If the brain were so simple that we could understand it, we wouldn't. Science. Music. Poetry.

Barcelona, Spain
Joined November 2019
Things are heating up on Terry Tao’s blog. In “If Math Is More Than Proof, We Need to Better Celebrate the Rest of It,” Grant Sanderson of @3blue1brown proposes “open exposition problems” -- rewarding the work of making math genuinely understandable. terrytao.wordpress.com/2026/…
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Francesca retweeted
About emergence... algorithmic style (compression rules!). Preprint updated (and submitted). Algorithmic emergence: the event where an observer/agent discovers a useful representation and reusable model that reveal regularity it could not use before. Compression may not exist—and even when it does, every reliable method that always halts has blind spots. @bcom_foundation @Castaldo_Fr doi.org/10.5281/zenodo.21008…
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Francesca retweeted
Wonderful paper, wonderful collaboration, wonderful collaborators! And a very fun paper to write... @bcom_foundation
Can AI spread like a virus and erode cognitive autonomy? Our new paper models how LLM adoption can cross tipping points, triggering runaway dependence and tech lock-in, suggesting routes to "cognitive immunization". arxiv.org/abs/2609.03344
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Extremely grateful to be joining the @RenPhilanthropy x @SPRIND Big if True Science Accelerator, alongside scientists and builders I can't wait to learn from. My program: computational customization of depression treatment, aligned with our mission at @bcom_foundation.
We’re delighted to introduce the @RenPhilanthropy and @SPRIND Big if True Science (BiTS) Accelerator 2026 cohort: eight exceptional scientists, technologists, and innovators developing ambitious R&D programs across AI for science, advanced materials, aging biology, nuclear energy, & more. renaissancephilanthropy.org/… Meet the Cohort↓ 1/9
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Francesca retweeted
The things that stay, with @Castaldo_Fr @bcom_foundation. You cannot step into the same river twice—but the river remains. 🌊 From Aristotle to Alan Turing, how do we persist when our atoms are constantly replaced? Dive into Kolmogorov Theory and the computational nature of identity. #Philosophy #CognitiveScience #KT giulioruffini.github.io/asse…
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Francesca retweeted
Download our "Rosetta Stone of Neural Mass Models" review paper for a limited time (preprint also available at arXiv)! By transforming a repertoire of disparate formalisms into a navigable ladder, we hope to help select NMM choice for brain modeling and translate between scales, modalities, and interventions.authors.elsevier.com/a/1nH4W…
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Francesca retweeted
Do you need to understand the world to survive in it? A classic 1970 cybernetics theorem says yes: "Every good regulator of a system must be a model of that system." But proving this mathematically for complex, unpredictable real-world scenarios has always been notoriously difficult. 2/5 In a new paper, "The Algorithmic Regulator" (published in Entropy), I tackle this using Algorithmic Information Theory and Kolmogorov Complexity. 🧠💻 It takes the classic Good Regulator Theorem and the Internal Model Principle and complements and extends them for non-linear, deterministic systems. 3/5 The paper looks at regulation as data compression. The proof shows that if a regulator successfully keeps a system (embedded in the world) stable (reducing the algorithmic complexity of its output), it mathematically must share "mutual algorithmic information" with the world with high probability. The key result: K(W∣R)mdpi.com/1099-4300/28/3/257
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Check out our new paper: Rosetta Stone of Neural Mass Models 🔅
1/ 🧠 New in Computational Neuroscience: "Rosetta Stone of Neural Mass Models." We pr,ovide a unifying framework for translating between them, connecting the harmonic oscillator with Stuart-Landau, Wilson-Cowan, NMM1, and NMM2 (next generation). With @Castaldo_Fr, Raul de Palma Aristides, Pau Clusella, and Jordi Garcia-Ojalvo - arxiv.org/abs/2512.10982
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📢Welcome to read the paper "Structured Dynamics in the Algorithmic Agent", by Giulio Ruffini, Francesca Castaldo, Jakub Vohryzek 👉Find full article at: mdpi.com/1099-4300/27/1/90 #DynamicalSystems #AlgorithmicInformationTheory #LieGroups #KolmogorovTheory #NeuralNetworks #AI
