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Ritter, P.

Publications and source records attributed to Ritter, P..

At least 19 recordsLinked to original sources

Multi-Methodological Characterization of Sleep Deprivation: From Standard EEG Power Spectra to Aperiodic Dynamics in Humans and Mice.

Sleep deprivation is a potent, rapid-acting therapeutic intervention for major depressive disorder, yet its underlying neural mechanisms remain poorly understood, hindering the development of predictive biomarkers. Here, we systematically characterize the electro-physiological signatures of prolonged wakefulness using a multi-methodological approach across three independent datasets in humans and mice. By integrating standard power spectral density analysis with aperiodic component fitting (SpecParam) and highly compar-ative time-series analysis (HCTSA), we identified robust cross-species biomarkers of sleep pressure. Machine learning models revealed that theta power is the most consistent feature for differentiating control and sleep deprivation states, achieving up to 90% classification accuracy. Sleep deprivation significantly increased the spectral offset - suggesting global cortical hyperexcitation - while simultaneously steepening the spectral slope. We interpret this simultaneous shift as a state uncoordinated state of hyperexcited and inefficient neu-ral processing. These findings establish reproducible EEG markers of sleep deprivation that transcend species. Given the clinical utility of wake therapy, we propose that prefrontal the-ta power and spectral offset/slope may serve as mechanism-based predictors of therapeu-tic response. Our results provide a framework for the clinical validation of these biomarkers, potentially enabling personalized chronotherapeutic interventions for psychiatric disorders.

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The Virtual Child Brain: Modeling Neuromaturational Trajectories

IntroductionUnderstanding the mechanisms of human neuromaturation constitutes one of the fundamental questions of neuroscience. While it is well described that large-scale brain maturation is initiated within sensorimotor brain regions and progresses to associative cortex, the underlying developmental neurobiology remains to be fully characterized. Animal models have indicated that cortical inhibitory upregulation might be a driver of neurodevelopment. To investigate the hypothesis that cortical inhibitory upregulation plays a similar role in human neuromaturation, we developed a The Virtual Brain (TVB) based computational model (TVB-Child) to explore potential mechanisms of human neurodevelopment. Material and methodWe created neurodevelopmental dynamic brain network models capturing neurobiological maturation by using the large-scale brain simulator TVB and fitting brain network models to developmental functional MRI (fMRI) from the Human Connectome Project-Development (HCP-D) data set with 640 subjects with an age range of 6-21 years. Age-dependent trajectories in the fMRI data set were first analyzed by combined group-ICA/Dual Regression extracting subject-specific resting-state networks (RSN). Maturational topographical and topological redistribution of these networks were analyzed by linear and non-linear regression of RSN size and degree and strength centrality. Brain network models were fitted to the fMRI functional connectivity obtained from the HCP-D data set. Hypothesizing that cortical inhibition is a driver of neuromaturation, we analyzed spatiotemporal inhibition parameter gradients in the dynamic brain network model for the hypothesized significant correlations with fMRI RSN maturational trajectories. ResultsWhile during development frontoparietal (FP) and default mode network (DMN) grew and exhibited an increase in both degree and strength centrality, becoming dominant network hubs, the attention network underwent network pruning with a decrease in size and node degree. The primary sensory network changed little. For the fitted brain network models, we obtained a high degree of reproduction with correlation coefficients between empirical and simulated functional connectivities ranging between 0.80 and 0.95. Values of the feed forward inhibition model parameter [Formula] representing the strength of regional feedforward inhibitory input exhibited the most significant increase with age within the FP and DMN networks. A less pronounced, but significant, age-dependent increase of the inhibitory parameter values were seen in attention networks and no change within primary sensory networks. ConclusionOur study shows that high order (FP, DMN), attention and primary sensory networks exhibit distinct topographical and topological maturation trajectories. Moreover, brain network modeling revealed RSN-specific age-dependent inhibition trajectories, indicating that the model is able to reproduce and thus support candidate mechanisms of neurodevelopment. Graphical abstractOverview of the study combining empirical and modeling analyses of neuromaturation in 640 study participants from the HCP-D data set, age range 6-21 years old. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=149 SRC="FIGDIR/small/737052v1_ufig1.gif" ALT="Figure 1"> View larger version (50K): org.highwire.dtl.DTLVardef@1764432org.highwire.dtl.DTLVardef@17740ceorg.highwire.dtl.DTLVardef@3fa9a6org.highwire.dtl.DTLVardef@19afc80_HPS_FORMAT_FIGEXP M_FIG C_FIG

