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Benali, H.

Publications and source records attributed to Benali, H..

8 recordsLinked to original sources

Sleep Spindle-Locked Targeted Memory Reactivation Enhances Declarative Memory Consolidation

Study ObjectivesSleep spindles are implicated in memory consolidation. Yet direct evidence linking spindle dynamics to declarative memory outcomes remains limited. We thus tested whether targeted memory reactivation (TMR) time-locked to sleep spindles enhances declarative memory, and whether the temporal organization of stimulated spindles-trains versus isolated events-is selectively associated with distinct memory outcomes. MethodsTwenty-eight healthy young adults learned image locations from two categories (animals, clothing) in a grid, each paired with a distinct auditory cue. During overnight NREM sleep, one cue was replayed time-locked to spindles detected in real-time using a closed-loop system (TMR condition); the other served as the non-reactivated control (No-TMR condition). Category-cue assignment was counterbalanced. Post-sleep recall, recognition accuracy, and movement time were assessed. ResultsRecall accuracy was significantly higher in the TMR than the No-TMR condition (93.96% vs. 90.61%, p = .024), whereas recognition accuracy (p = .139) and movement time (p = .651) did not differ. Stimulation intensity within spindle trains correlated with the TMR effect on recall (Spearman {rho} = .531, p = .004), whereas the proportion of isolated spindle stimulations correlated with the TMR effect on recognition ({rho} = .563, p = .002). Cross-associations were not significant. ConclusionsSpindle-locked TMR enhances recall-based declarative memory retention. The selective association between spindle temporal clustering and memory outcomes suggests that train-embedded and isolated spindles support different aspects of memory consolidation, highlighting spindle temporal context as a functionally relevant dimension of sleep-dependent memory processing.

neuroscience↗

Parameter Dependence in Identifiability Applied to FP-Fisher-KPP Reaction-Diffusion Equations Parameterized for Tauopathy Network Modeling

Parameterization and a priori identifiability analysis are two interconnected steps that should be carried out in advance of model calibration. In the first place, we propose a framework for parameterizing a recently introduced and analytically studied generalization of the celebrated Fisher-Kolmogorov-Petrovsky-Piskunov (Fisher-KPP) reaction-diffusion (Re-Di) equation with fractional polynomial (FP) terms to model heterogeneous nonlinear diffusion in the propagation of a given species through directed networks, exemplified by the tauopathy progression in Alzheimers disease (AD). Next, we present our results on identifiability in a generic sense for the parameterized FP-Fisher-KPP Re-Di equations with regular multi-experimental designs, seamlessly applicable to meromorphic systems, encompassing analytic systems. In particular, the concept of generic local minimal dependence of unknown parameters and regularly parameterized initial conditions will be formalized through the use of one-parameter Lie groups of transformations, and a decomposition method to explore this new concept will be devised. Finally, the Allen Mouse Brain Connectivity Atlas (AMBCA) dataset is utilized to develop a model for tauopathy progression in the mouse brain, which will subsequently be employed to implement the proposed methodology for analyzing a priori identifiability.

systems biology↗

Protocol for simultaneous evaluation of neuronal activity and neurotransmitter release following chronic amyloid-beta oligomer injections into the hippocampus

In Alzheimers disease, there is an imbalance in neurotransmitter release and altered neuronal activation. We present a novel approach to analyze neuronal activity by combining local field potential (LFP) recording with microdialysis within the same animal. This method measures glutamate and GABA levels following chronic hippocampal amyloid-beta oligomer (A{beta}o) injections in rats. We outline the design of our electrode and canula, the surgical procedure, and the steps for LFP recording, interstitial fluid collection, and A{beta}o injections simultaneously in living animal. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=182 HEIGHT=200 SRC="FIGDIR/small/614333v2_ufig1.gif" ALT="Figure 1"> View larger version (37K): org.highwire.dtl.DTLVardef@155f3c0org.highwire.dtl.DTLVardef@1f60289org.highwire.dtl.DTLVardef@207ba2org.highwire.dtl.DTLVardef@94eeb3_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

