FIRES is a rare and ferocious epileptic encephalopathy that typically announces itself in a previously healthy child. After an ordinary febrile infection, often nothing more sinister than a fever, the child plunges into超 refractory status epilepticus, a prolonged convulsive storm that resists conventional anti-seizure drugs. The syndrome is classified as a subtype of new-onset refractory status epilepticus, or NORSE, and its underlying etiology remains stubbornly unknown. Survivors of the acute phase frequently emerge into a chronic phase marked by drug-resistant epilepsy, cognitive impairment, and profound disability. The condition’s trajectory is so bleak that neurologists have long searched for anything that might bend its course, and growing evidence implicates a runaway neuroinflammatory process, with elevated cytokines detected in the cerebrospinal fluid of affected children.

Among the inflammatory messengers implicated in that storm, interleukin-6 has attracted particular attention. Laboratory and clinical studies have linked higher interleukin-6 signaling to seizure generation and to worse outcomes in NORSE, making the cytokine pathway a logical therapeutic target. Tocilizumab, a monoclonal antibody that binds the interleukin-6 receptor and prevents the cytokine from delivering its signal, is already approved for rheumatoid arthritis and other inflammatory conditions, and international consensus recommendations have endorsed it as an anti-inflammatory option during the acute phase of FIRES. What has been far less clear is whether the drug helps after the acute storm has passed and the child has settled into the chronic, seizure-burdened phase of the illness, when the window for rescuing the brain may seem to have closed.

To answer that question, the Beijing team assembled a retrospective cohort of twenty-seven pediatric patients with chronic-phase FIRES who received tocilizumab. These were children whose epilepsy had already become entrenched: the median duration of seizures at the time the first dose was given was sixteen months, with an interquartile range spanning six to thirty-four months. Over the course of treatment, each patient received a median of four doses of the drug, with a range of three to six. The investigators defined the primary outcome as the response rate at sixteen weeks after initiation, counting as responders those patients whose seizure frequency fell by at least fifty percent. Secondary outcomes included the response rate at twenty-eight weeks, changes in disability measured by the modified Rankin Scale, and treatment-related adverse events.

The results were striking for a syndrome with so few options. After sixteen weeks of tocilizumab, seventeen of the twenty-seven children, or 63 percent, had achieved at least a fifty percent reduction in seizure frequency, and two children, 7.4 percent, became entirely seizure free. Beyond seizure counts, the therapy appeared to change daily life: nineteen of twenty-seven patients, 70.4 percent, showed improvements in their modified Rankin Scale scores, a measure of functional disability. Perhaps equally telling, 81.5 percent of the children, twenty-two of twenty-seven, did not require any additional anti-seizure medications during the entire treatment period, suggesting that the drug’s benefit was not simply an artifact of polytherapy escalation. The benefits, however, were not uniformly durable. By twenty-eight weeks, the response rate had slipped to 48.1 percent, with thirteen of twenty-seven children still maintaining at least a halving of their seizures.

Safety data provided cautious reassurance. The most common adverse event was neutropenia, a depletion of a key class of infection-fighting white blood cells, which occurred in nine patients, or 33.3 percent of the cohort. Infections developed in four patients, 14.8 percent. Neither finding is surprising for a drug that deliberately dampens immune signaling, and both are manageable with monitoring, dose adjustment, and vigilance for early signs of infection. For families weighing the risks of a therapy against the relentless toll of uncontrolled seizures, the profile described in the study suggests that tocilizumab occupies a tolerable middle ground: powerful enough to matter, but not so hazardous that it cannot be given to children over repeated doses.

The study’s authors conclude that tocilizumab is effective in treating the epilepsy of chronic-phase FIRES, reducing seizure frequency in pediatric patients while remaining relatively safe. That conclusion carries weight beyond the twenty-seven patients enrolled. Because FIRES is so rare, randomized controlled trials are extraordinarily difficult to mount, and the field has advanced largely through case reports, small series, and expert consensus. A structured cohort study with predefined endpoints, quantified response rates, functional outcome measures, and systematic adverse-event tracking moves the evidence base a meaningful step forward. It also extends the therapeutic logic of the syndrome itself: if neuroinflammation ignites the acute catastrophe, the same inflammatory circuitry may continue to fuel seizures in the chronic phase, and blocking it can still yield clinical gains even after months of drug resistance.

