Research Topic: Brain Connectivity

Meditation, psychedelics, and brain connectivity: A randomized controlled resting-state fMRI study of N,N-dimethyltryptamine and harmine in a meditation retreat

Researchers studied how meditation combined with a psychedelic compound called DMT affects the brain. They scanned 40 experienced meditators before and after a 3-day retreat, with some receiving the psychedelic and others a placebo. While meditation alone reduced connections between different brain networks, the psychedelic enhanced certain connections, suggesting the two practices may complement each other in promoting mental health.

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N,N-dimethyltryptamine effects on connectome harmonics, subjective experience and comparative psychedelic experiences

Researchers studied how DMT, a powerful psychedelic drug, changes brain activity patterns and how these changes relate to what people experience. Using advanced brain imaging and network analysis, they found that DMT shifts brain activity away from large-scale network patterns toward smaller, more diverse patterns. Importantly, these brain changes directly tracked with how intensely participants reported experiencing the drug’s effects moment-to-moment.

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Psilocin, LSD, mescaline, and DOB all induce broadband desynchronization of EEG and disconnection in rats with robust translational validity

Researchers tested how different psychedelic drugs affect brain electrical activity in rats using EEG recordings. They found that psilocin, LSD, mescaline, and DOB all produced similar patterns of decreased brain activity and reduced communication between brain regions. Importantly, these effects in rats closely matched what scientists observe in human brain studies, suggesting that rats can be useful for understanding how psychedelics work in the brain.

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Long term worsening of amyloid pathology, cerebral function, and cognition after a single inoculation of beta-amyloid seeds with Osaka mutation

Researchers found that a single exposure to mutated amyloid-beta proteins (Aβ Osaka) in the brains of genetically modified mice caused lasting damage over four months. The mutated proteins triggered more severe memory loss, brain connectivity problems, and synapse damage compared to normal amyloid-beta. This suggests that even one encounter with mutated amyloid proteins can set off a chain reaction of disease progression that persists long after initial exposure.

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