dysregulation

Endocannabinoid System Dysregulations in Binge Eating Disorder and Obesity

Cholesterol and matrisome pathways dysregulated in Alzheimer’s disease brain astrocytes and microglia

The impact of apolipoprotein E ε4 (APOE4), the strongest genetic risk factor for Alzheimer’s disease (AD), on human brain cellular function remains unclear. Here, we investigated the effects of APOE4 on brain cell types derived from population and isogenic human induced pluripotent stem cells, post-mortem brain, and APOE targeted replacement mice. Population and isogenic models demonstrate that APOE4 local haplotype, rather than a single risk allele, contributes to risk. Global transcriptomic analyses reveal human-specific, APOE4-driven lipid metabolic dysregulation in astrocytes and microglia. APOE4 enhances de novo cholesterol synthesis despite elevated intracellular cholesterol due to lysosomal cholesterol sequestration in astrocytes. Further, matrisome dysregulation is associated with upregulated chemotaxis, glial activation, and lipid biosynthesis in astrocytes co-cultured with neurons, which recapitulates altered astrocyte matrisome signaling in human brain. Thus, APOE4 initiates glia-specific cell and non-cell autonomous dysregulation that may contribute to increased AD risk." https://doi.org/10.1016/j.cell.2022.05.017

Dopamine receptors dysregulation in BG disease

Untitled Seminar

Giordano Lippi – Beyond transcription – microRNA mechanisms of brain development; Maria Isabel Carreño-Muñoz– Role of GABAergic circuits in the generation of sensory processing dysregulations in SYNGAP1 haploinsufficiency; Rhys Knowles-TBA; Nigel Kee- That other half: Derivation of posterior axial tissues from human stem cells

Redox and mitochondrial dysregulation in epilepsy

Epileptic seizures render the brain uniquely dependent on energy producing pathways. Studies in our laboratory have been focused on the role of redox processes and mitochondria in the context of abnormal neuronal excitability associated with epilepsy. We have shown that that status epilepticus (SE) alters mitochondrial and cellular redox status, energetics and function and conversely, that reactive oxygen species and resultant dysfunction can lead to chronic epilepsy. Oxidative stress and neuroinflammatory pathways have considerable crosstalk and targeting redox processes has recently been shown to control neuroinflammation and excitability. Understanding the role of metabolic and redox processes can enable the development of novel therapeutics to control epilepsy and/or its comorbidities.

Dissecting the neural circuits underlying prefrontal regulation of reward and threat responsivity in a primate

Gaining insight into the overlapping neural circuits that regulate positive and negative emotion is an important step towards understanding the heterogeneity in the aetiology of anxiety and depression and developing new treatment targets. Determining the core contributions of the functionally heterogenous prefrontal cortex to these circuits is especially illuminating given its marked dysregulation in affective disorders. This presentation will review a series of studies in a new world monkey, the common marmoset, employing pathway-specific chemogenetics, neuroimaging, neuropharmacology and behavioural and cardiovascular analysis to dissect out prefrontal involvement in the regulation of both positive and negative emotion. Highlights will include the profound shift of sensitivity away from reward and towards threat induced by localised activations within distinct regions of vmPFC, namely areas 25 and 14 as well as the opposing contributions of this region, compared to orbitofrontal and dorsolateral prefrontal cortex, in the overall responsivity to threat. Ongoing follow-up studies are identifying the distinct downstream pathways that mediate some of these effects as well as their differential sensitivity to rapidly acting anti-depressants.

Mechanisms to medicines in neurodegeneration

Dysregulation of protein synthesis both globally and locally in neurons and astrocytes is a key feature of neurodegenerative diseases. Aberrant signalling through the Unfolded Protein Response (UPR) and related Integrated Stress Response (ISR) have become major targets for neuroprotection in these disorders. In addition, other homeostatic mechanisms and stress responses, including the cold shock response, appear to regulate local translation and RNA splicing to control synapse maintenance and regeneration and can also be targeted therapeutically for neuroprotection. We have defined the role of UPR/ISR and the cold-shock response in neurodegenerative disorders and have developed translational strategies targeting them for new treatments for dementia.

