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Delev, D.

Publications and source records attributed to Delev, D..

12 recordsLinked to original sources

Graph theory for the analysis of micro-electrode array recordings of human brain slices - framework and benchmarking

Micro-electrode array (MEA) recordings are widely used to characterize functional connectivity in neural cultures and have gained traction for the analysis of human brain slices. However, the impact of graph construction methodology on the resulting network topology has not been systematically quantified. Here, we benchmark three methods - shared spiking activity, Pearson cross-correlation, and the spike time tiling coefficient (STTC) - across 37 recordings from human cortical slice cultures classified into low, moderate, and high activity groups. We show that method choice alone produces large topological differences (Cohens d = 0.86-1.14 for clustering coefficient, d > 1.0 for node count), while higher-order features such as modularity remain stable. Each method exhibits a distinct sensitivity profile: shared spiking detects activity-dependent changes primarily through network size, correlation uniquely captures clustering differences, and STTC combines strong biological sensitivity with negligible parameter dependence across lag windows (all d < 0.1). Within shared spiking, z-score normalization dominates all other parameter choices (d > 1.0 versus bin size effects of d < 0.23), functioning as an implicit analytical null model that fundamentally reshapes the edge set rather than merely rescaling weights. Inter-method edge overlap is low (Jaccard index 0.08-0.45) and activity dependent, demonstrating that these methods identify substantially different connections from identical data. Our results reveal that methodological choices including construction method, threshold, and normalization introduce hidden degrees of freedom with effect sizes comparable to the biological signals being measured. We provide practical recommendations for parameter selection, reporting, and cross-method validation in MEA-based network neuroscience. Author SummaryWhen we record electrical activity from brain tissue using grids of electrodes, we can ask how different sites influence one another and map the tissue as a network of connections. Thanks to novel culturing methods, this approach is increasingly used to study human brain slices. However, deciding what is "connected" is not well defined. Researchers use several different methods, and it has never been clear how much this choice shapes the network they end up describing. Here we compared three widely used methods on 37 recordings from human cortical slices spanning a range of activity levels. We found that the method alone can change the apparent structure of the network as much as real biological differences do. The methods frequently disagreed about which connections exist and some technical choices, including normalization techniques, had surprisingly large effects. Because these hidden choices can rival the biological signal, we provide this benchmarking work with practical recommendations for selecting, reporting, and cross-checking methods, so that network studies of brain tissue become more transparent, comparable, and reproducible.

neuroscience↗

The Mechanical Fingerprint of Hippocampal Sclerosis Linking Neuronal Cell Loss and Gliosis to Tissue Stiffness

Hippocampal sclerosis (HS) is the most common pathology in drug-resistant temporal lobe epilepsy (TLE). However, clinical diagnosis, prevalent epileptogenicity, and drug drug-resistance in individuals with HS remain an ongoing challenge demanding multidisciplinary research efforts. In this study, we examined the mechanical properties of neurosurgically en bloc resected HS specimens (n=8) ex vivo under compression, tension, and torsional shear. We fitted a two-term Ogden hyperelastic model to the measured mechanical responses to quantify nonlinear mechanical tissue properties. The resulting parameters revealed higher strain stiffening under compression in HS compared to hippocampus obtained post mortem (n=7). The distinction was most noticeable in the large-strain regime, which has important implications for using mechanical tissue properties as valuable diagnostic biomarker. Furthermore, we correlated the tissue microstructure with mechanical parameters. We trained a deep-learning histopathology classifier to detect and classify neurons and glial cells from hematoxylin-stained whole slide images (WSI). We identified a strong association between the small-strain stiffness (shear modulus {micro}) and the overall cell density as well as the glial cell density. The negative relationship between the neuron-to-glia ratio and shear modulus is consistent with the hypothesis that neuronal cell loss and gliosis drives tissue stiffening, respectively. Magnetic resonance imaging (MRI) analysis of the specimens confirmed the previously reported negative association between MRI-derived fractional anisotropy and shear modulus {micro}. Taken together, our study establishes a direct link between tissue mechanics and microstructure, suggesting nonlinear continuum mechanics models as promising new tools for clinical diagnosis and novel research strategies.

bioengineering↗

Neuronal precursor cell persistence in Ganglioglioma is associated with ECM remodeling and immune cell infiltration

