glia
Latest
High Stakes in the Adolescent Brain: Glia Ignite Under THC’s Influence
Microglia regulate remyelination via inflammatory phenotypic polarization in CNS demyelinating disorders
The basal ganglia and addiction
Developmental and evolutionary perspectives on thalamic function
Brain organization and function is a complex topic. We are good at establishing correlates of perception and behavior across forebrain circuits, as well as manipulating activity in these circuits to affect behavior. However, we still lack good models for the large-scale organization and function of the forebrain. What are the contributions of the cortex, basal ganglia, and thalamus to behavior? In addressing these questions, we often ascribe function to each area as if it were an independent processing unit. However, we know from the anatomy that the cortex, basal ganglia, and thalamus, are massively interconnected in a large network. One way to generate insight into these questions is to consider the evolution and development of forebrain systems. In this talk, I will discuss the developmental and evolutionary (comparative anatomy) data on the thalamus, and how it fits within forebrain networks. I will address questions including, when did the thalamus appear in evolution, how is the thalamus organized across the vertebrate lineage, and how can the change in the organization of forebrain networks affect behavioral repertoires.
Astrocytes release glutamate by regulated exocytosis in health and disease
Astrocytes release glutamate by regulated exocytosis in health and disease Vladimir Parpura, International Translational Neuroscience Research Institute, Zhejiang Chinese Medical University, Hangzhou, P.R. China Parpura will present you with the evidence that astrocytes, a subtype of glial cells in the brain, can exocytotically release the neurotransmitter glutamate and how this release is regulated. Spatiotemporal characteristic of vesicular fusion that underlie glutamate release in astrocytes will be discussed. He will also present data on a translational project in which this release pathway can be targeted for the treatment of glioblastoma, the deadliest brain cancer.
The cellular phase of Alzheimer’s Disease and the path towards therapies
Rejuvenating the Alzheimer’s brain: Challenges & Opportunities
Unlocking the Secrets of Microglia in Neurodegenerative diseases: Mechanisms of resilience to AD pathologies
Dopaminergic Network Dynamics
Cholinergic Interneurons
Oligodendrocyte dyfunction drives human cognitive decline
Regulation of cortical circuit maturation and plasticity by oligodendrocytes and myelin
Honorary Lectures 2025
Schizophrenia and BG
SWEBAGS conference 2024: Shared network mechanisms of dopamine and deep brain stimulation for the treatment of Parkinson’s disease: From modulation of oscillatory cortex – basal ganglia communication to intelligent clinical brain computer interfaces
SWEBAGS conference 2024: The involvement of the striatum in autism spectrum disorder
SWEBAGS conference 2024: The basal ganglia in action
Decision and Behavior
This webinar addressed computational perspectives on how animals and humans make decisions, spanning normative, descriptive, and mechanistic models. Sam Gershman (Harvard) presented a capacity-limited reinforcement learning framework in which policies are compressed under an information bottleneck constraint. This approach predicts pervasive perseveration, stimulus‐independent “default” actions, and trade-offs between complexity and reward. Such policy compression reconciles observed action stochasticity and response time patterns with an optimal balance between learning capacity and performance. Jonathan Pillow (Princeton) discussed flexible descriptive models for tracking time-varying policies in animals. He introduced dynamic Generalized Linear Models (Sidetrack) and hidden Markov models (GLM-HMMs) that capture day-to-day and trial-to-trial fluctuations in choice behavior, including abrupt switches between “engaged” and “disengaged” states. These models provide new insights into how animals’ strategies evolve under learning. Finally, Kenji Doya (OIST) highlighted the importance of unifying reinforcement learning with Bayesian inference, exploring how cortical-basal ganglia networks might implement model-based and model-free strategies. He also described Japan’s Brain/MINDS 2.0 and Digital Brain initiatives, aiming to integrate multimodal data and computational principles into cohesive “digital brains.”