Dancing to a Different Tune: TANGO Gives Hope for Dravet Syndrome

The long-term goal of our research is to understand the mechanisms of SUDEP, defined as Sudden, Unexpected, witnessed or unwitnessed, nontraumatic and non-drowning Death in patients with EPilepsy, excluding cases of documented status epilepticus. The majority of SUDEP patients die during sleep. SUDEP is the most devastating consequence of epilepsy, yet little is understood about its causes and no biomarkers exist to identify at risk patients. While SUDEP accounts for 7.5-20% of all epilepsy deaths, SUDEP risk in the genetic epilepsies varies with affected genes. Patients with ion channel gene variants have the highest SUDEP risk. Indirect evidence variably links SUDEP to seizure-induced apnea, pulmonary edema, dysregulation of cerebral circulation, autonomic dysfunction, and cardiac arrhythmias. Arrhythmias may be primary or secondary to hormonal or metabolic changes, or autonomic discharges. When SUDEP is compared to Sudden Cardiac Death secondary to Long QT Syndrome, especially to LQT3 linked to variants in the voltage-gated sodium channel (VGSC) gene SCN5A, there are parallels in the circumstances of death. To gain insight into SUDEP mechanisms, our approach has focused on channelopathies with high SUDEP incidence. One such disorder is Dravet syndrome (DS), a devastating form of developmental and epileptic encephalopathy (DEE) characterized by multiple pharmacoresistant seizure types, intellectual disability, ataxia, and increased mortality. While all patients with epilepsy are at risk for SUDEP, DS patients may have the highest risk, up to 20%, with a mean age at SUDEP of 4.6 years. Over 80% of DS is caused by de novo heterozygous loss-of-function (LOF) variants in SCN1A, encoding the VGSC Nav1.1  subunit, resulting in haploinsufficiency. A smaller cohort of patients with DS or a more severe DEE have inherited, homozygous LOF variants in SCN1B, encoding the VGSC 1/1B non-pore-forming subunits. A related DEE, Early Infantile EE (EIEE) type 13, is linked to de novo heterozygous gain-of-function variants in SCN8A, encoding the VGSC Nav1.6. VGSCs underlie the rising phase and propagation of action potentials in neurons and cardiac myocytes. SCN1A, SCN8A, and SCN1B are expressed in both the heart and brain of humans and mice. Because of this, we proposed that cardiac arrhythmias contribute to the mechanism of SUDEP in DEE. We have taken a novel approach to the development of therapeutics for DS in collaboration with Stoke Therapeutics. We employed Targeted Augmentation of Nuclear Gene Output (TANGO) technology, which modulates naturally occurring, non-productive splicing events to increase target gene and protein expression and ameliorate disease phenotype in a mouse model. We identified antisense oligonucleotides (ASOs) that specifically increase the expression of productive Scn1a transcript in human and mouse cell lines, as well as in mouse brain. We showed that a single intracerebroventricular dose of a lead ASO at postnatal day 2 or 14 reduced the incidence of electrographic seizures and SUDEP in the F1:129S-Scn1a+/- x C57BL/6J mouse model of DS. Increased expression of productive Scn1a transcript and NaV1.1 protein were confirmed in brains of treated mice. Our results suggest that TANGO may provide a unique, gene-specific approach for the treatment of DS.