NREM sleep brain networks modulate cognitive recovery from sleep deprivation

Decrease in cognitive performance after sleep deprivation and its recovery following sleep suggests the key role of sleep, especially non-rapid eye movement (NREM) sleep, in maintaining cognition. It remains unknown whether brain network reorganization in NREM sleep stages N2 and N3 can uniquely be mapped onto individual differences in cognitive performance after a recovery nap following sleep deprivation. Using resting state functional magnetic resonance imaging (fMRI), we quantified the integration and segregation of brain networks during N2 and N3 sleep in a 1-hour nap following 24-hour sleep deprivation, compared to well-rested wakefulness. Here, we introduce a new analytic framework called the hierarchical segregation index (HSI) to quantify network segregation across spatial scales, from whole-brain to the voxel level, by identifying spatio-temporally overlapping large-scale networks and the corresponding voxel-to-region hierarchy. We found that network segregation increased in the posterior cingulate cortex during both N2 and N3 sleep compared to wakefulness. In contrast, increased segregation in the visual cortex and decreased segregation in the posterior ventromedial prefrontal cortex during N2 returned to levels comparable to wakefulness during N3. More segregation during N3 sleep was associated with worse recovery of working memory, executive attention, and psychomotor vigilance after the nap. Sleep-related changes in network segregation emerged at different spatial scales, with regional- and voxel-level alterations being associated with different cognitive tasks. Finally, we demonstrated the sensitivity and reliability of voxel-level HSI to provide key insights into within-region variation, suggesting a mechanistic understanding of how NREM sleep replenishes cognition after sleep deprivation.

neuroscience↗

Extended fractional-polynomial generalizations of diffusion and Fisher-KPP equations on directed networks: Modeling neurodegenerative progression

In a variety of practical applications, there is a need to investigate diffusion or reaction-diffusion processes on complex structures, including brain networks, that can be modeled as weighted undirected and directed graphs. As an instance, the celebrated Fisher-Kolmogorov-Petrovsky-Piskunov (Fisher-KPP) reaction-diffusion equation are becoming increasingly popular for use in graph frameworks by substituting the standard graph Laplacian operator for the continuous one to study the progression of neurodegenerative diseases such as tauopathies including Alzheimers disease (AD). However, due to the porous structure of neuronal fibers, the spreading of toxic species can be governed by an anomalous diffusion process rather than a normal one, and if this is the case, the standard graph Laplacian cannot adequately describe the dynamics of the spreading process. To capture such more complicated dynamics, we propose a diffusion equation with a nonlinear Laplacian operator and a generalization of the Fisher-KPP reaction-diffusion equation on undirected and directed networks using extensions of fractional polynomial (FP) functions. A complete analysis is also provided for the extended FP diffusion equation, including existence, uniqueness, and convergence of solutions, as well as stability of equilibria. Moreover, for the extended FP Fisher-KPP reaction-diffusion equation, we derive a family of positively invariant sets allowing us to establish existence, uniqueness, and boundedness of solutions. Finally, we conclude by investigating nonlinear diffusion on a directed one-dimensional lattice and then modeling tauopathy progression in the mouse brain to gain a deeper understanding of the potential applications of the proposed extended FP equations.

systems biology↗

Hierarchical Bayesian Modeling of the Relationship between Task Related Hemodynamic Responses and Neuronal Excitability: a Simultaneous fNIRS/TMS Study