Contribution of computational models of reinforcement learning to neurosciences/ computational modeling, reward, learning, decision-making, conditioning, navigation, dopamine, basal ganglia, prefrontal cortex, hippocampus
Basal Ganglia in Songbirds
Top-down models of learning and decision-making in BG
Physical Activity, Sedentary Behaviour and Brain Health
Cerebellum-Basal Ganglia Interactions
Updating our models of the basal ganglia using advances in neuroanatomy and computational modeling
Dopamine Acetylcholine interactions
Mitochondrial diversity in the mouse and human brain
The basis of the mind, of mental states, and complex behaviors is the flow of energy through microscopic and macroscopic brain structures. Energy flow through brain circuits is powered by thousands of mitochondria populating the inside of every neuron, glial, and other nucleated cell across the brain-body unit. This seminar will cover emerging approaches to study the mind-mitochondria connection and present early attempts to map the distribution and diversity of mitochondria across brain tissue. In rodents, I will present convergent multimodal evidence anchored in enzyme activities, gene expression, and animal behavior that distinct behaviorally-relevant mitochondrial phenotypes exist across large-scale mouse brain networks. Extending these findings to the human brain, I will present a developing systematic biochemical and molecular map of mitochondrial variation across cortical and subcortical brain structures, representing a foundation to understand the origin of complex energy patterns that give rise to the human mind.
Blood-brain barrier dysfunction in epilepsy: Time for translation
The neurovascular unit (NVU) consists of cerebral blood vessels, neurons, astrocytes, microglia, and pericytes. It plays a vital role in regulating blood flow and ensuring the proper functioning of neural circuits. Among other, this is made possible by the blood-brain barrier (BBB), which acts as both a physical and functional barrier. Previous studies have shown that dysfunction of the BBB is common in most neurological disorders and is associated with neural dysfunction. Our studies have demonstrated that BBB dysfunction results in the transformation of astrocytes through transforming growth factor beta (TGFβ) signaling. This leads to activation of the innate neuroinflammatory system, changes in the extracellular matrix, and pathological plasticity. These changes ultimately result in dysfunction of the cortical circuit, lower seizure threshold, and spontaneous seizures. Blocking TGFβ signaling and its associated pro-inflammatory pathway can prevent this cascade of events, reduces neuroinflammation, repairs BBB dysfunction, and prevents post-injury epilepsy, as shown in experimental rodents. To further understand and assess BBB integrity in human epilepsy, we developed a novel imaging technique that quantitatively measures BBB permeability. Our findings have confirmed that BBB dysfunction is common in patients with drug-resistant epilepsy and can assist in identifying the ictal-onset zone prior to surgery. Current clinical studies are ongoing to explore the potential of targeting BBB dysfunction as a novel treatment approach and investigate its role in drug resistance, the spread of seizures, and comorbidities associated with epilepsy.
Subthalamic nucleus
Of glia and macrophages, signaling hubs in development and homeostasis
We are interested in the biology of macrophages, which represent the first line of defense against pathogens. In Drosophila, the embryonic hemocytes arise from the mesoderm whereas glial cells arise from multipotent precursors in the neurogenic region. These cell types represent, respectively, the macrophages located outside and within the nervous system (similar to vertebrate microglia). Thus, despite their different origin, hemocytes and glia display common functions. In addition, both cell types express the Glide/Gcm transcription factor, which plays an evolutionarily conserved role as an anti-inflammatory factor. Moreover, embryonic hemocytes play an evolutionarily conserved and fundamental role in development. The ability to migrate and to contact different tissues/organs most likely allow macrophages to function as signaling hubs. The function of macrophages beyond the recognition of the non-self calls for revisiting the biology of these heterogeneous and plastic cells in physiological and pathological conditions across evolution.
Honorary Lecture 2024
The many roles of microglia in the pathogenesis of neurodegeneration
Cellular and genetic mechanisms of cerebral cortex folding
One of the most prominent features of the human brain is the fabulous size of the cerebral cortex and its intricate folding, both of which emerge during development. Over the last few years, work from my lab has shown that specific cellular and genetic mechanisms play central roles in cortex folding, particularly linked to neural stem and progenitor cells. Key mechanisms include high rates of neurogenesis, high abundance of basal Radial Glia Cells (bRGCs), and neuron migration, all of which are intertwined during development. We have also shown that primary cortical folds follow highly stereotyped patterns, defined by a spatial-temporal protomap of gene expression within germinal layers of the developing cortex. I will present recent findings from my laboratory revealing novel cellular and genetic mechanisms that regulate cortex expansion and folding. We have uncovered the contribution of epigenetic regulation to the establishment of the cortex folding protomap, modulating the expression levels of key transcription factors that control progenitor cell proliferation and cortex folding. At the single cell level, we have identified an unprecedented diversity of cortical progenitor cell classes in the ferret and human embryonic cortex. These are differentially enriched in gyrus versus sulcus regions and establish parallel cell lineages, not observed in mouse. Our findings show that genetic and epigenetic mechanisms in gyrencephalic species diversify cortical progenitor cell types and implement parallel cell linages, driving the expansion of neurogenesis and patterning cerebral cortex folds.