BackgroundGangliogliomas (GGs) are low-grade glioneuronal tumors that frequently present with drug-resistant epilepsy. Although their indolent course contrasts with their high epileptogenic potential, the oncogenic mechanisms sustaining neuronal precursor-like populations within the tumor microenvironment remain poorly defined. MethodsWe performed spatial transcriptomic profiling on eight histologically confirmed GGs and matched healthy cortex to map the cellular and molecular architecture of the tumor microenvironment. Integrated analysis with weighted gene correlation network analysis (WGCNA) defined recurrent oncogenic programs and spatially resolved tumor-stroma interactions. ResultsEight conserved gene modules emerged, encompassing physiological cortical, reactive glial, and oncopathological programs. The latter captured extracellular matrix (ECM) remodeling, vascular-immune signaling, and persistence of immature, proliferative neuronal-like states. Spatial modeling revealed that these oncopathological programs form structured niches at the tumor-brain interface, where radial glia-derived neuronal-like tumor cells coexist with immune and stromal elements engaged in ECM turnover and cytokine signaling. ConclusionsGanglioglioma represents a hybrid glioneuronal neoplasm in which developmental neuronal programs are co-opted by tumor-associated stromal and immune cues. This convergence establishes a permissive oncogenic niche that sustains precursor-like tumor cells and provides a mechanistic basis for both the tumors benign growth and its intrinsic epileptogenicity. Key PointsO_LISpatial transcriptomics identifies reproducible transcriptional programs that define the ganglioglioma microenvironment. C_LIO_LITumor-associated regions show transcriptional programs consistent with immature neuronal states together with ECM remodelling and immune activity. C_LIO_LISingle-cell reference data indicate that immature neuronal programs in ganglioglioma resemble radial glia-derived developmental states. C_LI Importance of the StudyGanglioglioma is a low-grade glioneuronal tumor that combines benign growth with pronounced epileptogenicity, yet the molecular basis of this dual behavior remains poorly understood. Through spatial transcriptomics integrated with single-cell analysis, we reveal that ganglioglioma architecture is defined by two interacting transcriptional axes: a residual glioneuronal network and a tumoral niche enriched for extracellular-matrix, vascular, and immune programs. Within these niches, immature neuronal-like tumor cells persist in a developmentally arrested state maintained by ECM-immune signaling. This spatially organized interplay between physiological and pathological programs explains both the low oncologic aggressiveness and high excitability of these lesions. Our findings provide molecular signatures that may refine diagnostic classification within the LEAT spectrum, delineate epileptogenic zones, and identify candidate pathways for therapeutic modulation of the ganglioglioma microenvironment.

neuroscience↗

Comprehensive Analysis of Human Dendritic Spine Morphology and Density: Exploring Diversity of Human Dendritic Spines

Dendritic spines, small protrusions on neuronal dendrites, play a crucial role in brain function by changing shape and size in response to neural activity. So far, in depth analysis of dendritic spines in human brain tissue is lacking. This study presents a comprehensive analysis of human dendritic spine morphology and density using a unique dataset from human brain tissue from 27 patients (8 females, 19 males, aged 18-71) undergoing tumor or epilepsy surgery at three neurosurgery sites. We used acute slices and organotypic brain slice cultures to examine dendritic spines, classifying them into the three main morphological subtypes: Mushroom, Thin, and Stubby, via 3D reconstruction using ZEISS arivis Pro software. A deep learning model, trained on 39 diverse datasets, automated spine segmentation and 3D reconstruction, achieving a 74% F1-score and reducing processing time by over 50%. We show significant differences in spine density by sex, dendrite type, and tissue condition. Females had higher spine densities than males, and apical dendrites were denser in spines than basal ones. Acute tissue showed higher spine densities compared to cultured human brain tissue. With time in culture, Mushroom spines decreased, while Stubby and Thin spine percentages increased, particularly from 7-9 to 14 days in vitro, reflecting potential synaptic plasticity changes. Our study underscores the importance of using human brain tissue to understand unique synaptic properties and shows that integrating deep learning with traditional methods enables efficient large-scale analysis, revealing key insights into sex- and tissue-specific dendritic spine dynamics relevant to neurological diseases. New and NoteworthyThis study presents a dataset of nearly 4,000 morphologically reconstructed human dendritic spines across different ages, gender, and tissue conditions. The dataset was further used to evaluate a deep learning algorithm for three-dimensional spine reconstruction, offering a scalable method for semi-automated spine analysis across various tissues and microscopy setups. The findings enhance understanding of human neurology, indicating potential connections between spine morphology, brain function, and the mechanisms of neurological and psychiatric diseases.

