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A foundation model of vision, audition, and language for in-silico neuroscience

‘The present results strengthen the possibility of a paradigm shift in neuroscience… moving from the fragmented mapping of isolated cognitive tasks toward the use of unified, predictive foundation models of brain and cognitive functions By aligning the representations of Al systems to those of the human brain, we demonstrate that a single architecture can integrate a vast range of fMRI responses across hundreds of individuals, extending the framework that led the 2025 Algonauts competition. The observed log-linear scaling of encoding accuracy mirroring power laws in both artificial intelligence and neuroscience suggests that the ceiling for predicting human brain activity is yet to be reached.’


Cognitive neuroscience is fragmented into specialized models, each tailored to specific experimental paradigms, hence preventing a unified model of cognition in the human brain. Here, we introduce TRIBE v2, a tri-modal (video, audio and language) foundation model capable of predicting human brain activity in a variety of naturalistic and experimental conditions. Leveraging a unified dataset of over 1,000 hours of fMRI across 720 subjects, we demonstrate that our model accurately predicts high-resolution brain responses for novel stimuli, tasks and subjects, superseding traditional linear encoding models, delivering several-fold improvements in accuracy. Critically, TRIBE v2 enables in silico experimentation: tested on seminal visual and neuro-linguistic paradigms, it recovers a variety of results established by decades of empirical research.

Characterization of a Splice Variant in FLNA Associated With Periventricular Nodular Heterotopia

This study broadens the phenotypic and genetic spectrum of PNH, demonstrating a dual PNH phenotype associated with a bi‑transcript mechanism and mosaic inheritance, including tissue‑specific mosaicism.


PNH is a neurodevelopmental brain malformation characterized by failure of the gray matter to properly migrate to the cerebral cortex during embryonic development. This results in ectopic localization around the ventricular ependyma.1 MRI serves as the primary diagnostic tool, showing bilateral periventricular gray matter nodules with a signal intensity similar to that of normal cortical gray matter.2,3 Its primary clinical manifestation is epilepsy, which is often accompanied by intellectual disabilities and learning difficulties.2,3 PNH is genetically heterogeneous and is linked to variants in multiple genes, including ARFGEF2, ERMARD, NEDD4L, ARF1, and MAP1B, as well as abnormalities in chromosome 5. Among these, pathogenic variants in FLNA are the most common genetic causes.4

FLNA is located at Xq28 and comprises 47 exons,5 encoding a 280 kDa actin binding protein, called filamin A. The N-terminal region contains an actin binding domain (ABD) and a rod-like structure composed of 24 immunoglobulin-like repeats. ABD interacts with actin to stabilize the cytoskeletal architecture and plays crucial roles in maintaining cell shape, migration, and transmitting mechanical force. FLNA regulates cellular migration and extension processes via interactions with several signaling proteins, including small GTPases Rac/Rho, TRAF2, integrins, and BRCA2.6–8 This gene possesses at least 2 transcription initiation sites (ENST00000369850.8 and ENST00000610817.4) that use distinct promoters and demonstrate tissue-specific expression.6–8 Rat FLNA-knockdown models exhibit impaired neuronal migration and elevated epileptic susceptibility.

Paralyzed army vet can now play World of Warcraft using ‘science fiction… magic… brilliant…’ Neuralink brain implant — ‘I’m now raiding, and exploring Azeroth hands-free at full speed’

Noble has been paralyzed from the shoulders down since a spinal cord injury in 2016.

Biohacks & Brain Mods

Biohacks and brain implants are coming fast. From memory upgrades to neural meshes, how will implant culture reshape identity, economics, and civilization itself?

Get Nebula using my link for 50% off an annual subscription: https://go.nebula.tv/isaacarthur.
Watch my exclusive video Lazarus Protocols: https://nebula.tv/videos/isaacarthur–… out Tech Alter: https://nebula.tv/techaltar?ref=isaac… and Day Pass: https://nebula.tv/daypass?ref=isaacar… 🛒 SFIA Merchandise: https://isaac-arthur-shop.fourthwall… 🌐 Visit our Website: http://www.isaacarthur.net ❤️ Support us on Patreon: / isaacarthur ⭐ Support us on Subscribestar: https://www.subscribestar.com/isaac-a… 👥 Facebook Group: / 1,583,992,725,237,264 📣 Reddit Community: / isaacarthur 🐦 Follow on Twitter / X: / isaac_a_arthur 💬 SFIA Discord Server: / discord Credits: Biohacks & Brain Mods — The Coming Age of Implant Culture Written, Produced & Narrated by: Isaac Arthur Edited by: Chris Gray & Donagh Broderick Select imagery/video supplied by Getty Images Chapters 0:00 Intro 1:28 The First Layer – The Implants Already Here 3:08 The Early Adoption Phase – Niche Enhancements 5:27 Safety vs Freedom 8:25 Implant Economics 14:31 The Social Shift – The Rise of Implant Culture 20:04 Minds in Motion – Cognitive Architecture as a Design Space 21:50 Implant Maximalism – Full-Stack Upgrades 23:03 Nebula 24:09 Post-Implant Society – Upgrades as Life Stages 25:40 The Far Horizon – When Implants Become Civilization.
Check out Tech Alter: https://nebula.tv/techaltar?ref=isaac
and Day Pass: https://nebula.tv/daypass?ref=isaacar