Imaging the subcortex; Microstructural and connectivity correlates of outcome variability in functional neurosurgery for movement disorders
We are very much looking forward to host Francisca Ferreira and Birte Forstmann on December 14th, 2023, at noon ET / 6PM CET. Francisca Ferreira is a PhD student and Neurosurgery trainee at the University College of London Queen Square Institute of Neurology and a Royal College of Surgeons “Emerging Leaders” program laureate. Her presentation title will be: “Microstructural and connectivity correlates of outcome variability in functional neurosurgery for movement disorders”. Birte Forstmann, PhD, is the Director of the Amsterdam Brain and Cognition Center, a Professor of Cognitive Neuroscience at the University of Amsterdam, and a Professor by Special Appointment of Neuroscientific Testing of Psychological Models at the University of Leiden. Besides her scientific presentation (“Imaging the human subcortex”), she will give us a glimpse at the “Person behind the science”. You can register via talks.stimulatingbrains.org to receive the (free) Zoom link!
Astrocyte reprogramming / activation and brain homeostasis
Astrocytes are multifunctional glial cells, implicated in neurogenesis and synaptogenesis, supporting and fine-tuning neuronal activity and maintaining brain homeostasis by controlling blood-brain barrier permeability. During the last years a number of studies have shown that astrocytes can also be converted into neurons if they force-express neurogenic transcription factors or miRNAs. Direct astrocytic reprogramming to induced-neurons (iNs) is a powerful approach for manipulating cell fate, as it takes advantage of the intrinsic neural stem cell (NSC) potential of brain resident reactive astrocytes. To this end, astrocytic cell fate conversion to iNs has been well-established in vitro and in vivo using combinations of transcription factors (TFs) or chemical cocktails. Challenging the expression of lineage-specific TFs is accompanied by changes in the expression of miRNAs, that post-transcriptionally modulate high numbers of neurogenesis-promoting factors and have therefore been introduced, supplementary or alternatively to TFs, to instruct direct neuronal reprogramming. The neurogenic miRNA miR-124 has been employed in direct reprogramming protocols supplementary to neurogenic TFs and other miRNAs to enhance direct neurogenic conversion by suppressing multiple non-neuronal targets. In our group we aimed to investigate whether miR-124 is sufficient to drive direct reprogramming of astrocytes to induced-neurons (iNs) on its own both in vitro and in vivo and elucidate its independent mechanism of reprogramming action. Our in vitro data indicate that miR-124 is a potent driver of the reprogramming switch of astrocytes towards an immature neuronal fate. Elucidation of the molecular pathways being triggered by miR-124 by RNA-seq analysis revealed that miR-124 is sufficient to instruct reprogramming of cortical astrocytes to immature induced-neurons (iNs) in vitro by down-regulating genes with important regulatory roles in astrocytic function. Among these, the RNA binding protein Zfp36l1, implicated in ARE-mediated mRNA decay, was found to be a direct target of miR-124, that be its turn targets neuronal-specific proteins participating in cortical development, which get de-repressed in miR-124-iNs. Furthermore, miR-124 is potent to guide direct neuronal reprogramming of reactive astrocytes to iNs of cortical identity following cortical trauma, a novel finding confirming its robust reprogramming action within the cortical microenvironment under neuroinflammatory conditions. In parallel to their reprogramming properties, astrocytes also participate in the maintenance of blood-brain barrier integrity, which ensures the physiological functioning of the central nervous system and gets affected contributing to the pathology of several neurodegenerative diseases. To study in real time the dynamic physical interactions of astrocytes with brain vasculature under homeostatic and pathological conditions, we performed 2-photon brain intravital imaging in a mouse model of systemic neuroinflammation, known to trigger astrogliosis and microgliosis and to evoke changes in astrocytic contact with brain vasculature. Our in vivo findings indicate that following neuroinflammation the endfeet of activated perivascular astrocytes lose their close proximity and physiological cross-talk with vasculature, however this event is at compensated by the cross-talk of astrocytes with activated microglia, safeguarding blood vessel coverage and maintenance of blood-brain integrity.