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Dopamine Depletion Drives Whole-Brain Oscillatory Disruptions via Cortico-Subcortical Resonance: A Multiscale Model of Parkinson's Disease in Mice

Parkinson's disease is defined by dopaminergic neuron loss in the substantia nigra, yet its hallmark, exaggerated beta-band synchrony, pervades motor cortex, thalamus, and cerebellum, implicating network dynamics far beyond any single circuit. How focal subcortical dopamine depletion translates into brain-wide oscillatory pathology remains unresolved. We use a connectome-constrained multiscale model of the mouse brain, embedding biophysically detailed spiking networks of basal ganglia and cerebellum within whole-brain corticothalamic dynamics grounded in the Allen Mouse Brain Connectivity Atlas. We show that confining dopamine depletion exclusively to subcortical circuits is sufficient to produce widespread beta hypersynchrony (10-30 Hz), accompanied by heterogeneous theta and gamma dysregulation. Virtual loop ablations reveal that cortical and cerebellar beta amplification strictly requires intact cortico-basal ganglia-thalamic feedback; severing this loop confines beta to subcortical generators. These results support resonance within closed large-scale loops, rather than local rhythmogenesis, as the mechanism underlying distributed Parkinsonian beta pathology.

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The Cerebellar Engine: Multiscale Digital Brain Co-simulations Reveal How Cerebellar Spiking Architecture Shapes Cortical Coherence

Cellular activities shape large-scale brain dynamics determining brain functioning and disease, yet the causal mechanisms across scales remain unclear. In particular, the cerebellum has been reported to modulate whole-brain dynamics during sensorimotor integration through unknown circuit interactions. To investigate the underlying mechanisms, we developed a novel multiscale digital brain simulator, in which a spiking neural network of the olivocerebellar microcircuit is embedded in a mean-field virtual mouse brain and wired using an atlas-based long-range connectome. Parameters were systematically tuned to match multiscale experimental data from primary sensory and motor cortices (S1 and M1) and cerebellum. We analyzed the role of cerebellar circuitry on sensorimotor integration by lesioning critical circuit connections in silico. Results suggested that Purkinje cell inhibition enhances the processing efficiency of the 'cerebellar engine' through decorrelation of cerebellar nuclei activity and that the pathway between mossy fibers and cerebellar nuclei is the specific pathway inside the microcircuit driving M1-S1 coherence. These results indicate a mechanistic link between cerebellar microcircuit and cortical sensorimotor processing. This novel framework opens new perspectives for the broader multiscale investigation of brain physiological and pathological states in relation to specific cellular and microcircuit properties.

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Brain network modeling with The Virtual Brain derives pharmacodynamics of ketamine