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🧵 Thread: The Laminar Neural Mass Model (LaNMM) — A Unified Framework for Oscillatory Dynamics in Health and Disease 1. Intro Let me introduce a modeling framework that my team has developed for computational neuroscience: the Laminar Neural Mass Model (LaNMM). This approach links circuit-level mechanisms to EEG/MEG biomarkers across brain states — from healthy function to disease and altered consciousness. 2. The Laminar Neural Mass Model (2022) sciencedirect.com/science/ar… biorxiv.org/content/10.1101/… Our original LaNMM papers (2019, 2022) introduced a physics-grounded neural mass model capable of generating both alpha/beta and gamma oscillations across cortical layers. It embeds synaptic sources into a spatially layered medium, enabling simulation of laminar LFPs and their spectral features. 3. Key Insight Alpha/beta (slow/fast) rhythms are generated in deep layers, gamma in superficial ones. The model’s structure allows us to simulate realistic depth-resolved LFP, bipolar LFP, and CSD — crucial for aligning with experimental macaque data and uncovering oscillatory origins. Now comes the trilogy of applied studies using LaNMM: 4. AD Study (2025) biorxiv.org/content/10.1101/… In this AD-focused work, the model simulates fast interneuron (PV+) dysfunction and later-stage pyramidal cell loss. This reproduces AD’s biphasic M/EEG trajectory: early hyperexcitability (↑gamma, ↑alpha), followed by slowing and hypoactivity. 5. Mechanistic Findings Aβ oligomers impair PV+ interneurons → disinhibition → hyperactivity. Later, tau pathology hits pyramidal neurons → hypoactivity. The LaNMM shows that PV+ dysfunction alone explains the early phase EEG biomarkers, but tau-induced hypoactivity is required to match reduced firing/metabolism in advanced stages. 6. Clinical Relevance This model suggests PV+ cells are a therapeutic target — and that EEG spectral changes can serve as early-stage biomarkers. It bridges molecular pathology and mesoscopic dynamics. 7. Psychedelics + AD (2024) biorxiv.org/content/10.1101/… In this follow-up study, the LaNMM is embedded in whole-brain models personalized to AD patients. Activation of 5-HT2A receptors (mimicking psychedelics) increases excitability in L5 pyramidal cells — counteracting AD-related oscillatory deficits. 8. Restoration of Dynamics Under 5-HT2A modulation: → ↓ Alpha power (reduces hypersynchrony) → ↑ Gamma power (restores PV-related processing) → ↑ Entropy/complexity (a proxy for cognitive flexibility) 9. Spatial Specificity Spectral changes correlate with PET-derived 5-HT2A receptor distributions — suggesting that psychedelics could restore oscillatory dynamics in AD via targeted circuit modulation. 10. Prediction Error & CFC (2025) biorxiv.org/content/10.1101/… Our latest paper goes deeper into theory. It proposes that LaNMM supports biologically plausible Comparator functions via cross-frequency coupling (CFC), enabling local prediction error evaluation in predictive coding. 11. Key Mechanisms • Signal-Envelope Coupling (SEC): Low-freq rhythms modulate the amplitude of fast oscillations (PAC-like). • Envelope-Envelope Coupling (EEC): Slow envelopes modulate fast envelopes — allowing gating and precision weighting (think Kalman gain). 12. Comparator Disruption Across Conditions → In AD: Interneuron loss disrupts CFC, leading to inflated early prediction errors and their later suppression. → In psychedelics: Increased gain weakens prediction precision → “relaxed beliefs” and increased error signaling. 13. Comparator Hypothesis CFC in LaNMM instantiates the analog version of the hierarchical XOR-like error computation central to predictive coding and KT/AIF. This formalization bridges algorithmic models with real electrophysiology. 14. Why This Matters Together, these papers show how LaNMM provides a unified, mechanistic scaffold for studying: • Neurodegeneration (AD) • Psychedelic states • Predictive inference • Oscillatory biomarkers • Interneuron dynamics 15. Conclusion LaNMM is not just another NMM — it’s a physically grounded, biophysically realistic platform that integrates structure, dynamics, and function. Expect to see more work where biology meets theory, with LaNMM at the core! @neurotwin @Neuroelectrics @KarlFristonNews @GustavoDeco @Castaldo_Fr @ne_sanchez_todo @galvani_lab @ERC_Research @alvaropleone @VohryzekJakub 🧵/end
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🚨 Don’t miss this week’s #NeurotechTalk with three incredible experts: @jacamprodon, @ruffini & @Castaldo_Fr! Register now and discover how neuroscience & brain stimulation are transforming #SuicidePrevention. Save your spot for Dec 12 here: neuroelectrics.com/webinar/8…
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Check this out! Our latest work on Major Depressive Disorder uses the algorithmic agent framework to bridge first-person and third-person perspectives, advancing computational neuropsychiatry. Happy birthday, Karl! #Neuropsychiatry #Depression