Effect of nutrient sensing by microglia on mouse behavior
Microglia are the brain macrophages, eliciting multifaceted functions to maintain brain homeostasis across lifetime. To achieve this, microglia are able to sense a plethora of signals in their close environment. In the lab, we investigate the effect of nutrients on microglia function for several reasons: 1) Microglia express all the cellular machinery required to sense nutrients; 2) Eating habits have changed considerably over the last century, towards diets rich in fats and sugars; 3) This so-called "Western diet" is accompanied by an increase in the occurrence of neuropathologies, in which microglia are known to play a role. In my talk, I will present data showing how variations in nutrient intake alter microglia function, including exacerbation of synaptic pruning, with profound consequences for neuronal activity and behavior. I will also show unpublished data on the mechanisms underlying the effects of nutrients on microglia, notably through the regulation of their metabolic activity.
The role of CNS microglia in health and disease
Microglia are the resident CNS macrophages of the brain parenchyma. They have many and opposing roles in health and disease, ranging from inflammatory to anti-inflammatory and protective functions, depending on the developmental stage and the disease context. In Multiple Sclerosis, microglia are involved to important hallmarks of the disease, such as inflammation, demyelination, axonal damage and remyelination, however the exact mechanisms controlling their transformation towards a protective or devastating phenotype during the disease progression remains largely unknown until now. We wish to understand how brain microglia respond to demyelinating insults and how their behaviour changes in recovery. To do so we developed a novel histopathological analysis approach in 3D and a cell-based analysis tool that when applied in the cuprizone model of demyelination revealed region- and disease- dependent changes in microglial dynamics in the brain grey matter during demyelination and remyelination. We now use similar approaches with the aim to unravel sensitive changes in microglial dynamics during neuroinflammation in the EAE model. Furthermore, we employ constitutive knockout and tamoxifen-inducible gene-targeting approaches, immunological techniques, genetics and bioinformatics and currently seek to clarify the specific role of the brain resident microglial NF-κB molecular pathway versus other tissue macrophages in EAE.
September webinar
Dopamine and Acetylcholine waves in the striatum
Workplace Experiences of LGBTQIA+ Academics in Psychology, Psychiatry, and Neuroscience
In this webinar, Dr David Pagliaccio discusses the findings of his recent pre-print on workplace bias and discrimination faced by LGBTQIA+ brain scientists in the US.
From pecking order to ketamine - neural mechanism of social and emotional behavior
Emotions and social interactions color our lives and shape our behaviors. Using animal models and engineered manipulations, we aim to understand how social and emotional behaviors are encoded in the brain, focusing on the neural circuits underlying dominance hierarchy and depression. This lecture will highlight our recent discoveries on how downward social mobility leads to depression; how ketamine tames depression by blocking burst firing in the brain’s antireward center; and, how glia-neuron interaction plays a surprising role in this process. I will also present our recent work on the mechanism underlying the sustained antidepressant activity of ketamine and its brain region specificity. With these results, we hope to illuminate on a more unified theory on ketamine’s mode of action and inspire new treatment strategies for depression.
From pecking order to ketamine - neural mechanism of social and emotional behavior
Emotions and social interactions color our lives and shape our behaviors. Using animal models and engineered manipulations, we aim to understand how social and emotional behaviors are encoded in the brain, focusing on the neural circuits underlying dominance hierarchy and depression. This lecture will highlight our recent discoveries on how downward social mobility leads to depression; how ketamine tames depression by blocking burst firing in the brain’s antireward center; and, how glia-neuron interaction plays a surprising role in this process. I will also present our recent work on the mechanism underlying the sustained antidepressant activity of ketamine and its brain region specificity. With these results, we hope to illuminate on a more unified theory on ketamine’s mode of action and inspire new treatment strategies for depression.
May Webinar
Auditory input to the basal ganglia; Deep brain stimulation and action-stopping: A cognitive neuroscience perspective on the contributions of fronto-basal ganglia circuits to inhibitory control
On Thursday, May 25th we will host Darcy Diesburg and Mark Richardson. Darcy Diesburg, PhD, is a post-doctoral research fellow at Brown University. She will tell us about “Deep brain stimulation and action-stopping: A cognitive neuroscience perspective on the contributions of fronto-basal ganglia circuits to inhibitory control”. Mark Richardson, MD, PhD, is the Director of Functional Neurosurgery at the Massachusetts General Hospital, Charles Pappas Associate Professor of Neurosciences at Harvard Medical School and Visiting Associate Professor of Brain and Cognitive Sciences at MIT. Beside his scientific presentation on “Auditory input to the basal ganglia”, he will give us a glimpse at the “Person behind the science”. The talks will be followed by a shared discussion. You can register via talks.stimulatingbrains.org to receive the (free) Zoom link!