Ketamine, an N-Methyl-D-aspartate receptor (NMDAR) antagonist, is used clinically as an anesthetic and antidepressant, and is also known for its psychotomimetic effects. Its impact on brain dynamics and behavior varies significantly with dosage likely via a dose-dependent modulation of the NMDARergic transmission. Currently, it is unclear how molecular changes at the microscopic level of NMDAR antagonism lead to large-scale changes in brain dynamics. We implement a dose-dependent NMDAR antagonism based on ketamines disinhibition theory into a biophysically grounded mean-field model within The Virtual Brain (TVB) framework to replicate ketamines key signatures across its dose spectrum. Our results imply that in low doses ketamine preferentially impairs excito-inhibitory neurotransmission while in higher doses antagonism on excito-excitatory connections plays a role. These findings highlight the utility of computational modeling for disentangling dose-specific mechanisms of action and provide a framework for exploring NMDAR-related interventions. Author summaryKetamine is a dissociative anesthetic at high doses, but at lower, sub-anesthetic doses, it has garnered significant interest for its rapid-acting antidepressant and anxiolytic effects. Despite its growing clinical use in psychiatric conditions, the precise neural mechanisms underlying ketamines dose-dependent effects remain incompletely understood. Ketamine primarily acts as a non-competitive antagonist of the NMDAR, which is expressed on both excitatory and inhibitory neurons throughout the cortex. One of the leading hypotheses explaining its antidepressant effects is the disinhibition theory which proposes that low doses of ketamine preferentially block NMDARs on inhibitory interneurons, resulting in increased cortical excitability. At high doses ketamine exerts anesthetic effects potentially through more widespread NMDAR antagonism including on excitatory neurons. In this study, we used a computational model to explore how selective NMDAR antagonism at different doses affects large-scale brain dynamics. A key novelty of our work is the integration of ketamines full dose spectrum within a single computational modeling framework, allowing us to relate distinct neural effects from disinhibition to anesthesia to experimental findings. This modeling approach contributes to a deeper understanding of how ketamine modulates cortical activity across different contexts.

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An Interactive Brain Atlas of Knowledge

Biomedical knowledge about the brain increases every day, with a rapidly growing number of scientific publications, datasets, and software tools. While this informational plethora is not merely comprehensible by human beings, recent developments in information science and computational linguistics aim to make this knowledge programmatically accessible by literature mining. However, integrating these semantic methods into neuroimaging standards remains insufficient, hindering researchers from unraveling their full potential. Therefore, we developed the semantic meta-analysis platform The Virtual Brain adapter of semantics (TVBase) that projects biomedical knowledge preserved in over 36 million scientific articles onto a 3D standardized brain. The literature-mining platform SCAIView was used to extract ontologically defined biomedical entities and their associations with brain anatomy from the PubMed database. By querying a specific concept, the association strength with each anatomical term was calculated using entropy. To project the data onto a standardized brain, we created a unique transformation matrix that links over 800 anatomical terms to voxel coordinates of a parcellated standard brain. This novel method of knowledge projection extracts region-specific information about biomedical concepts from the literature to support translational multi-scale approaches to computational neuroscience. The multi-purpose software framework TVBase is openly available as a Python library. It aims for hypothesis-free neuroimaging pattern interpretation, hypothesis generation, and applications in personalized medicine.

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From Ions to Chaos: exploring a whole-brain modelling framework in the mouse

Computational neuroscience offers powerful tools for understanding brain function in both healthy and diseased states. However, detailed data on microscale mechanisms--such as those involved in genetics and pharmacology--are often derived from mouse experiments and further lack integration into whole-brain models. In this work, we bridge microscale ion-channel dynamics and macroscale network behavior by employing the Larter-Breakspear neural mass model on The Virtual Brain platform with a mouse brain connectome. Our simulations reproduced key findings from prior computational studies with the Larter-Breakspear model, demonstrating its cross-species translation to the mouse. This included the emergence of chaotic dynamics and network synchrony as a function of coupling and delay parameters. Furthermore, we demonstrate that Calcium, Sodium, and Potassium-related parameters each critically shape the global dynamic regimes and that the response to external stimuli is highly sensitive to calcium concentrations. This work represents the first integration of the Larter-Breakspear model into a mouse-scale connectome, validating previous results in a new context. In addition, it establishes a framework for a detailed exploration of synchrony, ion dependency, and stimulus reactivity. By linking molecular simulations, genetic data, and mouse electrophysiology, this approach holds promise for mechanistic insights into neuropsychiatric disorders, such as schizophrenia and epilepsy.