The road ahead nevertheless demands caution. The study is retrospective, without a randomized control group, so spontaneous fluctuations in seizure burden or concurrent treatment changes cannot be fully excluded as contributors to improvement. The tapering of benefit between sixteen and twenty-eight weeks raises practical questions about dosing intervals, treatment duration, and whether maintenance strategies might consolidate early gains. Identifying which children are most likely to respond, perhaps through cytokine profiling or genetic markers, remains an open frontier. Larger, ideally prospective, multi-center studies will be needed to confirm the findings and to establish where tocilizumab belongs in the treatment algorithm relative to other immunotherapies such as anakinra, which blocks the related interleukin-1 pathway and has also shown promise in chronic-phase FIRES.

For now, the message for clinicians and families is one of tempered optimism. A child with chronic-phase FIRES who has endured more than a year of drug-resistant seizures may still respond to targeted immunotherapy, with nearly two-thirds of treated children in this cohort halving their seizure burden and most improving in functional status. In a field where therapeutic victories are measured in fewer seizures rather than cures, that is no small thing. The Beijing study gives neurologists a firmer evidence platform to offer tocilizumab earlier in the chronic phase, and it hands researchers a clear mandate: define the biology of interleukin-6 signaling in these young brains, and design the trials that will determine how long the benefit lasts.

Subject of Research: Efficacy and safety of tocilizumab, an interleukin-6 receptor antagonist, in treating chronic-phase febrile infection-related epilepsy syndrome in children

Article Title: Efficacy and safety of tocilizumab in the chronic phase of febrile infection-related epilepsy syndrome: a retrospective cohort study

Article References: Liu, W., Zhang, J., Deng, J., Yang, X.-L., Dong, H., Wu, Y., Sang, T., Ji, T.-Y., Zhu, Y., Jiang, Y.-W., & Wu, Y. (2026). Efficacy and safety of tocilizumab in the chronic phase of febrile infection-related epilepsy syndrome: a retrospective cohort study. World Journal of Pediatrics. https://doi.org/10.1007/s12519-026-01065-y

Image Credits: AI Generated

DOI: 10.1007/s12519-026-01065-y

Keywords: tocilizumab, FIRES, febrile infection-related epilepsy syndrome, new-onset refractory status epilepticus, interleukin-6 receptor, pediatric epilepsy, neuroinflammation, immunotherapy, seizure frequency, modified Rankin Scale, retrospective cohort study, World Journal of Pediatrics

The research, conducted by Noureldeen et al., embarks on a meticulous exploration of the cardiac function in children with drug-resistant epilepsy, a subgroup historically notorious for its complex management challenges. While epilepsy’s neurological manifestations are well-documented, this study pioneers focus on the subtle cardiovascular alterations that evade detection by traditional diagnostic tools. By harnessing the sophisticated imaging modality of speckle-tracking echocardiography, the authors have unveiled nuanced myocardial mechanics revealing reduced strain patterns indicative of early cardiac dysfunction despite the absence of overt clinical symptoms.

Speckle-tracking echocardiography represents a remarkable advancement beyond conventional echocardiography; it enables quantification of myocardial deformation by tracking natural acoustic markers or “speckles” within the cardiac tissue. This capability provides a sensitive and precise assessment of myocardial strain—parameters that offer robust insights into the contractile function of the heart muscle. The researchers capitalized on this technology to dissect left ventricular mechanics in children debilitated by intractable epilepsy, exposing subclinical cardiac changes that standard echocardiographic measures would overlook.

The implications of these findings are vast. Cardiac complications are an underappreciated dimension of epilepsy, often overshadowed by the primary neurological deficits. However, sudden unexpected death in epilepsy (SUDEP) is a recognized phenomenon with suspected cardiac etiologies. This study’s detection of subclinical myocardial dysfunction in a vulnerable pediatric population may unravel part of the mystery surrounding SUDEP, suggesting that early cardiac impairment might predispose these patients to adverse outcomes beyond seizure burden alone.

A critical factor highlighted in the study is the interplay between prolonged seizures and the autonomic nervous system, which may precipitate chronic cardiac stress and ultimately myocardial injury. Epileptic seizures induce surges in catecholamines and fluctuations in autonomic tone, setting the stage for arrhythmic vulnerability and myocardial strain accumulation. Over time, this pathophysiological cascade could depress cardiac function subtly yet relentlessly, as illustrated by the reduced global longitudinal strain recorded via speckle-tracking.

