disease

Convergent large-scale network and local vulnerabilities underlie brain atrophy across Parkinson’s disease stages

The tubulin code in neuron health and disease : focus on detyrosination

Cellular Crosstalk in Brain Development, Evolution and Disease

Cellular crosstalk is an essential process during brain development and is influenced by numerous factors, including cell morphology, adhesion, the local extracellular matrix and secreted vesicles. Inspired by mutations associated with neurodevelopmental disorders, we focus on understanding the role of extracellular mechanisms essential for the proper development of the human brain. Therefore, we combine 2D and 3D in vitro human models to better understand the molecular and cellular mechanisms involved in progenitor proliferation and fate, migration and maturation of excitatory and inhibitory neurons during human brain development and tackle the causes of neurodevelopmental disorders.

Cause & Consequences of neuronal Tau protein ‘activation’

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.

Expanding mechanisms and therapeutic targets for neurodegenerative disease

A hallmark pathological feature of the neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) is the depletion of RNA-binding protein TDP-43 from the nucleus of neurons in the brain and spinal cord. A major function of TDP-43 is as a repressor of cryptic exon inclusion during RNA splicing. By re-analyzing RNA-sequencing datasets from human FTD/ALS brains, we discovered dozens of novel cryptic splicing events in important neuronal genes. Single nucleotide polymorphisms in UNC13A are among the strongest hits associated with FTD and ALS in human genome-wide association studies, but how those variants increase risk for disease is unknown. We discovered that TDP-43 represses a cryptic exon-splicing event in UNC13A. Loss of TDP-43 from the nucleus in human brain, neuronal cell lines and motor neurons derived from induced pluripotent stem cells resulted in the inclusion of a cryptic exon in UNC13A mRNA and reduced UNC13A protein expression. The top variants associated with FTD or ALS risk in humans are located in the intron harboring the cryptic exon, and we show that they increase UNC13A cryptic exon splicing in the face of TDP-43 dysfunction. Together, our data provide a direct functional link between one of the strongest genetic risk factors for FTD and ALS (UNC13A genetic variants), and loss of TDP-43 function. Recent analyses have revealed even further changes in TDP-43 target genes, including widespread changes in alternative polyadenylation, impacting expression of disease-relevant genes (e.g., ELP1, NEFL, and TMEM106B) and providing evidence that alternative polyadenylation is a new facet of TDP-43 pathology.

The cellular phase of Alzheimer’s Disease and the path towards therapies

Unlocking the Secrets of Microglia in Neurodegenerative diseases: Mechanisms of resilience to AD pathologies

Dark Matter in the Locus coeruleus - Neuromelanin in Health and Disease

An inconvenient truth: pathophysiological remodeling of the inner retina in photoreceptor degeneration

Photoreceptor loss is the primary cause behind vision impairment and blindness in diseases such as retinitis pigmentosa and age-related macular degeneration. However, the death of rods and cones allows retinoids to permeate the inner retina, causing retinal ganglion cells to become spontaneously hyperactive, severely reducing the signal-to-noise ratio, and creating interference in the communication between the surviving retina and the brain. Treatments aimed at blocking or reducing hyperactivity improve vision initiated from surviving photoreceptors and could enhance the signal fidelity generated by vision restoration methodologies.

Impact of High Fat Diet on Central Cardiac Circuits: When The Wanderer is Lost

Cardiac vagal motor drive originates in the brainstem's cardiac vagal motor neurons (CVNs). Despite well-established cardioinhibitory functions in health, our understanding of CVNs in disease is limited. There is a clear connection of cardiovascular regulation with metabolic and energy expenditure systems. Using high fat diet as a model, this talk will explore how metabolic dysfunction impacts the regulation of cardiac tissue through robust inhibition of CVNs. Specifically, it will present an often overlooked modality of inhibition, tonic gamma-aminobuytric acid (GABA) A-type neurotransmission using an array of techniques from single cell patch clamp electrophysiology to transgenic in vivo whole animal physiology. It also will highlight a unique interaction with the delta isoform of protein kinase C to facilitate GABA A-type receptor expression.