Multi-scale synaptic analysis for psychiatric/emotional disorders

Dysregulation of emotional processing and its integration with cognitive functions are central features of many mental/emotional disorders associated both with externalizing problems (aggressive, antisocial behaviors) and internalizing problems (anxiety, depression). As Dr. Joseph LeDoux, our invited speaker of this program, wrote in his famous book “Synaptic self: How Our Brains Become Who We Are”—the brain’s synapses—are the channels through which we think, act, imagine, feel, and remember. Synapses encode the essence of personality, enabling each of us to function as a distinctive, integrated individual from moment to moment. Thus, exploring the functioning of synapses leads to the understanding of the mechanism of (patho)physiological function of our brain. In this context, we have investigated the pathophysiology of psychiatric disorders, with particular emphasis on the synaptic function of model mice of various psychiatric disorders such as schizophrenia, autism, depression, and PTSD. Our current interest is how synaptic inputs are integrated to generate the action potential. Because the spatiotemporal organization of neuronal firing is crucial for information processing, but how thousands of inputs to the dendritic spines drive the firing remains a central question in neuroscience. We identified a distinct pattern of synaptic integration in the disease-related models, in which extra-large (XL) spines generate NMDA spikes within these spines, which was sufficient to drive neuronal firing. We experimentally and theoretically observed that XL spines negatively correlated with working memory. Our work offers a whole new concept for dendritic computation and network dynamics, and the understanding of psychiatric research will be greatly reconsidered. The second half of my talk is the development of a novel synaptic tool. Because, no matter how beautifully we can illuminate the spine morphology and how accurately we can quantify the synaptic integration, the links between synapse and brain function remain correlational. In order to challenge the causal relationship between synapse and brain function, we established AS-PaRac1, which is unique not only because it can specifically label and manipulate the recently potentiated dendritic spine (Hayashi-Takagi et al, 2015, Nature). With use of AS-PaRac1, we developed an activity-dependent simultaneous labeling of the presynaptic bouton and the potentiated spines to establish “functional connectomics” in a synaptic resolution. When we apply this new imaging method for PTSD model mice, we identified a completely new functional neural circuit of brain region A→B→C with a very strong S/N in the PTSD model mice. This novel tool of “functional connectomics” and its photo-manipulation could open up new areas of emotional/psychiatric research, and by extension, shed light on the neural networks that determine who we are.

miRNA dysregulation in embryo results in autism spectrum disorder

Firing Rate Homeostasis in Neural Circuits: From basic principles to malfunctions

Maintaining average activity level within a set-point range constitutes a fundamental property of central neural circuits. Accumulated evidence suggests that firing rate distributions and their means represent physiological variables regulated by homeostatic systems during sleep-wake cycle in central neural circuits. While intracellular Ca2+ has long been hypothesized as a feedback control signal, the source of Ca2+ and the molecular machinery enabling network-wide homeostatic responses remain largely unknown. I will present our hypothesis and framework on identifying homeostatic regulators in neural circuits. Next, I will show our new results on the role of mitochondria in the regulation of activity set-points and feedback responses. Finally, I will provide an evidence on state-dependent dysregulation of activity set-points at the presymptomatic disease stage in familial Alzheimer’s models.

Dysregulation of mTOR Signaling Mediates Common Neurite and Migration Defects in Idiopathic and 16p11.2 Deletion Autism neural progenitors

A metabolic function of the hippocampal sharp wave-ripple

The hippocampal formation has been implicated in both cognitive functions as well as the sensing and control of endocrine states. To identify a candidate activity pattern which may link such disparate functions, we simultaneously measured electrophysiological activity from the hippocampus and interstitial glucose concentrations in the body of freely behaving rats. We found that clusters of sharp wave-ripples (SPW-Rs) recorded from both dorsal and ventral hippocampus reliably predicted a decrease in peripheral glucose concentrations within ~10 minutes. This correlation was less dependent on circadian, ultradian, and meal-triggered fluctuations, it could be mimicked with optogenetically induced ripples, and was attenuated by pharmacogenetically suppressing activity of the lateral septum, the major conduit between the hippocampus and subcortical structures. Our findings demonstrate that a novel function of the SPW-R is to modulate peripheral glucose homeostasis and offer a mechanism for the link between sleep disruption and blood glucose dysregulation seen in type 2 diabetes and obesity.