Importantly, the study differentiates children with drug-resistant epilepsy from those responsive to medical therapy, underscoring the unique cardiovascular risks borne by the former group. Drug-resistant cases tend to endure more refractory, frequent, and severe seizures, exposing their myocardium to greater injury through repeated autonomic disturbance. This work thus calls for integrated cardiovascular surveillance in these high-risk patients as part of comprehensive epilepsy care, a paradigm shift away from exclusively neurologic focus.

Furthermore, the methodology of the study warrants appreciation for its precision and rigor. The researchers systematically applied echocardiographic protocols standardized for pediatric populations, ensuring age-appropriate normative strain values as reference points. This methodological sophistication lends credence to their conclusion that subclinical dysfunction observed is indeed pathological rather than developmental variance. The quantitative nature of speckle-tracking also enables longitudinal tracking, potentially facilitating early intervention before clinical heart disease ensues.

The study’s authors advocate for routine implementation of speckle-tracking echocardiography in the evaluation of children with drug-resistant epilepsy. This recommendation challenges current clinical guidelines but resonates with a growing recognition of epilepsy as a multisystem disorder. Armed with the capacity to detect cryptic cardiac involvement, clinicians may better stratify risk, tailor treatments, and guide informed family counseling, potentially improving both neurological and cardiac outcomes for these patients.

Beyond clinical practice, the discovery opens fertile ground for further research. Future investigations might deepen understanding of the temporal relationship between seizure burden and cardiac dysfunction progression, examine reversible components after seizure control, or explore cardioprotective strategies within epileptic care frameworks. Additionally, integrating other modalities such as cardiac MRI and electrophysiological studies could complement speckle-tracking findings, enriching the diagnostic arsenal against hidden cardiac risks.

The significance of this research extends into the realm of public health as well. Drug-resistant epilepsy remains a substantial contributor to pediatric morbidity worldwide. Unmasking covert cardiac impairments in this population not only elevates clinical vigilance but also underscores the necessity for multidisciplinary approaches in chronic neurological diseases. Policymakers may harness these insights to prioritize resource allocation for comprehensive cardiac monitoring capabilities in epilepsy centers, ensuring vulnerable children receive holistic care.

Moreover, this study epitomizes the symbiotic advancement of medical imaging technology and translational research. The evolution of speckle-tracking echocardiography from investigative tool to potential clinical staple exemplifies how innovation can unveil unsuspected disease facets. Such interdisciplinary fusion drives progress, ultimately delivering refined diagnostic acumen and enhancing patient-centered care—an aspiration that resonates across the spectrum of medicine.

In conclusion, Noureldeen and colleagues’ pioneering work delivers a vital wakeup call to the epilepsy community. Their demonstration that subclinical cardiac dysfunction, detected by speckle-tracking echocardiography, pervades children with drug-resistant epilepsy challenges existing paradigms and paves the way for novel interventional strategies. By exposing the silent cardiac threat intertwined with refractory seizures, this study heralds a new era of integrated neurological and cardiovascular assessment, promising better prevention, prognosis, and quality of life for affected children globally.

Subject of Research: Children with drug-resistant epilepsy and subclinical cardiac dysfunction detected through speckle-tracking echocardiography.

Article Title: Subclinical cardiac dysfunction detected by speckle-tracking echocardiography in children with drug-resistant epilepsy.

Article References:
Noureldeen, M.M., Tohamy, M.M., Botrous, O.E. et al. Subclinical cardiac dysfunction detected by speckle-tracking echocardiography in children with drug-resistant epilepsy. Pediatr Res (2026). https://doi.org/10.1038/s41390-026-04769-z

Image Credits: AI Generated

DOI: 03 February 2026

Focal cortical dysplasia represents a spectrum of cortical malformations characterized by disrupted neuronal organization and architecture, frequently culminating in intractable epileptic seizures. Historically, differentiating between FCD type I and II has been riddled with diagnostic challenges due to overlapping clinical and radiological features. Precise subtype identification is crucial, however, as it can inform surgical planning and prognostication. The advent of microRNA-based biomarkers offers an unprecedented, minimally invasive window into neuropathological heterogeneity.