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The Virtual Brain Ontology: A Digital Knowledge Framework for Reproducible Brain Network Modeling

Computational models of brain network dynamics offer mechanistic insights into brain function and disease, and are utilized for hypothesis generation, data interpretation, and the creation of personalized digital brain twins. However, results remain difficult to reproduce and compare because equations, parameters, networks, and numerical settings are reported inconsistently across the literature, and shared code is often not fully documented, standardized, or executable. We introduce The Virtual Brain Ontology (TVB-O), a semantic knowledge base, minimal metadata standard, and Python toolbox that simplifies the description, execution, and sharing of network simulations. TVB-O offers 1) a common vocabulary and ontology for core concepts and axioms representing current domain knowledge for simulating brain network dynamics, 2) a minimal, human- and machine-readable metadata specification for the information needed to reproduce an experiment, 3) a curated database of published models, brain networks, and study configurations, and 4) software that generates executable code for various simulation platforms and programming languages, including The Virtual Brain, Jax, or Julia. FAIR metadata and provenance-aware reports can be exported from TVB-Os model specification. It hereby enables a flexible framework for adopting new models and enhances reproducibility, comparability, and portability across simulators, while making assumptions explicit and linking models to biomedical knowledge and observation pathways. By reducing technical barriers and standardizing workflows, TVB-O broadens access to computational neuroscience and establishes a foundation for transparent, shareable "digital brain twins" that integrate with clinical pipelines and large-scale data resources.

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Fast and Easy Whole-Brain Network Model Parameter Estimation with Automatic Differentiation

Personalized brain modeling at clinically relevant scales requires integrating biophysical models with empirical neuroimaging data, yet high-dimensional parameter estimation in whole-brain network models remains computationally prohibitive. We present TVB-Optim, an open-source Python library providing a general and extensible framework for gradient-based optimization of brain network models build on JAX. Leveraging automatic differentiation, we demonstrate direct optimization of thousands of parameters, from global coupling (N=2) to regional dynamics (N=168) to full structural connectivity matrices (N=14,028), across functional MRI and magnetoencephalography data. Forward simulations achieve 10x CPU speedup over reference implementations and scale efficiently to GPU and multi-device configurations. We establish best practices through documented workflows that combine coarse parameter space exploration with gradient refinement, often yielding superior solutions faster than gradient methods alone. By bridging mechanistic neuroscience with modern machine learning infrastructure, TVB-Optim enables large-scale personalized brain models, bringing computational neuroscience closer to clinical translation.

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Biological Database Mining for LLM-Driven Alzheimer's Disease Drug Repurposing

BACKGROUNDThis study presents a software pipeline that leverages LLMs to apply knowledge stored in natural language (such as in pharmacological texts) and ontologies in a transparent Drug Repurposing (DR) information structure. METHODSAlzheimers Disease (AD) related entries in Gene Ontology and DrugBank were integrated into a Knowledge Graph database to inform LLM prompts. 16,581 drugs were screened for their DR potential by the LLM Llama3:8b. The vector embedding representation of the drugs in the LLM was investigated to asses if LLMs store pharmacological information in alignment with domain expert understanding of pharmacological groups. By measuring the semantic similarity of drugs quantitatively, the performance of the DR pipeline was examined. A manual hallucination check was performed to assess the impact of the ontology-database combination on LLM-hallucination performance. The results were compared against registered clinical trials (RCTs) and proposed medications in meta-analyses to evaluate their predictive value. RESULTSThe embedding analysis showed that the vector representations of drugs in the LLM show clusters in alignment with pharmacological groups. The ontologically enhanced prompt was closer to the expert domain proposals than a zero-shot control prompt without that knowledge. The results of the ontology-based prompt showed fewer hallucinations in their responses compared to the zero-shot control prompting. CONCLUSIONSOntology-augmented LLM interaction leads to fewer hallucinations and output closer to expert assessment in comparison with a zero-shot control. We propose retrospective analyses, considering the high-rated drugs and their effect on AD patients as a starting point for further (prospective) research.