Genetic Analysis of Alzheimer's disease from mechanism to therapies (with some analogies to other diseases)

Constructing and deconstructing the human nervous system to study development and disease

Pharmacological exploitation of neurotrophins and their receptors to develop novel therapeutic approaches against neurodegenerative diseases and brain trauma

Neurotrophins (NGF, BDNF, NT-3) are endogenous growth factors that exert neuroprotective effects by preventing neuronal death and promoting neurogenesis. They act by binding to their respective high-affinity, pro-survival receptors TrkA, TrkB or TrkC, as well as to p75NTR death receptor. While these molecules have been shown to significantly slow or prevent neurodegeneration, their reduced bioavailability and inability to penetrate the blood-brain-barrier limit their use as potential therapeutics. To bypass these limitations, our research team has developed and patented small-sized, lipophilic compounds which selectively resemble neurotrophins’ effects, presenting preferable pharmacological properties and promoting neuroprotection and repair against neurodegeneration. In addition, the combination of these molecules with 3D cultured human neuronal cells, and their targeted delivery in the brain ventricles through soft robotic systems, could offer novel therapeutic approaches against neurodegenerative diseases and brain trauma.

The synaptic functions of Alpha Synuclein and Lrrk2

Alpha synuclein and Lrrk2 are key players in Parkinson's disease and related disorders, but their normal role has been confusing and controversial. Data from acute gene-editing based knockdown, followed by functional assays, will be presented.

Defining Molecular Mechanisms Underlying Neurodegenerative Diseases

Rett syndrome, MECP2 and therapeutic strategies

The development of the iPS cell technology has revolutionized our ability to study development and diseases in defined in vitro cell culture systems. The talk will focus on Rett Syndrome and discuss two topics: (i) the use of gene editing as an approach to therapy and (ii) the role of MECP2 in gene expression (i) The mutation of the X-linked MECP2 gene is causative for the disease. In a female patient, every cell has a wt copy that is, however, in 50% of the cells located on the inactive X chromosome. We have used epigenetic gene editing tools to activate the wt MECP2 allele on the inactive X chromosome. (ii) MECP2 is thought to act as repressor of gene expression. I will present data which show that MECP2 binds to Pol II and acts as an activator for thousands of genes. The target genes are significantly enriched for Autism related genes. Our data challenge the established model of MECP2’s role in gene expression and suggest novel therapeutic approaches.

Genetic and epigenetic underpinnings of neurodegenerative disorders

Pluripotent cells, including embryonic stem (ES) and induced pluripotent stem (iPS) cells, are used to investigate the genetic and epigenetic underpinnings of human diseases such as Parkinson’s, Alzheimer’s, autism, and cancer. Mechanisms of somatic cell reprogramming to an embryonic pluripotent state are explored, utilizing patient-specific pluripotent cells to model and analyze neurodegenerative diseases.

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

Brain-on-a-Chip: Advanced In Vitro Platforms for Drug Screening and Disease Modeling

Virtual and experimental approaches to the pathogenicity of SynGAP1 missense mutations

Targeting gamma oscillations to improve cognition

The molecular basis of prion diseases

How the brain barriers ensure CNSimmune privilege”

Britta Engelhard’s research is devoted to understanding thefunction of the different brain barriers in regulating CNS immunesurveillance and how their impaired function contributes toneuroinflammatory diseases such as Multiple Sclerosis (MS) orAlzheimer’s disease (AD). Her laboratory combines expertise invascular biology, neuroimmunology and live cell imaging and hasdeveloped sophisticated in vitro and in vivo approaches to studyimmune cell interactions with the brain barriers in health andneuroinflammation.

Prosocial Learning and Motivation across the Lifespan

2024 BACN Early-Career Prize Lecture Many of our decisions affect other people. Our choices can decelerate climate change, stop the spread of infectious diseases, and directly help or harm others. Prosocial behaviours – decisions that help others – could contribute to reducing the impact of these challenges, yet their computational and neural mechanisms remain poorly understood. I will present recent work that examines prosocial motivation, how willing we are to incur costs to help others, prosocial learning, how we learn from the outcomes of our choices when they affect other people, and prosocial preferences, our self-reports of helping others. Throughout the talk, I will outline the possible computational and neural bases of these behaviours, and how they may differ from young adulthood to old age.