Extracellular vesicles (EVs), nanoscale membrane-bound particles secreted by cells, have emerged as pivotal mediators of intercellular communication and reservoirs of diverse molecular cargo, including microRNAs (miRNAs). These miRNAs, short non-coding RNA sequences, regulate gene expression at the post-transcriptional level and have been increasingly implicated in neurodevelopmental and neuropathological processes. By analyzing miRNAs encapsulated within plasma EVs, the researchers leveraged a robust, stable source of biomolecules reflective of central nervous system pathology.

This innovative approach involved isolating plasma EVs from pediatric patients diagnosed with different FCD histopathologic subtypes. Advanced sequencing platforms and rigorous bioinformatics analyses were employed to profile the miRNA expression landscape, uncovering distinct divergent expression patterns correlating with FCD type I versus type II. Notably, several miRNAs previously unlinked to cortical dysplasia were identified as discriminatory markers, underscoring the untapped biological insight harbored within vesicular RNA cargo.

The implications of these findings extend far beyond mere diagnostics. MicroRNAs operate as master regulators, orchestrating gene networks that govern cellular proliferation, migration, and differentiation—processes inherently deranged in cortical dysplasia. By delineating subtype-specific miRNA fingerprints, the study opens avenues for elucidating molecular mechanisms underlying FCD pathogenesis and progression. Therein lies potential for targeted therapeutic interventions aimed at modulating miRNAs or their downstream pathways.

Critically, the study also highlights the translational potential of plasma EV-derived miRNAs as non-invasive biomarkers. Traditional diagnostic modalities for FCD, such as high-resolution MRI and invasive electrocorticography, carry inherent limitations and risks. Blood-based assays measuring EV-associated miRNAs could revolutionize diagnostic workflows by providing rapid, accurate, and repeatable assessments, facilitating early intervention and personalized treatment strategies tailored to the dysplasia subtype.

The methodological rigor of the study deserves emphasis. The isolation of pure EV populations from plasma amidst a milieu of lipoproteins and protein aggregates demanded stringent ultracentrifugation protocols, validated by nanoparticle tracking analysis and electron microscopy. Subsequent miRNA extraction and quantitative analyses employed state-of-the-art next-generation sequencing and qPCR validation, ensuring reproducibility and robustness of results. Statistical modeling further refined candidate biomarker panels capable of classifying FCD subtypes with high diagnostic performance.

In examining the biological relevance of the identified miRNAs, pathway enrichment analyses implicated dysregulated signaling cascades involved in neuroinflammation, synaptic plasticity, and cellular apoptosis. These insights collectively suggest that subtype-distinct molecular programs are reflected in plasma EV miRNA profiles, offering a holistic snapshot of neuropathological alterations accessible via peripheral blood.

Moreover, this research sets a precedent for expanding liquid biopsy applications in neurological disorders. While EV-derived miRNAs have been studied extensively in oncology and cardiovascular diseases, their clinical utility in pediatric epilepsy and cortical malformations remains nascent. The study by Zhou et al. bridges this gap, advocating for broader integration of extracellular vesicle biomarker platforms in routine clinical practice to enhance diagnostic accuracy and patient outcomes.

The study also raises intriguing questions about EV biogenesis and release dynamics in pathological versus healthy cortical tissue. Understanding how neuronal and glial cells package specific miRNAs into EVs and how these vesicles traverse the blood-brain barrier could further refine biomarker discovery and utility. Additionally, longitudinal monitoring of EV miRNA profiles might enable tracking of disease progression or response to therapy, a transformative prospect in managing refractory epilepsy.

Potential challenges ahead include standardizing EV isolation and miRNA detection techniques across laboratories to ensure consistency and comparability of results. Furthermore, large-scale multicenter validation studies are imperative to confirm the specificity and sensitivity of identified miRNA panels across diverse populations. Integration with other biomarker modalities—imaging, electrophysiology, and genetic profiling—could crystallize a comprehensive diagnostic algorithm for FCD.

From a translational perspective, the identification of miRNA biomarkers tailored to FCD subtypes paves the way for novel treatment paradigms. Modulating miRNA activity via mimics or inhibitors—technologies already under investigation in other neurological disorders—could be harnessed to rectify aberrant gene expression patterns driving dysplasia formation or seizure genesis. Such interventions may complement current surgical and pharmacologic approaches, ultimately improving seizure control and quality of life for affected children.