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The Virtual Brain links transcranial magnetic stimulation evoked potentials and inhibitory neurotransmitter changes in major depressive disorder

BackgroundTranscranial magnetic stimulation evoked potentials (TEPs) show promise as a biomarker in major depressive disorder (MDD), but the origin of the increased TEP amplitude in these patients remains unclear. Gamma aminobutyric acid (GABA) may be involved, as TEP peak amplitude is known to increase with GABAergic activity in healthy controls. We employed a computational modeling approach to investigate this phenomenon. MethodsWhole-brain simulations in The Virtual Brain (thevirtualbrain.org), employing the Jansen and Rit neural mass model, were optimized to simulate TEPs of healthy individuals (Nsubs=20, 14 females, 24.5{+/-}4.9 years). To mimic MDD-like impaired inhibition, a GABAergic deficit was introduced to the simulations by altering one of two selected inhibitory parameters, the inhibitory synaptic decay rate b or the number of inhibitory synapses C4. The TEP amplitude was quantified and compared for all simulations. ResultsThe inhibitory synaptic decay rate showed a quadratic correlation (r=0.99, p<0.001) and the number of inhibitory synapses a negative exponential correlation (r=0.99, p<0.001) with the TEP amplitude. Moreover, significant correlations between these simulation-derived values and all TEP peaks and troughs were detected (p<0.001). Thus, under local parameter changes, we were able to alter the TEP amplitude towards pathological levels, i.e. creating an MDD-like increase of the global mean field amplitude in line with empirical results. ConclusionsOur model suggests specific GABAergic deficits as the cause of increased TEP amplitude in MDD patients, which may serve as therapeutic targets. This work highlights the potential of whole-brain simulations in the investigation of neuropsychiatric diseases.

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Whole-brain dynamics and hormonal shifts throughout women's lifespan: From reproductive stages to menopausal transition and beyond

Neuroimaging studies have identified significant age-related disruptions in whole-brain dynamics, yet the influence of womens reproductive stages and associated hormonal shifts remains underexplored. This study leverages resting-state fMRI data from the Human Connectome Project in Aging to examine brain dynamics through five reproductive stages: reproductive, late reproductive, perimenopause, early postmenopause, and late postmenopause. Our results indicate that the late reproductive stage is characterized by the highest dynamical complexity across whole-brain and resting-state networks, while brain dynamics significantly decline at menopause onset. Additionally, we employ machine learning classifiers using two approaches: (1) brain dynamics alone and (2) brain dynamics combined with follicle-stimulating hormone (FSH) and estradiol (brain-hormone model). Both models accurately distinguished reproductive stages, but the brain-hormone model outperformed the brain dynamics model. Key predictors included decreased estradiol, increased FSH, and altered brain dynamics in later life stages. These results offer a framework for assessing brain health across womens reproductive lifespan.

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Off-Equilibrium Fluctuation-Dissipation Theorem Paves the Way in Alzheimer's Disease Research

INTRODUCTIONAlzheimers disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline. Although traditional methods have provided insights into brain dynamics in AD, they have limitations in capturing non-equilibrium dynamics across disease stages. Recent studies suggest that dynamic functional connectivity in resting-state networks (RSNs) may serve as a biomarker for AD, but the role of deviations from dynamical equilibrium remains underexplored. OBJECTIVEThis study applies the off-equilibrium fluctuation-dissipation theorem (FDT)1 to analyze brain dynamics in AD, aiming to compare deviations from equilibrium in healthy controls, patients with mild cognitive impairment (MCI), and those with AD. The goal is to identify potential biomarkers for early AD detection and understand disease progressions mechanisms. METHODSWe employed a model-free approach based on FDT to analyze functional magnetic resonance imaging (fMRI) data, including healthy controls, MCI patients, and AD patients. Deviations from equilibrium in resting-state brain activity were quantified using fMRI scans. In addition, we performed model-based simulations incorporating Amyloid-Beta (A{beta}), tau burdens, and Generative Effective Connectivity (GEC) for each subject. RESULTSOur findings show that deviations from equilibrium increase during the MCI stage, indicating hyperexcitability, followed by a significant decline in later stages of AD, reflecting neuronal damage. Model-based simulations incorporating A{beta} and tau burdens closely replicated these dynamics, especially in AD patients, highlighting their role in disease progression. Healthy controls exhibited lower deviations, while AD patients showed the most significant disruptions in brain dynamics. DISCUSSIONThe study demonstrates that the off-equilibrium FDT framework can accurately characterize brain dynamics in AD, providing a potential biomarker for early detection. The increase in non-equilibrium deviations during the MCI stage followed by their decline in AD offers a mechanistic explanation for disease progression. Future research should explore how combining this framework with other dynamic brain measures could further refine diagnostic tools and therapeutic strategies for AD and other neurodegenerative diseases.