The cell biology of Parkinson’s disease: a role for primary cilia and synaptic vesicle pleomorphism in dopaminergic neurons

SYNGAP1 Natural History Study/ Multidisciplinary Clinic at Children’s Hospital Colorado

Personalized medicine and predictive health and wellness: Adding the chemical component

Wearable sensors that detect and quantify biomarkers in retrievable biofluids (e.g., interstitial fluid, sweat, tears) provide information on human dynamic physiological and psychological states. This information can transform health and wellness by providing actionable feedback. Due to outdated and insufficiently sensitive technologies, current on-body sensing systems have capabilities limited to pH, and a few high-concentration electrolytes, metabolites, and nutrients. As such, wearable sensing systems cannot detect key low-concentration biomarkers indicative of stress, inflammation, metabolic, and reproductive status.  We are revolutionizing sensing. Our electronic biosensors detect virtually any signaling molecule or metabolite at ultra-low levels. We have monitored serotonin, dopamine, cortisol, phenylalanine, estradiol, progesterone, and glucose in blood, sweat, interstitial fluid, and tears. The sensors are based on modern nanoscale semiconductor transistors that are straightforwardly scalable for manufacturing. We are developing sensors for >40 biomarkers for personalized continuous monitoring (e.g., smartwatch, wearable patch) that will provide feedback for treating chronic health conditions (e.g., perimenopause, stress disorders, phenylketonuria). Moreover, our sensors will enable female fertility monitoring and the adoption of more healthy lifestyles to prevent disease and improve physical and cognitive performance.

Beyond the synapse: SYNGAP1 in primary and motile cilia

The Roles of Distinct Functions of SynGAP1 in SYNGAP1-Related Disorders

Investigating dynamiCa++l mechanisms underlying cortical development and disease

Use of human systems for neuroinflammatory/neurodegenerative diseases

Modeling human brain development and disease: the role of primary cilia

Neurodevelopmental disorders (NDDs) impose a global burden, affecting an increasing number of individuals. While some causative genes have been identified, understanding the human-specific mechanisms involved in these disorders remains limited. Traditional gene-driven approaches for modeling brain diseases have failed to capture the diverse and convergent mechanisms at play. Centrosomes and cilia act as intermediaries between environmental and intrinsic signals, regulating cellular behavior. Mutations or dosage variations disrupting their function have been linked to brain formation deficits, highlighting their importance, yet their precise contributions remain largely unknown. Hence, we aim to investigate whether the centrosome/cilia axis is crucial for brain development and serves as a hub for human-specific mechanisms disrupted in NDDs. Towards this direction, we first demonstrated species-specific and cell-type-specific differences in the cilia-genes expression during mouse and human corticogenesis. Then, to dissect their role, we provoked their ectopic overexpression or silencing in the developing mouse cortex or in human brain organoids. Our findings suggest that cilia genes manipulation alters both the numbers and the position of NPCs and neurons in the developing cortex. Interestingly, primary cilium morphology is disrupted, as we find changes in their length, orientation and number that lead to disruption of the apical belt and altered delamination profiles during development. Our results give insight into the role of primary cilia in human cortical development and address fundamental questions regarding the diversity and convergence of gene function in development and disease manifestation. It has the potential to uncover novel pharmacological targets, facilitate personalized medicine, and improve the lives of individuals affected by NDDs through targeted cilia-based therapies.

Activity-Dependent Gene Regulation in Health and Disease

In the last of this year’s Brain Prize webinars, Elizabeth Pollina (Washington University, USA), Eric Nestler (Icahn School of Medicine Mount Sinai, USA) and Michelle Monje (Stanford University, USA) will present their work on activity-dependent gene regulation in health and disease. Each speaker will present for 25 minutes, and the webinar will conclude with an open discussion. The webinar will be moderated by the winners of the 2023 Brain Prize, Michael Greenberg, Erin Schuman and Christine Holt.