This pioneering work also underscores the broader paradigm shift towards precision medicine in neurology. As molecularly informed diagnoses become mainstream, leveraging minimally invasive biofluid assays to decode complex neurodevelopmental conditions promises to transform clinical paradigms. Detecting subtle molecular aberrations in easily accessible samples reduces diagnostic uncertainty, accelerates therapeutic decisions, and personalizes care on an unprecedented scale.

In summary, Zhou and colleagues’ elucidation of plasma extracellular vesicle-derived microRNA signatures as discriminators of focal cortical dysplasia subtypes represents a monumental stride in pediatric epilepsy research. This innovative strategy melds cutting-edge molecular biology with clinical neurology, offering robust, non-invasive biomarkers that may soon become indispensable tools in diagnosing and managing FCD. As validation efforts progress and miRNA-targeted therapies evolve, this approach heralds a new era of biomarker-driven precision neurotherapeutics tailored to the molecular underpinnings of cortical malformations.

With epilepsy affecting millions worldwide and focal cortical dysplasia being a leading cause in pediatric cases, such advancements could reverberate through clinical practice globally. The promise of harnessing circulating extracellular vesicles to unlock the molecular fingerprints of complex brain malformations heralds transformative potential. This study exemplifies how interdisciplinary research at the nexus of neurology, molecular genetics, and bioengineering can catalyze breakthroughs with profound clinical impact.

As research continues to unravel the complexities of EV-associated miRNAs in neurological disease, it is conceivable that this paradigm will extend beyond focal cortical dysplasia to encompass other neurodevelopmental and neurodegenerative disorders. The non-invasive nature and molecular specificity of EV-derived miRNA biomarkers position them at the forefront of next-generation diagnostics and therapeutics—a beacon of hope for countless patients and clinicians striving to combat neurological disease with precision and efficacy.

Subject of Research:
Plasma extracellular vesicles-derived microRNAs as biomarkers for distinguishing between focal cortical dysplasia type I and II in pediatric epilepsy.

Article Title:
Plasma extracellular vesicles-derived microRNAs provide potential biomarkers in distinguishing between focal cortical dysplasia type I and II.

Article References:
Zhou, B., Yu, H., Liu, C. et al. Plasma extracellular vesicles-derived microRNAs provide potential biomarkers in distinguishing between focal cortical dysplasia type I and II. Pediatr Res (2025). https://doi.org/10.1038/s41390-025-04343-z

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41390-025-04343-z

Focal cortical dysplasia is a malformation of cortical development characterized by disrupted lamination and aberrant neuronal morphology, which culminates in the generation of epileptogenic tissue. Historically, investigations into FCD have been hampered by the tissue heterogeneity and limitations in resolving individual cellular contributions. The authors overcome these challenges by harnessing single-cell sequencing technologies that allow the dissection of genetic mutations and transcriptional landscapes at the resolution of individual cells. This approach reveals the mosaicism inherent to FCD lesions, where only subsets of neurons and glial cells harbor pathogenic variants, while neighboring cells may remain genetically unaffected.

Central to this investigation is the application of comprehensive single-cell whole-genome genotyping. By isolating thousands of individual cells from resected cortical tissue of affected patients, the researchers identified somatic mutations in key mTOR pathway genes, which have long been implicated in cortical malformations and epilepsy. These mutations are not uniformly distributed but rather restricted to discrete cellular populations, which define the mosaic nature of the dysplastic tissue. This evidence challenges prior assumptions of uniform mutation across lesions and emphasizes the complexity of mosaicism in neurodevelopmental disorders.

Going beyond genotyping, the study performs single-cell RNA sequencing to interrogate transcriptomic profiles and reveal the functional consequences of somatic mutations at a molecular level. Intriguingly, dysplastic cells with mutations exhibit altered gene expression patterns notably enriched in pathways governing cell growth, synaptic signaling, and inflammation. This aberrant transcriptional state likely contributes to the epileptogenicity of the lesion and offers clues to the cellular processes that could be therapeutically targeted to modulate disease progression or seizure activity.

What sets this research apart is the integration of genotypic and transcriptomic data within the same single cells, providing unparalleled insight into how genetic mosaicism shapes cellular phenotypes in FCD. The team’s data convincingly demonstrate that mutant and wild-type cells coexist within one lesion, creating a microenvironment with unique intercellular interactions that may drive pathological network hyperexcitability. This nuanced understanding permits a new conceptual model of FCD pathology as a stable mosaic network rather than a homogenous mass of defective cells.