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Connectomes, simultaneous EEG-fMRI resting-state data and brain simulation results from 50 healthy subjects

We present raw and processed multimodal empirical data as well as simulation results from a study with The Virtual Brain (TVB). Simultaneous electroencephalography (EEG) - functional magnetic resonance imaging (fMRI) resting-state data, diffusion-weighted MRI, and structural MRI were acquired for 50 healthy adult subjects (18 - 80 years of age) at the Charite University Medicine, Berlin, Germany. We constructed personalized models from this multimodal data with TVB by optimizing parameters on an individual basis that predict multiple empirical features in fMRI and EEG, e.g. dynamic functional connectivity and bimodality in the alpha band power. We annotated this large comprehensive empirical and simulated dataset according to the openMINDS metadata framework and structured it following Brain Imaging Data Structure (BIDS) standards for EEG and MRI as well as the BIDS Extension Proposal for computational modeling data. This dataset provides ready-to-use data for future research at various levels of processing including the thereof inferred brain simulation results for a large dataset of healthy subjects with a wide age range.

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Multiscale Detrended Cross-Correlation Coefficient: Estimating Coupling in Nonstationary Neurophysiological Signals

The brain consists of a vastly interconnected network of regions, the connectome. By estimating the statistical interdependence of neurophysiological time series, we can measure the functional connectivity (FC) of this connectome. Pearsons correlation (rP) is a common metric of coupling in FC studies. Yet rP does not account properly for the non-stationarity of the signals recorded in neuroimaging. In this study, we introduced a novel estimator of coupled dynamics termed multiscale detrended cross-correlation coefficient (MDC3). Firstly, we showed that MDC3 had higher accuracy compared to rP using simulated time series with known coupling, as well as simulated functional magnetic resonance imaging (fMRI) signals with known underlying structural connectivity. Next, we computed functional brain networks based on empirical magnetoencephalography (MEG) and fMRI. We found that by using MDC3 we could construct networks of healthy populations with significantly different properties compared to rP networks. Based on our results, we believe that MDC3 is a valid alternative to rP that should be incorporated in future FC studies. Author SummaryThe brain consists of a vastly interconnected network of regions. To estimate the connection strength of such networks the coupling between different brain regions should be calculated. This can be achieved by using a series of statistical methods that capture the connection strength between signals originating across the brain, one of them being Pearsons correlation (rP). Despite its benefits, rP is not suitable for realistic estimation of brain network architecture. In this study, we introduced a novel estimator called multiscale detrended cross-correlation coefficient (MDC3). Firstly, we showed that MDC3 was more accurate than rP using simulated signals with known connection strength, as well as simulated brain activity emerging from realistic brain simulations. Next, we constructed brain networks based on real-life brain activity, recorded using two different methodologies. We found that by using MDC3 we could construct networks of healthy populations with significantly different properties compared to rP networks. Based on our results, we believe that MDC3 is a valid alternative to rP that should be incorporated in future studies of brain networks.

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Whole-Brain Dynamics Disruptions in the Progression of Alzheimer's Disease: Understanding the Influence of Amyloid-Beta and Tau