Our KT-MDD paper has been published! "The Algorithmic Agent Perspective and Computational Neuropsychiatry: From Etiology to Advanced Therapy in Major Depressive Disorder (MDD)," with @Castaldo_Fr, Ed Lopez-Sola, @ne_sanchez_todo, and @VohryzekJakub, is now part of the Special Entropy issue to honor Karl Friston's 65th birthday. mdpi.com/1099-4300/26/11/953 Here is a summary: By using the algorithmic agent framework drawn from Kolmogorov theory of consciousness (KT), we link first-person and third-person phenomena to analyze MDD. Some important concepts we use: Def 1 (agent): An algorithmic agent is an information-processing system with an Objective Function that interacts bidirectionally with the external world, creating and running compressive Models (Model=Program in AIT language), Planning, and acting to maximize its Objective Function. Def 2 (Emotion): The emotional state of the Agent is the tuple E = (Model, Valence). In first-person language, emotion is structured experience with valence, and can be described along dimensions characterizing world/self model structure plus valence (positive/negative). Def 3: (Depressed Agent). Depression is a pathological state in which the output value of the Objective Function (valence) of an agent is persistently low. A cornerstone in KT is this hypothesis: Hypothesis (Structured Experience). An agent has structured experience (𝒮) to the extent it has access to encompassing, accurate, and compressive models to interact with the world. The key question is this: what drives an agent to a state of persistent low valence? Depression is characterized as a "disorder of the agent" arising from issues in how the brain evaluates valence (positive or negative feelings). We suggest that the complexity and multi-etiology of depression stem from the many systems involved in valence evaluation, including the structure of world models. The framework divides complex neural processes into three agent components: the Modeling Engine, Objective Function, and Planning Engine. Each element connects to specific brain regions and circuits. For example, the Modeling Engine is linked to areas like the posterior cingulate cortex and hippocampus, which are involved in learning (compression) and prediction. In contrast, the Objective Function is connected with the amygdala and ventral striatum. We also propose a path toward personalized depression treatments and the importance of using "neurotwins" of a patient's brain to simulate and optimize treatments like brain stimulation and medication. For example, we highlight the potential of combining brain stimulation with neuroplastogens (substances that promote changes in the brain). We acknowledge that mapping the abstract agent framework onto the intricate biological reality of the brain is complex. However, this approach is crucial for moving toward personalized, model- and data-driven treatments in neuropsychiatry. Related talk at #techspiritbarcelona: youtube.com/watch?v=iihG8b9O… See also this related call for papers in Entropy on The Mathematics of Structured Experience: Exploring Dynamics, Topology, and Complexity in the Brain mdpi.com/journal/entropy/spe… This paper is part of the KT research program. You can learn more here: arxiv.org/abs/0704.1147 (2007) arxiv.org/abs/0903.1193 (2009) arxiv.org/abs/1612.05627 (2017) academic.oup.com/nc/article/… (2017) doi.org/10.1142/S27050785225… (2023) mdpi.com/1099-4300/26/1/90 (2024) biorxiv.org/content/10.1101/… (2024) @Neuroelectrics @neurotwin @galvani_lab
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We have released an updated version of our AIT/KT MDD paper, "The algorithmic agent perspective and computational neuropsychiatry: from etiology to advanced therapy in major depressive disorder." osf.io/preprints/psyarxiv/eq…. 1/n
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Despite feeling a bit awkward giving a talk about 🧠 modelling to some of the world’s top experts at #BrainModes2023 without being in the field myself, I enjoyed the experience. It helped that I presented the great work of @Castaldo_Fr with the beautiful slides she made.
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Our modelling paper led by @Castaldo_Fr and @francpsantos has just come out in Neuroimage (handled by the 'classic' editorial board). Thanks to all the co-authors again and the reviewers for their helpful guidance. sciencedirect.com/science/ar…
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How to do a principled stimulation paradigm? We argue for "Dynamic Sensitivity Analysis" where in-silico whole-brain perturbations are leveraged in guiding experiments. sciencedirect.com/science/ar… @Joana_Cabral__ @Castaldo_Fr @ysanz6 @LDLord13 @henrique_frnnds @LitvakVladimir
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So happy to see our efforts recognized by @Biotech_Spain to advance our mechanistic understanding of brain rhythms detected with EEG and MEG! @Castaldo_Fr, @VohryzekJakub, @LitvakVladimir @BickMath @RenaudLambiotte @BecariosFLC
.@UPFBarcelona A mechanical model to explain brain rhythms is the focus of an international research project involving the Center for Brain and Cognition biotech-spain.com/en/article…
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A new preprint! Ever used pwelch, or signal.welch? 1960s stats for spectra are widely used today though statistical methods have greatly advanced. We modernise this with the GLM-spectrum... @OHBA_Oxford @OxfordWIN @OxPsychiatry @TheCHBH @UoB_SoP biorxiv.org/cgi/content/shor…
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