Unique Molecular Regulation of Prefrontal Cortex Confers Vulnerability to Cognitive Disorders

The Arnsten lab studies molecular influences on the higher cognitive circuits of the dorsolateral prefrontal cortex (dlPFC), in order to understand mechanisms affecting working memory at the cellular and behavioral levels, with the overarching aim of identifying the actions that render the dlPFC so vulnerable in cognitive disorders. Her lab has shown that the dlPFC has unique neurotransmission and neuromodulation compared to the classic actions found in the primary visual cortex, including mechanisms to rapidly weaken PFC connections during uncontrollable stress. Reduced regulation of these stress pathways due to genetic or environmental insults contributes to dlPFC dysfunction in cognitive disorders, including calcium dysregulation and tau phosphorylation in the aging association cortex. Understanding these unique mechanisms has led to the development of a new treatment, IntunivTM, for a variety of PFC disorders.

Neurocircuits in control of integrative physiology

This open colloquia session is part of the special workshop entitled "Obesity at the Interface of Neuroscience and Physiology II". Abstract: Proopiomelanocortin (POMC)- and agouti related peptide (AgRP)-expressing neurons in the arcuate nucleus of the hypothalamus (ARH) are critical regulators of food intake and energy homeostasis. They rapidly integrate the energy state of the organism through sensing fuel availability via hormones, nutrient components and even rapidly upon sensory food perception. Importantly, they not only regulate feeding responses, but numerous autonomic responses including glucose and lipid metabolism, inflammation and blood pressure. More recently, we could demonstrate that sensory food cue-dependent regulation of POMC neurons primes the hepatic endoplasmic reticulum (ER) stress response to prime liver metabolism for the postpramndial state. The presentation will focus on the regulation of these neurons in control of integrative physiology, the identification of distinct neuronal circuitries targeted by these cells and finally on the broad range implications resulting from dysregulation of these circuits as a consequence of altered maternal metabolism.

Molecular controls over corticospinal neuron axon branching at specific spinal segments

Corticospinal neurons (CSN) are the cortical projection neurons that innervate the spinal cord and some brainstem targets with segmental precision to control voluntary movement of specific functional motor groups, limb sections, or individual digits, yet molecular regulation over CSN segmental target specificity is essentially unknown. CSN subpopulations exhibit striking axon targeting specificity from development into maturity: Evolutionarily newer rostrolateral CSN exclusively innervate bulbar-cervical targets (CSNBC-lat), while evolutionarily older caudomedial CSN (CSNmed) are more heterogeneous, with distinct subpopulations extending axons to either bulbar-cervical or thoraco-lumbar segments. The cervical cord, with its evolutionarily enhanced precision of forelimb movement, is innervated by multiple CSN subpopulations, suggesting inter-neuronal interactions in establishing corticospinal connectivity. I identify that Lumican, previously unrecognized in axon development, controls the specificity of cervical spinal cord innervation by CSN. Remarkably, Lumican, an extracellular matrix protein expressed by CSNBC-lat, non-cell-autonomously suppresses axon collateralization in the cervical cord by CSNmed. Intersectional viral labeling and mouse genetics further identify that Lumican controls axon collateralization by multiple subpopulations in caudomedial sensorimotor cortex. These results identify inter-axonal molecular crosstalk between CSN subpopulations as a novel mechanism controlling corticospinal connectivity and competitive specificity. Further, this mechanism has potential implications for evolutionary diversification of corticospinal circuitry with finer scale precision. "" Complementing this work, to comprehensively elucidate related axon projection mechanisms functioning at tips of growing CSN axons in vivo, I am currently applying experimental and analytic approaches recently developed in my postdoc lab (Poulopoulos*, Murphy*, Nature, 2019) to quantitatively and subcellularly “map” RNA and protein molecular machinery of subtype-specific growth cones, in parallel to their parent somata, isolated directly in vivo from developing subcerebral projection neurons (SCPN; the broader cortical output neuron population targeting both brainstem and spinal cord; includes CSN). I am investigating both normal development and GC-soma dysregulation with mutation of central CSN-SCPN transcriptional regulator Ctip2/Bcl11b.