Investigating activity-dependent processes during cortical neuronal assembly in development and disease

Cortical interneurons from brain development to disease

Dysfunctional translation in disease

In the fifth of this year’s Brain Prize webinars, Emily Osterweil (Harvard Medical School, USA), Gary Bassell (Emory University, USA) and Giovanna Mallucci (Altos Labs, UK) will present their work on dysfunctional translation in disease. Each speaker will present for 25 minutes, and the webinar will conclude with an open discussion. The webinar will be moderated by two of the winners of the 2023 Brain Prize, Michael Greenberg and Erin Schuman.

Alpha synuclein in parkinson's Disease: From the bedside to the bench and back again

From rare Genetic cohorts of Parkinsonism to biomarkers and to understanding broader neurodegenerative disease mechanisms

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.

Connectome-based models of neurodegenerative disease

Neurodegenerative diseases involve accumulation of aberrant proteins in the brain, leading to brain damage and progressive cognitive and behavioral dysfunction. Many gaps exist in our understanding of how these diseases initiate and how they progress through the brain. However, evidence has accumulated supporting the hypothesis that aberrant proteins can be transported using the brain’s intrinsic network architecture — in other words, using the brain’s natural communication pathways. This theory forms the basis of connectome-based computational models, which combine real human data and theoretical disease mechanisms to simulate the progression of neurodegenerative diseases through the brain. In this talk, I will first review work leading to the development of connectome-based models, and work from my lab and others that have used these models to test hypothetical modes of disease progression. Second, I will discuss the future and potential of connectome-based models to achieve clinically useful individual-level predictions, as well as to generate novel biological insights into disease progression. Along the way, I will highlight recent work by my lab and others that is already moving the needle toward these lofty goals.

Gut/Body interactions in health and disease

The adult intestine is a major barrier epithelium and coordinator of multi-organ functions. Stem cells constantly repair the intestinal epithelium by adjusting their proliferation and differentiation to tissue intrinsic as well as micro- and macro-environmental signals. How these signals integrate to control intestinal and whole-body homeostasis is largely unknown. Addressing this gap in knowledge is central to an improved understanding of intestinal pathophysiology and its systemic consequences. Combining Drosophila and mammalian model systems my laboratory has discovered fundamental mechanisms driving intestinal regeneration and tumourigenesis and outlined complex inter-organ signaling regulating health and disease. During my talk, I will discuss inter-related areas of research from my lab, including:1- Interactions between the intestine and its microenvironment influencing intestinal regeneration and tumourigenesis. 2- Long-range signals from the intestine impacting whole-body in health and disease.

Effects of Presenilin1 FAD mutants on brain angiogenic functions and neuroprotection in Alzheimer’s Disease

Circadian modulation by time-restricted feeding rescues brain pathology and improves memory in mouse models of Alzheimer’s disease

Metabolic Remodelling in the Developing Forebrain in Health and Disease

Little is known about the critical metabolic changes that neural cells have to undergo during development and how temporary shifts in this program can influence brain circuitries and behavior. Motivated by the identification of autism-associated mutations in SLC7A5, a transporter for metabolically essential large neutral amino acids (LNAAs), we utilized metabolomic profiling to investigate the metabolic states of the cerebral cortex across various developmental stages. Our findings reveal significant metabolic restructuring occurring in the forebrain throughout development, with specific groups of metabolites exhibiting stage-specific changes. Through the manipulation of Slc7a5 expression in neural cells, we discovered an interconnected relationship between the metabolism of LNAAs and lipids within the cortex. Neuronal deletion of Slc7a5 influences the postnatal metabolic state, resulting in a shift in lipid metabolism and a cell-type-specific modification in neuronal activity patterns. This ultimately gives rise to enduring circuit dysfunction.

From primate anatomy to human neuroimaging: insights into the circuits underlying psychiatric disease and neuromodulation; Large-scale imaging of neural circuits: towards a microscopic human connectome

On Thursday, October 26th, we will host Anastasia Yendiki and Suzanne Haber. Anastasia Yendiki, PhD, is an Associate Professor in Radiology at the Harvard Medical School and an Associate Investigator at the Massachusetts General Hospital and Athinoula A. Martinos Center. Suzanne Haber, PhD, is a Professor at the University of Rochester and runs a lab at McLean hospital at Harvard Medical School in Boston. She has received numerous awards for her work on neuroanatomy. Beside her scientific presentation, she 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!