Richly structured reward predictions in dopaminergic learning circuits
Theories from reinforcement learning have been highly influential for interpreting neural activity in the biological circuits critical for animal and human learning. Central among these is the identification of phasic activity in dopamine neurons as a reward prediction error signal that drives learning in basal ganglia and prefrontal circuits. However, recent findings suggest that dopaminergic prediction error signals have access to complex, structured reward predictions and are sensitive to more properties of outcomes than learning theories with simple scalar value predictions might suggest. Here, I will present recent work in which we probed the identity-specific structure of reward prediction errors in an odor-guided choice task and found evidence for multiple predictive “threads” that segregate reward predictions, and reward prediction errors, according to the specific sensory features of anticipated outcomes. Our results point to an expanded class of neural reinforcement learning algorithms in which biological agents learn rich associative structure from their environment and leverage it to build reward predictions that include information about the specific, and perhaps idiosyncratic, features of available outcomes, using these to guide behavior in even quite simple reward learning tasks.
Microbial modulation of zebrafish behavior and brain development
There is growing recognition that host-associated microbiotas modulate intrinsic neurodevelopmental programs including those underlying human social behavior. Despite this awareness, the fundamental processes are generally not understood. We discovered that the zebrafish microbiota is necessary for normal social behavior. By examining neuronal correlates of behavior, we found that the microbiota restrains neurite complexity and targeting of key forebrain neurons within the social behavior circuitry. The microbiota is also necessary for both localization and molecular functions of forebrain microglia, brain-resident phagocytes that remodel neuronal arbors. In particular, the microbiota promotes expression of complement signaling pathway components important for synapse remodeling. Our work provides evidence that the microbiota modulates zebrafish social behavior by stimulating microglial remodeling of forebrain circuits during early neurodevelopment and suggests molecular pathways for therapeutic interventions during atypical neurodevelopment.
Perivascular cells induce microglial phagocytic states and synaptic engulfment via SPP1 in mouse models of Alzheimer's disease
Microglia regulate central nervous system myelin growth and integrity
Off-policy learning in the basal ganglia
I will discuss work with Jack Lindsey modeling reinforcement learning for action selection in the basal ganglia. I will argue that the presence of multiple brain regions, in addition to the basal ganglia, that contribute to motor control motivates the need for an off-policy basal ganglia learning algorithm. I will then describe a biological implementation of such an algorithm that predicts tuning of dopamine neurons to a quantity we call "action surprise," in addition to reward prediction error. In the same model, an implementation of learning from a motor efference copy also predicts a novel solution to the problem of multiplexing feedforward and efference-related striatal activity. The solution exploits the difference between D1 and D2-expressing medium spiny neurons and leads to predictions about striatal dynamics.
Basal Ganglia in addiction
My evolution in invasive human neurophysiology: From basal ganglia single units to chronic electrocorticography; Therapies orchestrated by patients' own rhythms
On Thursday, April 27th, we will host Hayriye Cagnan and Philip A. Starr. Hayriye Cagnan, PhD, is an associate professor at the MRC Brain Network Dynamics Unit and University of Oxford. She will tell us about “Therapies orchestrated by patients’ own rhythms”. Philip A. Starr, MD, PhD, is a neurosurgeon and professor of Neurological Surgery at the University of California San Francisco. Besides his scientific presentation on “My evolution in invasive human neurophysiology: from basal ganglia single units to chronic electrocorticography”, he will give us a glimpse at the person behind the science. The talks will be followed by a shared discussion. You can register via talks.stimulatingbrains.org to receive the (free) Zoom link!