Transposable element activation in Alzheimer's disease and related tauopathies

Transposable elements, known colloquially as ‘jumping genes’, constitute approximately 45% of the human genome. Cells utilize epigenetic defenses to limit transposable element jumping, including formation of silencing heterochromatin and generation of piwi-interacting RNAs (piRNAs), small RNAs that facilitate clearance of transposable element transcripts. We have utilized fruit flies, mice and postmortem human brain samples to identify transposable element dysregulation as a key mediator of neuronal death in tauopathies, a group of neurodegenerative disorders that are pathologically characterized by deposits of tau protein in the brain. Mechanistically, we find that heterochromatin decondensation and reduction of piwi and piRNAs drive transposable element dysregulation in tauopathy. We further report a significant increase in transcripts of the endogenous retrovirus class of transposable elements in human Alzheimer’s disease and progressive supranuclear palsy, suggesting that transposable element dysregulation is conserved in human tauopathy. Taken together, our data identify heterochromatin decondensation, piwi and piRNA depletion and consequent transposable element dysregulation as a pharmacologically targetable, mechanistic driver of neurodegeneration in tauopathy.

Mechanisms of pathogenesis in the tauopathies

The distribution of pathological tau in the brain of patients with AD is highly predicable, and as disease worsens, it spreads transynaptically from initial regions of vulnerability. The reason why only some neurons are vulnerable to the accumulation and propagation of pathological forms of tau, and the mechanisms by which tauopathy spreads through the brain are not well understood. Using a combination of immunohistochemistry and computational analysis we have examined pathway differences between vulnerable and resistant neurons. How tau spreads across a synapse has been examined in vitro using different model systems. Our data show that dysregulation of tau homeostasis determines the cellular and regional vulnerability of specific neurons to tau pathology (H. Fu et al. 2019. Nat. Neuro. 22 (1):47-56) and that deficits in tau homeostasis can exacerbate tau accumulation and propagation. Aging appears to impact similar neuronal populations. Mechanisms and consequences of abnormal tau accumulation within neurons, its transfer between cells, pathology propagation and therapeutic opportunities will be discussed.

DYSREGULATION OF SK AND KV2.1 POTASSIUM CHANNELS ACROSS BRAIN REGIONS IN THE RNLS8 MOUSE MODEL OF ALS-FTD

FENS Forum 2026

EXPLORING NEUROBIOLOGICAL FACTORS UNDERLYING RISK AND RESILIENCY FOR EMOTIONAL DYSREGULATION AND THE THERAPEUTIC POTENTIAL OF FECAL MICROBIOTA TRANSPLANTATION IN ANIMALS PRENATALLY EXPOSED TO ALCOHOL

FENS Forum 2026

TECPR2 DEFICIENCY INDUCES AXONAL AUTOPHAGY DYSREGULATION IN HEREDITARY SENSORY AND AUTONOMIC NEUROPATHY TYPE IX

FENS Forum 2026

CIRCUIT-SPECIFIC ACTIVATION OF THE DORSAL CA1 - MPFC PATHWAY AS A MECHANISM FOR DOPAMINE DYSREGULATION IN SCHIZOPHRENIA RELEVANT BEHAVIORS

FENS Forum 2026

MEMBRANE DISRUPTION OF THE GANGLIOSIDE-NEUROPLASTIN-PMCA NETWORK DRIVES CALCIUM DYSREGULATION IN GLIOBLASTOMA

FENS Forum 2026

ENDOCANNABINOID DYSREGULATION CONTRIBUTES TO COGNITIVE IMPAIRMENT AND MYELINATION DEFICITS IN AN EXPERIMENTAL MODEL OF FASD