Neuroinflammation in Epilepsy: what have we learned from human brain tissue specimens ?

Epileptogenesis is a gradual and dynamic process leading to difficult-to-treat seizures. Several cellular, molecular, and pathophysiologic mechanisms, including the activation of inflammatory processes.  The use of human brain tissue represents a crucial strategy to advance our understanding of the underlying neuropathology and the molecular and cellular basis of epilepsy and related cognitive and behavioral comorbidities,  The mounting evidence obtained during the past decade has emphasized the critical role of inflammation  in the pathophysiological processes implicated in a large spectrum of genetic and acquired forms of  focal epilepsies. Dissecting the cellular and molecular mediators of  the pathological immune responses and their convergent and divergent mechanisms, is a major requisite for delineating their role in the establishment of epileptogenic networks. The role of small regulatory molecules involved in the regulation of  specific pro- and anti-inflammatory pathways  and the crosstalk between neuroinflammation and oxidative stress will be addressed.    The observations supporting the activation of both innate and adaptive immune responses in human focal epilepsy will be discussed and elaborated, highlighting specific inflammatory pathways as potential targets for antiepileptic, disease-modifying therapeutic strategies.

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.

Spatial and Single Cell Genomics for Next Generation Neuroscience

The advent of next generation sequencing ushered in a ten-year period of exuberant technology development, enabling the quantification of gene expression and epigenetic features within individual cells, and within intact tissue sections.  In this seminar, I will outline our technological contributions, beginning with the development of Drop-seq, a method for high-throughput single cell analysis, followed by the development of Slide-seq, a technique for measuring genome-wide expression at 10 micron spatial resolution.  Using a combination of these techniques, we recently constructed a comprehensive cell type atlas of the adult mouse brain, positioning cell types within individual brain structures.  I will discuss the major findings from this dataset, including emerging principles of neurotransmission, and the localization of disease gene signatures to specific cell types.  Finally, I will introduce a new spatial technology, Slide-tags, that unifies single cell and spatial genomics into a single, highly scalable assay.

How Intermittent Bioenergetic Challenges Enhance Brain and Body Health

Humans and other animals evolved in habitats fraught with a range of environmental challenges to their bodies and brains. Accordingly, cells and organ systems possess adaptive stress-responsive signaling pathways that enable them to not only withstand environmental challenges, but also to prepare for future challenges and function more efficiently. These phylogenetically conserved processes are the foundation of the hormesis principle in which repeated exposures to low to moderate amounts of an environmental challenge improve cellular and organismal fitness. Here I describe cellular and molecular mechanisms by which cells in the brain and body respond to intermittent fasting and exercise in ways that enhance performance and counteract aging and disease processes. Switching back and forth between adaptive stress response (during fasting and exercise) and growth and plasticity (eating, resting, sleeping) modes enhances the performance and resilience of various organ systems. While pharmacological interventions that engage a particular hormetic mechanism are being developed, it seems unlikely that any will prove superior to fasting and exercise.

ASTROCYTE-NEURON INTERACTIONS ARE PROTECTIVE AGAINST SYNAPSE LOSS IN AN EX VIVO MODEL OF EARLY-STAGE OF ALZHEIMER’S DISEASE

FENS Forum 2026

​SEVERE PARKINSON'S DISEASE DRIVEN ​BY <EM>SNCA </EM>TRIPLICATION: ​PLATELET AND BLOOD ​EXPRESSION REVEAL SYSTEMIC INVOLVEMENT

FENS Forum 2026

NEGATIVE ALLOSTERIC MODULATORS OF Α5 GABA TYPE A RECEPTORS CAN PREVENT Β-AMYLOID-INDUCED PATHOLOGY IN AN <EM >EX VIVO </EM>MODEL OF ALZHEIMER’S DISEASE