🛒 SFIA Merchandise: https://isaac-arthur-shop.fourthwall
🌐 Visit our Website: http://www.isaacarthur.net.
❤️ Support us on Patreon: / isaacarthur.
⭐ Support us on Subscribestar: https://www.subscribestar.com/isaac-a
👥 Facebook Group: / 1583992725237264
📣 Reddit Community: / isaacarthur.
🐦 Follow on Twitter / X: / isaac_a_arthur.
💬 SFIA Discord Server: / discord.
Credits:
Biohacks & Brain Mods — The Coming Age of Implant Culture.
Written, Produced & Narrated by: Isaac Arthur.
Edited by: Chris Gray & Donagh Broderick.
Select imagery/video supplied by Getty Images.

Chapters.
0:00 Intro.
1:28 The First Layer – The Implants Already Here.
3:08 The Early Adoption Phase – Niche Enhancements.
5:27 Safety vs Freedom.
8:25 Implant Economics.
14:31 The Social Shift – The Rise of Implant Culture.
20:04 Minds in Motion – Cognitive Architecture as a Design Space.
21:50 Implant Maximalism – Full-Stack Upgrades.
23:03 Nebula.
24:09 Post-Implant Society – Upgrades as Life Stages.
25:40 The Far Horizon – When Implants Become Civilization.

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Adversarial AI reveals mechanisms and treatments for disorders of consciousness

Researchers led by UCLA have developed an adversarial AI framework that may help explain how consciousness breaks down after brain injury — and how it might one day be restored. Published in Nature Neuroscience, the study used deep neural networks trained on more than 680,000 neuroelectrophysiology samples and validated findings across 565 patients, healthy volunteers, and animals. The model identified specific circuit-level disruptions linked to disorders of consciousness, including the basal ganglia indirect pathway and altered inhibitory cortical wiring.

What makes this so important is that it pushes consciousness research closer to mechanism. Instead of only asking what consciousness is, this kind of work asks: what specific brain circuitry fails when consciousness is lost, and can that failure be targeted? The study also identified high-frequency stimulation of the subthalamic nucleus as a promising intervention, supported by human electrophysiological data. This is the kind of neuroscience that makes consciousness feel less like pure philosophy — and more like something we may eventually model, test, and repair.

Abstract: Nature Neuroscience Adversarial AI reveals mechanisms and treatments for disorders of consciousness.


Toker et al. present an AI framework that identifies mechanisms of consciousness. The model predicts new drivers of unconsciousness and identifies subthalamic nucleus stimulation as a potential therapy for disorders of consciousness.

Phagocytosis and neuroinflammation: orchestrating central nervous system homeostasis, repair, and the resolution of inflammation

Brain phagocytosis and neuroinflammation.

Phagocytes in the central nervous system (CNS), including astrocytes, microglia, and macrophages, shape development and homeostasis by pruning synapses and removing apoptotic debris.

Phagocytosis is mediated by various ligand–receptor dyads and signaling pathways, enabling CNS phagocytes to respond to neuroimmune shifts across the lifespan and during pathology.

Phagocytosis pathways regulate recovery in various models of CNS pathology, including multiple sclerosis, CNS injury, ischemic stroke, and age-associated neurodegeneration.

Phagocytosis pathways are intimately integrated with the inflammatory cell state and remove viable cells in pathology-adjacent tissue, highlighting the complexity of targeting these systems.

To maximize benefit and minimize off target damage, new phagocytic-based approaches should optimize drug delivery timing and location, tailored to each CNS pathology. sciencenewshighlights ScienceMission https://sciencemission.com/resolution-of-inflammation


Hearing research traces evolution of key inner ear protein

In the intricate machinery of the inner ear, hearing begins with a protein that moves a few billionths of a meter up to 100,000 times per second. That protein, called TMC1, sits at the tips of sensory hair cells deep in the snail-shaped cochlea. When sound waves move these microscopic hairs, TMC1 acts as a channel, opening and allowing charged particles to flow into the cell and trigger an electrical signal to the brain.

Without TMC1, that signal never starts. Mutations in the TMC1 gene are a well-known cause of hereditary hearing loss in humans. Because of this central role, TMC1 is an attractive target for researchers designing gene therapies aimed at restoring hearing. Several groups are testing ways to supply working copies of the gene or fix harmful mutations.

For these efforts to be safe and effective, scientists need to know in detail how TMC1 is built, how it opens, and which parts of the protein are most sensitive to change. However, the hair-cell system that includes TMC1 is so complex, sensitive, and hard to access that it is notoriously difficult to take apart and study directly.

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