Furthermore, the authors explore the diversity of affected cell types within dysplastic tissue. They identify not only neurons but also astrocytes and oligodendrocyte precursor cells harboring mutations, indicating that multiple lineages contribute to the malformation and its epileptogenic potential. This multi-lineage mosaicism extends the potential impact of somatic mutations beyond neuronal circuits and into glial-mediated modulation of brain function, opening new avenues for research into neuroglial interactions in epilepsy.

A particularly striking discovery from the transcriptomic data is the activation of neuroinflammatory pathways selectively in mutant cells, suggesting that inflammation and immune signaling may play a crucial role in the pathogenesis of focal cortical dysplasia. This aligns with emerging evidence that immune-mediated processes influence epileptogenesis and highlights potential targets for adjunctive anti-inflammatory therapy to complement surgical intervention.

The study also leverages advanced computational algorithms to reconstruct developmental lineage trajectories of mutated cells, revealing how somatic mutations emerge during corticogenesis and lead to clonal expansion of dysplastic cells. This temporal and spatial mapping of mutant clones provides critical insights into the timing and cellular context for effective therapeutic intervention, emphasizing the potential for early detection and precision medicine approaches.

Clinically, these findings have profound implications. They suggest that future diagnostic regimes for epilepsy patients with FCD may benefit from single-cell molecular profiling to accurately characterize lesion heterogeneity and identify actionable mutations. Such precision diagnostics could be pivotal in stratifying patients who may respond to targeted inhibitors of pathogenic pathways like mTOR, thereby moving away from one-size-fits-all epilepsy surgery.

Moreover, the data serve as a foundation for developing molecular biomarkers that predict seizure frequency, prognosis, or response to therapy. For instance, the gene expression signatures uncovered could be translated into imaging or cerebrospinal fluid markers that non-invasively monitor disease activity or treatment efficacy, significantly improving patient management.

On the therapeutic front, the delineation of mutation-bearing cell populations prompts exciting possibilities for cell-type specific interventions, such as gene editing tools or molecular therapies delivered to discrete cellular subtypes. By precisely targeting mutant cells while sparing normal tissue, such approaches hold promise for minimizing side effects and maximizing treatment success in notoriously challenging refractory epilepsy.

The research also underscores the value of interdisciplinary collaboration, merging expertise in neurogenetics, bioinformatics, neuropathology, and clinical neurology. The use of extensive patient-derived tissue and the development of bespoke analytical pipelines exemplify how state-of-the-art technology platforms can be harnessed to decode complex neurological disorders systematically.

Looking beyond FCD, the methodologies and findings presented may have broad ramifications for other neurodevelopmental and neuropsychiatric diseases characterized by somatic mosaicism, including autism spectrum disorders and schizophrenia. This study paves the way for a paradigm shift in brain disease research, emphasizing the mosaic architecture of pathology as a fundamental principle.

Additionally, the high-resolution data generated offer a valuable resource for the neuroscience community, providing a reference map to explore gene regulatory networks, cellular interactions, and mutation-driven pathobiology. By publicly sharing their datasets, the authors foster an open scientific atmosphere encouraging further discovery and validation.

One of the most compelling aspects of this work is its potential to inspire novel experimental models. By identifying exact mutation profiles and affected cell types, researchers can engineer more faithful in vitro and in vivo models to study epileptogenesis or screen candidate drugs, accelerating translation from bench to bedside.

In summary, Baldassari et al. deliver a tour de force study that redefines our understanding of focal cortical dysplasia through single-cell resolution genetic and transcriptomic characterization. Their findings elucidate the mosaicism that orchestrates the lesion’s pathogenesis, identify critical molecular pathways driving disease, and chart a course toward precision diagnostics and targeted therapeutics for patients with epileptic brain malformations. This landmark study not only advances epilepsy research but also exemplifies the transformative power of single-cell technologies in tackling intricate brain disorders.

Subject of Research: Single-cell genetic and transcriptomic analysis of mosaic focal cortical dysplasia in drug-resistant epilepsy patients

Article Title: Single-cell genotyping and transcriptomic profiling of mosaic focal cortical dysplasia

Article References:
Baldassari, S., Klingler, E., Teijeiro, L.G. et al. Single-cell genotyping and transcriptomic profiling of mosaic focal cortical dysplasia. Nat Neurosci (2025). https://doi.org/10.1038/s41593-025-01936-z

Image Credits: AI Generated