neuroscience↗

Transport-Related Effects on Intrinsic and Synaptic Properties of Human Cortical Neurons: A Comparative Study

Transporting human brain tissue from the operating theater to an off-site laboratory may affect sample integrity for electrophysiological studies. This study investigated how a 30-40 minute transport influenced the intrinsic, synaptic, and morphological properties of human cortical neurons. Electrophysiological recordings were performed on Layer 2/3 (L2/3 pyramidal cells and fast-spiking (FS) interneurons from human cortical slices (n = 200 neurons from 32 surgeries), comparing on-site recordings at RWTH Aachen University Hospital and off-site at Research Centre Juelich. Action potential firing patterns remained largely preserved across both recording sites, but several differences were observed. Off-site recorded pyramidal cells showed a slightly depolarized resting membrane potential and a significantly lower rheobase current. In off-site recorded FS interneurons, we found a narrower action potential half-width and an increased amplitude, suggesting altered ion channel kinetics and/or neuromodulatory environment. Additionally, a significant reduction in large rhythmic depolarizations (LRDs) and the amplitudes of excitatory postsynaptic potentials (EPSPs) in off-site recorded FS interneurons indicated an impaired synaptic efficacy. The dendritic spine densities in apical oblique and apical tuft dendrites of off-site recorded pyramidal cells were also reduced. These findings emphasize the need for optimized transport conditions to preserve synaptic integrity, network properties, and neuronal morphology. Standardized protocols are crucial for ensuring reliable and reproducible results in studies of human cortical microcircuits. Significance StatementThis study demonstrates that transporting live human brain tissue for neuronal recordings significantly impacts the intrinsic, synaptic, and network properties of cortical neurons. By comparing on-site and off-site recordings, we found that even a brief transportation (30-40 minutes) induces increased neuronal excitability, reduced synaptic efficacy, and diminished network events such as LRDs. These alterations are likely due to the mechanical stress and washout of critical neuromodulators, which compromise tissue integrity and neuronal function. The findings underscore the necessity for optimizing transport protocols to preserve synaptic and network integrity, ensuring reliable and reproducible results in human brain research. Ultimately, this work advances our understanding of cortical microcircuitry and informs best practices for handling human brain tissue in experimental settings.

neuroscience↗

Linking Altered Neuronal and Synaptic Properties to Nicotinic Receptor Alpha5 Subunit Gene Dysfunction: A Translational Investigation in Rat mPFC and Human Cortical Layer 6

BackgroundGenetic variation in the 5 nicotinic acetylcholine receptor (nAChR) subunit of mice results in behavioral deficits linked to the prefrontal cortex (PFC). A Single Nucleotide Polymorphisms (SNP) in CHRNA5 imparts a partial loss of function to the 5 subunit-containing (5*) nAChRs and have been demonstrated to be associated with psychiatric disorders in humans, including schizophrenia, nicotine dependence, cocaine and alcohol addiction. MethodsWe performed single cell-electrophysiology combined with morphological reconstructions on layer 6 (L6) excitatory neurons in the medial PFC (mPFC) of wild type (WT) rats (n = 25), rats carrying the human coding polymorphism rs16969968 in Chrna5 (n = 11) and 5 knockout (KO) rats (n = 28). Neuronal and synaptic properties were compared among three rat genotypes. Galantamine was applied to identified L6 neuron populations to specifically boost the nicotinic responses mediated by 5*nAChRs in the rat mPFC and human neocortex (n = 6 patients). ResultsCompared with neurons in WT rats, L6 regular spiking (RS) neurons in the 5KO group exhibited altered electrophysiological properties, while those in 5SNP rats remained unchanged. L6 RS neurons in mPFC of 5SNP and 5KO rats differed from WT rats in dendritic morphology, spine density and spontaneous synaptic activity. Galantamine acted as a positive allosteric modulator of 5*nAChRs in RS but not burst spiking (BS) neurons in both rat and human cortical L6. ConclusionOur findings suggest that dysfunction in the 5 subunit gene leads to aberrant neuronal and synaptic properties, shedding light on the underlying mechanisms of cognitive deficits observed in human populations carrying 5SNPs. They highlight a potential pharmacological target for restoring the relevant behavioral output.