FENS Forum 2026

CHARACTERIZATION OF A TRANSLATIONAL MOUSE MODEL OF STROKE INTEGRATING ATHEROSCLEROSIS AND CHRONIC NEUROIMMUNE DYSREGULATION

FENS Forum 2026

SELECTIVE VULNERABILITY OF HIPPOCAMPAL PRINCIPAL CELLS ASSOCIATED WITH EXTRASYNAPTIC Δ-GABAA RECEPTOR DYSREGULATION IN ALZHEIMER’S DISEASE

FENS Forum 2026

MODELING MTOR PATHWAY DYSREGULATION IN PATIENT-DERIVED NEURONS

FENS Forum 2026

VASCULAR DYSREGULATION AND BLOOD-BRAIN BARRIER IMPAIRMENT IN A MURINE MODEL OF NEURODEGENERATION

FENS Forum 2026

BDNF RECEPTOR DYSREGULATION IN ALZHEIMER'S-DISEASE: EXTRACELLULAR VESICLE-MEDIATED TRANSPORT OF A SYNAPTOTOXIC TRKB FRAGMENT

FENS Forum 2026

LONG-LASTING GLUCOCORTICOID AND IMMUNE DYSREGULATION SUSTAIN ANOREXIA NERVOSA BEYOND WEIGHT RECOVERY

FENS Forum 2026

DYSREGULATION OF THE AGRP–PVH CIRCUIT DISRUPTS SYMPATHETIC CONTROL OF BONE MARROW IN EXPERIMENTAL MULTIPLE SCLEROSIS

FENS Forum 2026

DIO2 POLYMORPHISM AS A LESS-INVASIVE PERIPHERAL BIOMARKER INDEXING BRAIN THYROID HORMONE DYSREGULATION IN SCHIZOPHRENIA

FENS Forum 2026

DYSREGULATION OF LIPID HANDLING AND NEURONAL ACTIVITY-DEPENDENT GENES IN HIPPOCAMPUS OF PRECLINICAL MODELS OF DIABETES

FENS Forum 2026

SMALL NON-CODING RNA DYSREGULATION IN THE MICROGLIA FROM A MOUSE MODEL OF DOWN SYNDROME

FENS Forum 2026

CHARACTERIZATION OF NOGO-A–MEDIATED MECHANISMS UNDERLYING DOPAMINERGIC AND MITOCHONDRIAL DYSREGULATION IN AN IPSC-DERIVED PARKINSON’S DISEASE MODEL

FENS Forum 2026

DYSREGULATION OF THE TRYPTOPHAN-KYNURENINE PATHWAY AND ITS IMPLICATIONS FOR SEIZURE SUSCEPTIBILITY IN TEMPORAL LOBE EPILEPSY

FENS Forum 2026

DYSREGULATION OF JANUS KINASE- AND MICROTUBULE-INTERACTING PROTEIN 1 (JAKMIP1) IS ASSOCIATED WITH ALTERED STAT3 SIGNALLING, SOMATOSENSORY CORTICAL HYPEREXCITABILITY, AND AUTISM-LIKE BEHAVIOURS

FENS Forum 2026

FROM MITOCHONDRIA TO MOTOR NEURONS FAILURE : MITOPHAGY DYSREGULATION IN <EM>CHCHD10</EM>-ASSOCIATED AMYOTROPHIC LATERAL SCLEROSIS &AMP; FRONTOTEMPORAL DEMENTIA

FENS Forum 2026

DYRK1A OVEREXPRESSION INCREASES NORADRENERGIC TONE AND IMPAIRS CONTEXTUAL MEMORY THROUGH LOCUS COERULEUS DYSREGULATION IN BAC-DYRK1A MICE