Basal Ganglia feedback loops as possible candidates for generation of beta oscillation
COSYNE 2022
Exploration of learning by dopamine D1 and D2 receptors by a spiking network model of the basal ganglia
COSYNE 2022
Basal ganglia-dependent expression of recent song learning in the juvenile finch
COSYNE 2023
A computational model of cortico-basal ganglia circuits for deciding between reaching actions
COSYNE 2025
Glial ensheathment of inhibitory synapses drives hyperactivity and increases correlations
COSYNE 2025
Integrator dynamics in the cortico-basal ganglia loop underlie flexible motor timing
COSYNE 2025
Modeling rapid neuromodulation in the cortex-basal ganglia-thalamus loop
COSYNE 2025
Unifying reward and error-driven learning: a theory of cerebello-basal ganglia interactions
COSYNE 2025
2P-STED imaging of the microglial tripartite synapse in vivo
FENS Forum 2024
3-Photon in vivo imaging reveals breakdown of microglia surveillance upon glioma invasion in the corpus callosum
FENS Forum 2024
OPCs-microglia cross-talk in Alzheimer's disease: Roles and mechanisms
FENS Forum 2024
α-Synuclein propagation leads to synaptic abnormalities in the cortex through microglial synapse phagocytosis
FENS Forum 2024
Aberrant microglial activation in mice lacking the dsRNA editing enzyme ADAR1 is rescued by removing the gene encoding PKR
FENS Forum 2024
PKC activators orchestrate neuronal immune modulation: Unveiling microglial dynamics in NF-kB activation and phagocytosis
FENS Forum 2024
Aged microglia in Alzheimer’s disease display a senescent and pro-inflammatory profile associated with mitochondrial oxidative stress
FENS Forum 2024
AI-driven image analysis for label-free quantification of chemotherapeutic cytotoxicity in glial cells
FENS Forum 2024
Agmatine downregulates LPS-promoted glycolysis in microglial cells
FENS Forum 2024
Assessment of gradual perceptual learning by behaviour and neuron-glia imaging in AD model mice
FENS Forum 2024
Astroglial control of prefrontal dopamine tone shapes behavior
FENS Forum 2024
Astroglial connexins differentially drive chronic seizures in mice and humans
FENS Forum 2024
Astroglial networks shape collicular visual maps
FENS Forum 2024
Atypical astrocytes in the aging brain: An underreported phenotype where downregulated membrane proteins disrupt glial regulated homeostatic capacities
FENS Forum 2024
Autophagy modulation of glial neuroinflammatory responses in Parkinson’s disease
FENS Forum 2024
Avalanche transition matrices reflect basal ganglia-cortical alterations in Parkinson’s disease
FENS Forum 2024
Basal ganglia pathways for regulating motor skill variability
FENS Forum 2024
Bergmann glia suppress Purkinje cell firing via interneurons
FENS Forum 2024
Breaking the circulus vitiosus of neuroinflammation: Resveratrol attenuates the human glial cell response to cytokines
FENS Forum 2024
Calcium released by dying neurons mediates Iba-1 dependent polarization of microglial cells in Parkinsonian neurodegeneration
FENS Forum 2024
Caspr2 autoantibody pathology is mediated by altered excitability of sensory dorsal root ganglia
FENS Forum 2024
Cell-specific regulation of neuronal and glial glucose metabolism by neurodegeneration-associated protein TDP-43
FENS Forum 2024
CellRemorph: A Blender-based toolkit for constructing and optimizing morphologically detailed astroglial cell models
FENS Forum 2024
CD8+ T cells induce interferon-responsive oligodendrocytes and microglia in white matter aging
FENS Forum 2024
Cerebellar neurodegeneration in phospholipid flippases ATP8A1/ATP8A2 double knock-out mice can be ameliorated by inactivating a microglial PS receptor
FENS Forum 2024
Cerebral malaria leads to persistent microglial activation, long-term behavioural changes and electrographic seizures in mice
FENS Forum 2024
Characterization of astroglia-noradrenergic neuron communication in the locus coeruleus
FENS Forum 2024
Chemogenetic activation of Gq in microglia leads to deficits in synaptic plasticity and neuronal communication
FENS Forum 2024
Chemogenetic modulation of CX3CR1+ microglia in the intrahippocampal kainic acid mouse model of drug-resistant temporal lobe epilepsy
FENS Forum 2024
Chimeric in vitro model to study human microglia
FENS Forum 2024
Chronic demyelinating pathology induces lysosomal exhaustion and dysfunction of lipid recycling pathways in microglia
FENS Forum 2024
Deep Brain Stimulation in the Globus Pallidus internus Promotes Habitual Behavior by Modulating Cortico-Thalamic Shortcuts and Basal Ganglia Plasticity
Bernstein Conference 2024
glia coverage
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