neuroscience↗

Long-term human organotypic brain slice cultures: a detailed protocol to provide a comprehensive framework for single-neuron and neuronal network investigations

BackgroundThe investigation of the human brain at cellular and microcircuit level remains challenging due to the fragile viability of neuronal tissue, inter- and intra-variability of the samples and limited availability of human brain material. New methodHere, we present an optimized work-up to use resected tissue from brain surgeries for live cell experiments in vitro. Comparison with existing methodsWe provide a reworked, detailed protocol of the production, culturing and viral transduction of human organotypic brain slice cultures for research purposes. ResultsWe highlight the critical pitfalls of the culturing process of the human brain tissue and present results on viral expression, single-cell Patch-Clamp recordings, as well as multi-electrode array recordings over a prolonged period of time. Additionally, our statistics show that brain tissue from patients of any age and morbidity can be used for organotypic brain slice cultures if carefully selected. ConclusionsOrganotypic brain slice cultures are of great value for basic neuroscience and disease modeling over a time course of three weeks. HighlightsO_LILong-term human organotypic brain slice cultures are viable for 2-3 weeks and provide a framework for basic neuroscience and disease modeling C_LIO_LIWe provide a reworked, detailed protocol for organotypic human brain slice culture production and maintenance C_LIO_LIWe show results of long-term culturing of human organotypic brain slice cultures in terms of viral transduction, whole-cell Patch-Clamp recordings and multi-electrode array recordings C_LIO_LIStatistics of 16 surgeries show the correlation between the overall success rates of efficient culturing and viral transduction with the patient age and morbidity C_LI O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=139 SRC="FIGDIR/small/561508v1_fig1.gif" ALT="Figure 1"> View larger version (28K): org.highwire.dtl.DTLVardef@17c985aorg.highwire.dtl.DTLVardef@f651fdorg.highwire.dtl.DTLVardef@180d32eorg.highwire.dtl.DTLVardef@a896b5_HPS_FORMAT_FIGEXP M_FIG O_FLOATNOFigure 1, Graphical abstract.C_FLOATNO Schematic overview of preparation, maintenance and experimental workup of human organotypic brain slice cultures. After surgical resection, human brain tissue is prepared, sliced and cultured at air-liquid-interface between human cerebrospinal fluid and defined incubator atmosphere, allowing for week-long viability. This enables extensive experimental workup such as viral transduction, single cell and multi-electrode array electrophysiological recordings. C_FIG

neuroscience↗

Epigenetic neural glioblastoma enhances synaptic integration and predicts therapeutic vulnerability

Neural-tumor interactions drive glioma growth as evidenced in preclinical models, but clinical validation is nascent. We present an epigenetically defined neural signature of glioblastoma that independently affects patients survival. We use reference signatures of neural cells to deconvolve tumor DNA and classify samples into low- or high-neural tumors. High-neural glioblastomas exhibit hypomethylated CpG sites and upregulation of genes associated with synaptic integration. Single-cell transcriptomic analysis reveals high abundance of stem cell-like malignant cells classified as oligodendrocyte precursor and neural precursor cell-like in high-neural glioblastoma. High-neural glioblastoma cells engender neuron-to-glioma synapse formation in vitro and in vivo and show an unfavorable survival after xenografting. In patients, a high-neural signature associates with decreased survival as well as increased functional connectivity and can be detected via DNA analytes and brain-derived neurotrophic factor in plasma. Our study presents an epigenetically defined malignant neural signature in high-grade gliomas that is prognostically relevant.

neuroscience↗

Modulation of Giant Depolarizing Potentials (GDPs) in Human Large Basket Cells by Norepinephrine and Acetylcholine