FENS Forum 2026

CBP HAPLOINSUFFICIENCY LEADS TO AGE-RELATED SOCIAL DEFICITS AND HIPPOCAMPAL TRANSCRIPTOMIC AND EPIGENOMIC DYSREGULATION

FENS Forum 2026

CENTRAL REDOX DYSREGULATION AND MITOCHONDRIAL STRESS IN FATAL COVID-19 SEPSIS: A POSTMORTEM CSF STUDY

FENS Forum 2026

THC DISRUPTS MEMORY CONSOLIDATION VIA GLUTAMATERGIC DYSREGULATION IN THE HIPPOCAMPAL CA1 REGION

FENS Forum 2026

MAPPING SEX‑SPECIFIC SENSORY–PSYCHOMOTOR DYSREGULATION IN A NEURONAL GROWTH REGULATOR 1 (NEGR1) KNOCKOUT MICE

FENS Forum 2026

PTEN LOSS IN MATURE DENTATE GYRUS GRANULE CELLS DISRUPTS CIRCUIT COMPUTATION AN DRIVES EPILEPSY THROUGH COMPARTMENTALIZED DYSREGULATION OF MTOR/ERK SIGNALING

FENS Forum 2026

NKCC1 INHIBITION PREVENTS DYSREGULATION OF STRESS AND INFLAMMATORY SIGNALING, INTERGENERATIONAL BRAIN-GUT-MICROBIOTA AXIS DISRUPTION AND BEHAVIORAL ABNORMALITIES FOLLOWING MATERNAL PRECONCEPTION TBI

FENS Forum 2026

ROLE OF ASTROCYTIC TRPA1 IN CALCIUM DYSREGULATION UNDER PATHOLOGICAL CONDITIONS

FENS Forum 2026

FLAV-27 COUNTERACTS TRANSCRIPTIONAL DYSREGULATION AND FERROPTOSIS SUSCEPTIBILITY IN HUNTINGTON’S DISEASE MODELS BY REPROGRAMMING H3K9ME2 EPIGENETICS

FENS Forum 2026

INVESTIGATING LIPID DYSREGULATION ACROSS <EM>APOE4 </EM>GLIAL CELL-TYPES AND DRUG CANDIDATES FOR RESCUING LIPID PATHOLOGY

FENS Forum 2026

SYNAPTIC MIRNA DYSREGULATION IN ALZHEIMER’S DISEASE HUMAN TISSUE

FENS Forum 2026

DECIPHERING AUTONOMIC DYSREGULATION IN EPILEPSY THROUGH VAGUS NERVE ACTIVITY

FENS Forum 2026

MOLECULAR PROFILING OF MICROGLIA-ASTROCYTE CROSSTALK IN C9ORF72 ALS/FTD REVEALS DYSREGULATION OF CRITICAL SIGNALING PATHWAYS

FENS Forum 2026

MONOAMINERGIC AND TRYPTOPHAN PATHWAY DYSREGULATION UNDERLIES EARLY ANHEDONIC-LIKE BEHAVIOR IN EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS

FENS Forum 2026

CONVERGENT DYSREGULATION OF THE UBIQUITIN PROTEASOME SYSTEM IN <EM>FMR1</EM><SUP>-/Y</SUP> RATS

FENS Forum 2026

DIFFERENTIAL ROLE OF NEURONAL AND ASTROGLIAL TRPV4 CHANNELS IN CELLULAR VOLUME AND ION DYSREGULATION DURING ENERGY DEPRIVATION

FENS Forum 2026

LOSS OF FUNCTION OF <EM>MECP2</EM> LEADS TO PUBERTAL DYSREGULATION AND ALTERED VASOPRESSINERGIC CIRCUITS IN A MOUSE MODEL OF RETT SYNDROME

FENS Forum 2026

Chloride dysregulation underlies cognitive deficits associated with Alzheimer’s disease-related mutations in mice

Connecting metabolics and epigenetics dysregulations in Huntington’s disease

Dopamine dysregulation syndrome in a mouse model of Parkinson’s disease