BackgroundInvestigating the relationship between task-related hemodynamic responses and cortical excitability is challenging because it requires simultaneous measurement of hemodynamic responses while applying non-invasive brain stimulation. Moreover, cortical excitability and task-related hemodynamic responses are both associated with inter-/intra-subject variability. To reliably assess such a relationship, we applied hierarchical Bayesian modeling. MethodsThis study involved 16 healthy subjects who underwent simultaneous Paired Associative Stimulation (PAS10, PAS25, Sham) while monitoring brain activity using functional Near-Infrared Spectroscopy (fNIRS), targeting the primary motor cortex (M1). Cortical excitability was measured by Motor Evoked Potentials (MEPs), and the motor task-related hemodynamic responses were measured using fNIRS 3D reconstructions. We constructed three models to investigate: 1) PAS effects on the M1 excitability; 2) PAS effects on fNIRS hemodynamic responses to a finger tapping task, and 3) the correlation between PAS effects on M1 excitability and PAS effects on task-related hemodynamic responses. ResultsSignificant increase in cortical excitability was found following PAS25, whereas a small reduction of the cortical excitability was shown after PAS10 and a subtle increase occurred after sham. Both HbO and HbR absolute amplitudes increased after PAS25 and decreased after PAS10. The probability of the positive correlation between modulation of cortical excitability and hemodynamic activity was 0.77 for HbO and 0.79 for HbR. ConclusionWe demonstrated that PAS stimulation modulates task-related cortical hemodynamic responses in addition to M1 excitability. Moreover, the positive correlation between PAS modulations of excitability and hemodynamics brought insight into understanding the fundamental properties of cortical function and cortical excitability.

neuroscience↗

Altered functional integration of brain activity is a marker of impaired cognitive performance following sleep deprivation

Sleep deprivation (SD) leads to impairments in cognitive function. Here, we tested the hypothesis that cognitive changes in the sleep-deprived brain can be explained by information processing within and between large-scale cortical networks. We acquired functional magnetic resonance imaging (fMRI) scans of 20 healthy volunteers during attention and executive tasks following a regular night of sleep, a night of sleep deprivation, and a recovery nap containing non-rapid eye movement (NREM) sleep. Overall, sleep deprivation was associated with increased cortex-wide functional integration, driven by a rise of integration within cortical networks. The ratio of within vs between network integration in the cortex increased further in the recovery nap, suggesting that prolonged wakefulness drives the cortex toward a state resembling sleep. This balance of integration and segregation in the sleep-deprived state was tightly associated with deficits in cognitive performance. This was a distinct and better marker of cognitive impairment than conventional indicators of homeostatic sleep pressure, as well as the pronounced thalamo-cortical connectivity changes that occurs towards falling asleep. Importantly, restoration of the balance between segregation and integration of cortical activity was also related to performance recovery after the nap, demonstrating a bi-directional effect. These results demonstrate that intra- and inter-individual differences in cortical network integration and segregation during task performance may play a critical role in vulnerability to cognitive impairment in the sleep deprived state. Significance StatementSleep deprivation has significant negative consequences for cognitive function. Understanding how changes in brain activity underpin changes in cognition is important not only to discover why performance declines following extended periods of wakefulness, but also for answering the fundamental question of why we require regular and recurrent sleep for optimal performance. Finding neural correlates that predict performance following sleep deprivation also has the potential to understand which individuals are particularly vulnerable to sleep deprivation, and what aspects of brain function may protect them from these negative consequences on performance. Finally, understanding how perturbations to regular (well-rested) brain functioning affect cognitive performance, will provide important insight into how underlying principles of information processing in the brain may support cognition generally.

neuroscience↗

Consolidation alters motor sequence-specific distributed representations

FMRI studies investigating the acquisition of sequential motor skills in humans have revealed learning-related functional reorganizations of the cortico-striatal and cortico-cerebellar motor systems in link with the hippocampus. Yet, the functional significance of these activity level changes is not fully understood as they convey the evolution of both sequence-specific knowledge and unspecific task expertise. Moreover, these changes do not specifically assess the occurrence of learning-related plasticity. To address these issues, we investigated local circuits tuning to sequence-specific information using multivariate distances between patterns evoked by consolidated or newly acquired motor sequences production. Results reveal that representations in dorsolateral striatum, prefrontal and secondary motor cortices are greater when executing consolidated sequences than untrained ones. By contrast, sequence representations in the hippocampus and dorsomedial striatum are less engaged. Our findings show, for the first time in humans, that complementary sequence-specific motor representations evolve distinctively during critical phases of skill acquisition and consolidation.

neuroscience↗