FENS Forum 2026

CEREBELLAR AND HIPPOCAMPAL AMMONIA ELEVATION ACROSS LIVER DISEASE STAGES: IMPLICATION OF GLUTAMINASE

FENS Forum 2026

CANNABIDIOL IN ALZHEIMER’S DISEASE: A MULTI-TARGET APPROACH TO PATHOLOGY AND COGNITIVE DYSFUNCTION

FENS Forum 2026

MICROGLIA GABA<SUB>B1</SUB> SIGNALING LINKS PARVALBUMIN INTERNEURON HYPERACTIVITY TO SYNAPTIC PATHOLOGY IN ALZHEIMER DISEASE

FENS Forum 2026

MICROGLIAL STRUCTURAL SIMPLIFICATION AROUND AMYLOID PLAQUES LINKED TO MEMBRANE LOSS IN AN ALZHEIMER’S DISEASE MOUSE MODEL

FENS Forum 2026

<EM>CIRCHTT(2,3,4,5,6)</EM> REGULATES PROTEIN TRANSLATION, MODULATING HUNTINGTON`S DISEASE PHENOTYPES

FENS Forum 2026

TRANSIENT ACTIVATION OF HIPPOCAMPAL PV NEURONS INDUCES LONG-LASTING COGNITIVE RESCUE IN A MOUSE MODEL OF ALZHEIMER’S DISEASE

FENS Forum 2026

EVALUATING DIAGNOSTIC TOOL PERFORMANCE AND SEX-SPECIFIC NEUROPSYCHIATRIC DIFFERENCES IN PARKINSON’S DISEASE IN TAIWAN

FENS Forum 2026

DEVELOPING NOSE-TO-BRAIN DELIVERY OF AAV2-MEDIATED GENE-THERAPY FOR NEURODEGENERATIVE DISEASES

FENS Forum 2026

HYPOXIA AS POTENTIAL REGULATOR OF INFLAMMATION IN PARKINSON’S DISEASE

FENS Forum 2026

REGIONAL VULNERABILITY OF WHITE MATTER MICROSTRUCTURE IN EARLY ALZHEIMER’S DISEASE: EVIDENCE FROM 5XFAD MICE

FENS Forum 2026

UNRAVELING THE LINK BETWEEN CIRCADIAN RHYTHM-NEURAL ACTIVITY AND ALZHEIMER’S DISEASE WITH HUMAN CORTICAL ORGANOID MODELS

FENS Forum 2026

NEUROPHYSIOLOGICALLY REALISTIC ENVIRONMENT FOR COMPARING ADAPTIVE DEEP BRAIN STIMULATION ALGORITHMS IN PARKINSON'S DISEASE

FENS Forum 2026

<STRONG STYLE="">PHARMACOLOGICAL TARGETING OF MICROGLIAL REACTIVITY IN PRECLINICAL MODEL OF PARKINSON´S DISEASE</STRONG>

FENS Forum 2026

ENGINEERING A MULTICELLULAR NEUROIMMUNE COMPETENT HUMAN BRAIN ORGANOID MODEL FOR ALZHEIMER’S DISEASE

FENS Forum 2026

VOLTAGE-GATED CALCIUM CHANNELS AS A POSSIBLE NEW APPROACH FOR NEURODEGENERATIVE DISEASES

FENS Forum 2026

CANNABIDIOL PREVENTS COGNITIVE AND SOCIAL DEFICITS AND REDUCES NEUROINFLAMMATION IN A RAT MODEL OF ALZHEIMER’S DISEASE

FENS Forum 2026

CELL-DEPENDENT SYNAPTIC PLASTICITY ALTERATION IN THE SUBICULUM AT AN EARLY STAGE OF ALZHEIMER'S DISEASE

FENS Forum 2026

SV2A <EM >IN VIVO</EM>-POSTMORTEM CORRELATION: UTILISING HIGH-RESOLUTION ARRAY TOMOGRAPHY TO VALIDATE SV2A PET AS A BIOMARKER FOR SYNAPSE DENSITY IN ALZHEIMER'S DISEASE

FENS Forum 2026

TARGETING VNUT: NEW INSIGHTS INTO BIOMARKER DISCOVERY AND THERAPY IN ALZHEIMER’S DISEASE

FENS Forum 2026

H3K4ME1 AND H3K4ME3 EPIGENETIC MODULATION OF MICROGLIA IN PARKINSON’S DISEASE: IMPLICATIONS FOR DOPAMINERGIC NEURODEGENERATION