Rhythmic brain activity has been implicated in many brain functions and it is sensible to neuromodulation, but so far very few studies have investigated this activity on the cellular level in vitro in human tissue samples. In this study we revealed and characterized a novel rhythmic network activity in human neocortex. Intracellular patch-clamp recordings showed that giant depolarizing potentials (GDPs) were frequently found in human cortical neurons. GDPs appeared in a low frequency band ([~] 0.3 Hz) similar to that described for slow oscillations in vivo and displayed large amplitudes and long decay times. Under the same experimental conditions, no rhythmic activity was found in L2/3 of the rat neocortex. GDPs were predominantly observed in a subset of L2/3 interneurons considered to be large basket cells based on previously described morphological features. In addition, GDPs are highly sensitive to norepinephrine (NE) and acetylcholine (ACh), two neuromodulators known to modulate low frequency oscillations. NE increased the frequency of the GDPs by enhancing {beta}-adrenergic receptor activity while ACh decreased GDP frequency through M4 muscarinic receptor-activation. Multi-electrode array (MEA) recordings demonstrated that NE promoted synchronous oscillatory network activity while the application of ACh led to a desynchronization of neuronal activity. Our data indicate that the human neocortex is more prone to generate slow wave activity, which was reflected by more pronounced GDPs in L2/3 large basket cells. The distinct modulation of GDPs and slow wave activity by NE and ACh exerts a specific modulatory control over the human neocortex.

neuroscience↗

Spatiotemporal heterogeneity of glioblastoma is dictated by microenvironmental interference

Glioblastomas are highly malignant tumors of the central nervous system. Evidence suggests that these tumors display large intra- and inter-patient heterogeneity hallmarked by subclonal diversity and dynamic adaptation amid developmental hierarchies1-3. However, the source for dynamic reorganization of cellular states within their spatial context remains elusive. Here, we in-depth characterized glioblastomas by spatially resolved transcriptomics, metabolomics and proteomics. By deciphering exclusive and shared transcriptional programs across patients, we inferred that glioblastomas develop along defined neural lineages and adapt to inflammatory or metabolic stimuli reminiscent of reactive transformation in mature astrocytes. Metabolic profiling and imaging mass cytometry supported the assumption that tumor heterogeneity is dictated by microenvironmental alterations. Analysis of copy number variation (CNV) revealed a spatially cohesive organization of subclones associated with reactive transcriptional programs, confirming that environmental stress gives rise to selection pressure. Deconvolution of age-dependent transcriptional programs in malignant and non-malignant specimens identified the aging environment as the major driver of inflammatory transformation in GBM, suggesting that tumor cells adopt transcriptional programs similar to inflammatory transformation in astrocytes. Glioblastoma stem cells implanted into human neocortical slices of varying age levels, independently confirmed that the ageing environment dynamically shapes the intratumoral heterogeneity towards reactive transcriptional programs. Our findings provide insights into the spatial architecture of glioblastoma, suggesting that both locally inherent tumor as well as global alterations of the tumor microenvironment shape its transcriptional heterogeneity. Global age-related inflammation in the human brain is driving distinct transcriptional transformation in glioblastomas, which requires an adjustment of the currently prevailing glioma models.

cancer biology↗

Inferring spatially transient gene expression pattern from spatial transcriptomic studies

Spatial transcriptomic is a technology to provide deep transcriptomic profiling by preserving the spatial organization. Here, we present a framework for SPAtial Transcriptomic Analysis (SPATA, https://themilolab.github.io/SPATA), to provide a comprehensive characterization of spatially resolved gene expression, regional adaptation of transcriptional programs and transient dynamics along spatial trajectories.

bioinformatics↗

Lineage and Spatial Mapping of Glioblastoma-associated Immunity

The diversity of molecular states and cellular plasticity of immune cells in the glioblastoma environment is still poorly understood. Here, we performed scRNA sequencing of the immune compartment and mapped potential cellular interactions leading to an immunosuppressive microenvironment and dysfunction of T cells. Through inferring the dynamic adaptation during T cell activation, we identified three different terminal states with unique transcriptional programs. Modeling of driver genes for terminal T cell fate identified IL-10 signaling alterations in a subpopulation of HAVCR2(+) T cells. To explore in depth cellular interactions, we established an in-silico model by the integration of spatial transcriptomic and scRNA-sequencing, and identified a subset of HMOX1+ myeloid cells defined by IL10 release leading to T cell exhaustion. We found a spatial overlap between HMOX(+) myeloid and HAVCR2(+) T cells, suggesting that myeloid-lymphoid interaction causes immunosuppression present in tumor regions with enriched mesenchymal gene expression. Using human neocortical GBM model, coupled with patient-derived T cells, we confirmed that the functional interaction between myeloid and lymphoid cells, leads to a dysfunctional state of T cells. This IL-10 driven T cell exhaustion was found to be rescued by JAK/STAT inhibition. A comprehensive understanding of the cellular states and plasticity of lymphoid cells in GBM will aid towards successful immunotherapeutic approaches.

cancer biology↗