diversity, beta-diversity, and genus-level composition revealed that liraglutide changed the microbial structure in CUS mice, although specific compositional shifts differed between WT and Glp1r−/− mice (Figure S6). However, linear discriminant analysis (LDA) identified the genus Lactobacillus as the most significantly enriched taxon following liraglutide treatment in both WT and Glp1r−/− mice (Figures 2 H and 2I). Consistent with this finding, the abundance of Lactobacillus, which was reduced by CUS, was restored by liraglutide in both WT and Glp1r−/− mice (Figure 2 J). To identify the specific Lactobacillus species affected, we performed metagenomic sequencing on fecal samples from CUS mice treated with liraglutide. The Venn diagram showed that L. delbrueckii emerged as the most markedly altered species following liraglutide intervention in CUS mice (Figures 2 K and 2L). Targeted qPCR further validated that CUS-induced reduction in L. delbrueckii abundance was restored by liraglutide treatment in both WT and Glp1r−/− mice (Figures S7 A and S7B). Moreover, semaglutide, another GLP-1R agonist, similarly reversed the CUS-induced reduction of L. delbrueckii, suggesting a shared effect within this class of drugs (Figure S7 C). Together, these results demonstrated that liraglutide enriches intestinal L. delbrueckii in a manner that does not require canonical GLP-1R signaling. Notably, subcutaneous administration of liraglutide reached the gut lumen, and L. delbrueckii was most abundant in the ileum (Figure S8), supporting the in vivo relevance of the proposed mechanism.
To establish the causal role of liraglutide-induced microbial remodeling in mediating its behavioral effects, we performed fecal microbiota transplantation (FMT) from either untreated CUS or liraglutide-treated CUS donors into ABX-pretreated CUS recipients (Figure 2M). Recipients colonized with microbiota from liraglutide-treated donors exhibited significant improvements in depressive-like behaviors, as evidenced by increased sucrose preference in the SPT and reduced immobility in both the TST and FST, whereas microbiota from untreated CUS donors produced no significant behavioral change (Figures 2N–2P). Additionally, we found that FMT from liraglutide-treated donors similarly ameliorated depressive-like behaviors in lipopolysaccharide (LPS)-exposed recipients (Figure S9). We further quantified L. delbrueckii abundance in recipient feces and found that FMT from liraglutide-treated donors elevated L. delbrueckii abundance in recipients (Figure 2Q). Notably, the abundance of L.
Dementia is a degenerative disease that no known drug can completely stop or reverse, despite decades of tests.
Now, a historically vilified psychedelic is emerging as a possible new avenue for controlling Alzheimer’s symptoms.
Neuroscientists around the world are starting to investigate if psilocybin – the psychoactive ingredient in magic mushrooms – can help protect the aging brain.
An unexpected lab observation has led a team of scientists to discover how diet can influence survival in animal models of glioma, one of the most aggressive and deadly forms of brain cancer. Researchers at Baylor College of Medicine, the Duncan Neurological Research Institute (Duncan NRI) at Texas Children’s Hospital and collaborating institutions report in the Proceedings of the National Academy of Sciences how limiting a single nutrient, the amino acid methionine, in the diet destabilized DNA organization and led to cancer cell death and increased animal survival. These findings open new possibilities for treating one of the most challenging forms of brain cancer.
“Cancer cells, including gliomas, often depend on methionine. Methionine is an essential amino acid, meaning that the body does not produce it on its own; it must be consumed in the diet. Glioma cells are unusually dependent on methionine to fuel rapid growth and control gene activity,” said corresponding author Dr. Benjamin Deneen, professor and Dr. Russell J. and Marian K. Blattner Chair in the Department of Neurosurgery and director of the Center for Cancer Neuroscience, all at Baylor.
“In the current study, we wanted to know, if tumors depend so much on methionine, what happens if we reduce the supply?” said first author Brittney Lozzi, a graduate student in the Deneen lab.