FENS Forum 2026

MICROGLIA INTEGRATION ACCELERATES PATHOLOGICAL PHENOTYPES IN A HUMAN MULTICELLULAR BRAIN ORGANOID MODEL OF ALZHEIMER’S DISEASE (AD HMBO)

FENS Forum 2026

WASTEOSOME BURDEN IN THE HUMAN BRAIN SUGGESTS CHRONIC GLYMPHATIC INSUFFICIENCY IN NEURODEGENERATIVE DISEASES

FENS Forum 2026

A COMPARATIVE STUDY ON THE EFFECTS OF "ANTI-PD GRANULES" AND PROBIOTICS ON THE INTESTINAL FLORA OF PARKINSON'S DISEASE MODEL MICE

FENS Forum 2026

​ANALYSIS OF THE EFFECT OF A MUTANT VARIANT OF E2F4 IN OLIGODENDROCYTES IN A MOUSE MODEL OF ALZHEIMER´S DISEASE

FENS Forum 2026

DISRUPTION OF VISUAL CORTICO-STRIATAL ENSEMBLES IN A MOUSE MODEL OF PARKINSON’S DISEASE

FENS Forum 2026

AUTOPHAGY-LYSOSOMAL PATHWAY PROTEINS IN DERMAL FIBROBLASTS AS POTENTIAL PERIPHERAL BIOMARKERS FOR ALZHEIMER'S DISEASE DIAGNOSIS

FENS Forum 2026

EFFECTS OF MULTISENSORY GAIT INTEGRATION TRAINING ON SENSORY ORGANIZATION AND GAIT PERFORMANCE IN PEOPLE WITH PARKINSON’S DISEASE

FENS Forum 2026

INVOLVEMENT OF ASTROCYTIC TRPA1 IN THE DISRUPTION OF NEURON-ASTROCYTE INTERACTIONS INVOLVED IN THE INITIATION OF ALZHEIMER'S DISEASE

FENS Forum 2026

EFFECT OF CHEMOGENETIC SUBTHALAMIC NUCLEUS INHIBITION ON MOTOR SYMPTOMS IN A 6-OHDA RAT MODEL OF PARKINSON’S DISEASE AND L-DOPA-INDUCED DYSKINESIA

FENS Forum 2026

TRPV1 ALTERS THE EXPRESSION AND ACTIVITIES OF P2X3 RECEPTORS IN MUSCLE DORSAL ROOT GANGLION NEURONS OF EXPERIMENTAL PERIPHERAL ARTERY DISEASE

FENS Forum 2026

SOCIAL COGNITION DEFICITS IN THE J20 MOUSE MODEL OF ALZHEIMER’S DISEASE

FENS Forum 2026

CHARACTERIZATION OF NEUROPROTECTIVE EFFECTS MEDIATED BY PROLYL ENDOPEPTIDASE-INHIBITORY COMPOUNDS FOR THE TREATMENT OF PARKINSON’S DISEASE

FENS Forum 2026

ASTROCYTIC ACTIVATION CORRECTS MEMORY PERFORMANCE IN AN ALZHEIMER'S DISEASE MODEL

FENS Forum 2026

DECODING RETINAL CIRCUIT FUNCTION WITH TWO-PHOTON CALCIUM IMAGING ACROSS HEALTH AND DISEASE

FENS Forum 2026

OXYTOCIN NEURON ACTIVATION AMELIORATES SOCIAL ISOLATION-INDUCED COGNITIVE IMPAIRMENT AND AMYLOID-Β PATHOLOGY IN MICE MODEL OF ALZHEIMER'S DISEASE

FENS Forum 2026

TEMPORAL DYNAMICS OF COGNITIVE AND NON-COGNITIVE BEHAVIORAL PHENOTYPES IN THE ICV-STZ RAT MODEL OF SPORADIC ALZHEIMER’S DISEASE

FENS Forum 2026

THE INTERPLAY BETWEEN CB<SUB >2</SUB> AND NMDA RECEPTORS IN PARKINSON’S DISEASE

FENS Forum 2026