Alzheimers disease (AD) progressively alters brain structure and function, yet the associated changes in large-scale brain network dynamics remain poorly understood. We applied the intrinsic ignition framework to resting-state functional MRI (rs-fMRI) data from AD patients, individuals with mild cognitive impairment (MCI), and cognitively healthy controls (HC) to elucidate how AD shapes intrinsic brain activity. We assessed node-metastability at the whole-brain level and in 7 canonical resting-state networks (RSNs). Our results revealed a progressive decline in dynamical complexity across the disease continuum. HC exhibited the highest node-metastability, whereas it was substantially reduced in MCI and AD patients. The cortical hierarchy of information processing was also disrupted, indicating that rich-club hubs may be selectively affected in AD progression. Furthermore, we used linear mixed-effects models to evaluate the influence of Amyloid-{beta} (A{beta}) and tau pathology on brain dynamics at both regional and whole-brain levels. We found significant associations between both protein burdens and alterations in node-metastability. Lastly, a machine learning classifier trained on brain dynamics, A{beta}, and tau burden features achieved high accuracy in discriminating between disease stages. Together, our findings highlight the progressive disruption of intrinsic ignition across whole-brain and RSNs in AD and support the use of node-metastability in conjunction with proteinopathy as a novel framework for tracking disease progression.

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Using an ODE model to separate Rest and Task signals in fMRI

Cortical activity results from the interplay between network-connected regions that integrate information and stimulus-driven processes originating from sensory motor networks responding to specific tasks. Separating the information due to each of these components has been challenging, and the relationship as measured by fMRI in each of these cases Rest (network) and Task (stimulus-driven) remains a significant open question in the study of large-scale brain dynamics. In this study, we develop a network ordinary differential equation (ODE) model using advanced system identification tools to analyze fMRI data from both rest and task conditions. We demonstrate that task-specific ODEs are essentially a subset of rest-specific ODEs across four different tasks from the Human Connectome Project. By assuming that task activity is a relative complement of rest activity, our model significantly improves predictions of reaction times on a trial-by-trial basis, leading to a 9 % increase in explanatory power (R2) across the 14 sub-tasks tested. We have additionally shown that these results hold for predicting missing trials and accuracy on a per individual basis as well as classifying Tasks trajectories or resulting dynamic Task functional connectivity. Our findings establish the principle of the Active Cortex Model, which posits that the cortex is always active and that Rest State encompasses all processes, while certain subsets of processes get elevated to perform specific task computations. Thus, this study is an important milestone in the development of the fMRI equation - to causally link large-scale brain activity, brain structural connectivity, and behavioral variables within a single framework.

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A multiscale closed-loop neurotoxicity model of Alzheimer's disease progression explains functional connectivity alterations

While the accumulation of amyloid-beta (A{beta}) and hyperphosphorylated-tau (hp-tau) as two classical histopathological biomarkers are crucial in Alzheimers disease (AD), their detailed interaction with the electrophysiological changes at the meso- and macroscale are not yet fully understood. We developed a mechanistic mequltiscale model of AD progression, linking proteinopathy to its effects on neural activity and vice-versa. We integrated a heterodimer model of prion-like protein propagation, and a network of Jansen-Rit electrical oscillators whose model parameters varied due to neurotoxicity. Changes in inhibition guided the electrophysiological alterations found in AD, and both A{beta} and hp-tau-related inhibition changes were able to produce similar effects independently. Additionally, we found a causal disconnection between cellular hyperactivity and interregional hypersynchrony. Finally, we demonstrated that early A{beta} and hp-tau depositions location determine the spatiotemporal profile of the proteinopathy. The presented model combines the molecular effects of bothA{beta} and hp-tau together with a mechanistic protein propagation model and network effects within a unique closed-loop model. This holds the potential to enlighten the interplay between AD mechanisms on various scales, aiming to develop and test novel hypotheses on the contribution of different AD-related variables to the disease evolution. Significance StatementThis research presents a groundbreaking closed-loop model of AD mechanisms, bridging the gap between protein distribution and neural activity. Contrary to prior assumptions, the study reveals that interregional hyper-synchrony and cellular hyperactivity are not directly linked. Notably, the model identifies neural inhibition as a potential causal factor in neurophysiological AD alterations and posits early depositions of A{beta} as a determinant of the spatiotemporal profile of proteinopathy. The significance of this mechanistic disease framework lies in its potential to produce insights into AD evolution and to guide novel treatment strategies. It underscores the importance of further experiments and modelling efforts to refine our understanding of AD, offering hope for more effective treatments and personalized care in the fight against dementia.

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