Gina van Kleef is a Researcher and Teacher at the Faculty of Veterinary Medicine , Utrecht University , affiliated with the Institute for Risk Assessment Sciences (IRAS) and Department of Population Health Sciences . Her work focuses on neurotoxicity screening , developmental neurotoxicity , and environmental health using in vitro and hiPSC-derived neuronal models . Specializes in occupational health & safety and environmental toxicology Employing microelectrode array (MEA) recordings for neurotoxicity assessment Research trends from 2025-2020 reveal her focus on: Chemical neurotoxicity (insecticides, PFAS, flame retardants) Viral neurotoxicity (Enterovirus D-68, snake venom) Neurotransmitter receptor interactions (GABAA, nicotinic acetylcholine receptors) Novel assay development for high-throughput toxicity screening Contact: g.vankleef@uu.nl Location: Jeannette Donker-Voetgebouw, Yalelaan 104-106, Utrecht
Mikko Hiltunen is a Professor of Tissue and Cell Biology at the Institute of Biomedicine, School of Medicine, University of Eastern Finland. His research focuses on molecular mechanisms of neurodegenerative disorders, particularly Alzheimer's disease and idiopathic normal pressure hydrocephalus (iNPH). He leads several research groups including the Molecular Genetics of Alzheimer's Disease (Hiltunen Lab) and participates in the Brain Research Unit and Genome Center of Eastern Finland. Research interests span Alzheimer's pathogenesis, neuroinflammation, genetic risk factors, biomarker discovery, and therapeutic development. His work integrates molecular biology, genetics, and clinical neuroscience to investigate microglial function, amyloid pathology, and cerebrospinal fluid biomarkers. Key areas include APOE genetics, PLCγ2-mediated neuroprotection, and machine learning applications in neurodegeneration. His recent publications demonstrate a strong focus on cerebrospinal fluid biomarkers, genetic association studies, neuroinflammation mechanisms, and therapeutic interventions. Article themes consistently emphasize microglial biology, genetic risk modifiers, and translational approaches for Alzheimer's and iNPH. Collaborative projects include Neuro-Innovation (2021-2026) and NOVEL MSCA Postdoctoral Programme (2024-2029). Hiltunen leads the Clinical Alzheimer Research group and co-directs the UEF Brain Research Unit. His team utilizes advanced models including iPSC-derived microglia and pericyte systems to study neurovascular interactions. Current work explores phospho-tau immunotherapy, lysosomal dysfunction, and polygenic risk score applications across diverse populations.
Professor Lachlan Thompson is a leading academic in neurogenesis and neural transplantation, affiliated with the School of Medical Sciences. His work focuses on advancing stem cell therapies for neurodegenerative diseases like Parkinson’s, particularly through engineered neural grafts and hydrogel-based delivery systems. He leads research on optimizing stem cell differentiation, immune evasion, and functional integration within host neural circuits. Current research students include Laura Ancellotti and Alex Johnson. Key grants include a 2024 NHMRC Ideas Grant for improving Parkinson’s cell therapies and 2023 startup funding for establishing his research programs. His lab collaborates with the Charles Perkins Centre, focusing on translational neuroregenerative strategies. Research interests span stem cell engineering, neural circuit reconstruction, and disease modeling using patient-derived iPSCs. Recent work emphasizes hydrogel oxygen reservoirs, suicide gene activation in grafts, and developmental timing of neural progenitors. Over 80 publications detail advancements in neural transplantation safety, gene therapy approaches, and rodent models of neurological disorders. Awards and recognitions are not explicitly mentioned, though his high-impact publications and NHMRC grants highlight his academic standing. His lab integrates biomaterials science, genetic engineering, and clinical translation to address unmet needs in neurodegenerative therapies.
Ivy E. Dick, PhD is an Associate Professor in the Department of Pharmacology & Physiology at the University of Maryland School of Medicine. Her laboratory is located in Howard Hall Room 511B, with office space in BRB 5031. Dr. Dick leads a research team focused on understanding the biophysical properties of calcium channels and their role in both cardiac and neurological disorders. Dr. Dick began her career as an electrophysiologist at Merck, where she characterized voltage-gated sodium channels. In 2004, she joined the Calcium Signals Lab at Johns Hopkins as a graduate student under Dr. David Yue, focusing on calmodulin regulation of voltage-gated calcium channels. After completing her PhD, she continued her research in the same lab as a post-doctoral researcher and later as a Research Associate before joining the University of Maryland faculty. Dr. Dick's research centers on voltage-gated calcium channels (CaV), particularly their regulation by calmodulin and how disruptions in this regulation lead to channelopathies like Timothy Syndrome (LQT8). Her work examines the critical balance of calcium entry into heart, smooth muscle, and brain cells, focusing on the two major forms of feedback regulation: voltage-dependent inactivation (VDI) and calcium-dependent inactivation (CDI). Her laboratory employs a range of techniques including whole-cell and single-channel patch clamp electrophysiology, molecular biology, calcium and FRET imaging, tissue culture with induced pluripotent stem cells (iPSCs), and CRISPR gene editing. Analysis of Dr. Dick's recent publications reveals a strong focus on calcium channelopathies, particularly those involving CACNA1C (LQT8/Timothy Syndrome) and calmodulin mutations. Her work spans both cardiac and neurological manifestations of these channelopathies, with increasing use of iPSC-derived cardiomyocytes and neurons for disease modeling. Recent publications show expansion into gene editing approaches for rare disease modeling and potential therapeutic strategies. Dr. Dick has received notable recognition for her work, including: Paul F. Cranefield Award from the Society of General Physiologists (2023) for the paper 'CaV1.2 channelopathic mutations evoke diverse pathophysiological mechanisms' John C. Hemmeter Scholar appointment (2016) Dr. Dick has played a significant role in high-impact research, including work that contributed to re-examining the conviction of Kathleen Folbigg, who was convicted of murdering her children but may have had a genetic explanation related to calmodulin mutations. Her laboratory at the University of Maryland School of Medicine investigates the biology of excitable cells in both the heart and brain, with current projects using electrophysiological recording, patient-derived iPSCs, brain organoids, and calcium imaging. The Dick laboratory is part of a collaborative research environment focused on understanding calcium dynamics in health and disease, with implications for disorders ranging from cardiac arrhythmias to schizophrenia. Her team works at the intersection of basic biophysics and clinical applications, aiming to translate mechanistic understanding into potential therapeutic interventions for calcium channelopathies.
Gary E. Gibson is a tenured Professor of Neuroscience at Weill Cornell Medicine , where he serves as Lab Director at the Laboratory for Mitochondrial Biology and Metabolic Dysfunction in Neurodegeneration . He also holds the position of Associate Director at the Dementia Research Service within the Burke Neurological Institute . His academic career spans institutions including UCLA (where he completed postdoctoral work and faculty appointments) and Cornell University , where he earned his Ph.D. Education: B.S. in Zoology and Chemistry, University of Wyoming Ph.D. in Physiology (Biochemistry/Neuroscience), Cornell University Research Focus: Dr. Gibson's work centers on mitochondrial dysfunction and oxidative stress in neurodegenerative diseases (Alzheimer's, Huntington's, Parkinson's). His lab investigates: Mechanisms of α-ketoglutarate dehydrogenase complex (KGDHC) deficiency Metabolism-calcium signaling interactions Protein post-translational modifications (succinylation, acetylation) Thiamine-dependent metabolic pathways Translational studies using induced pluripotent stem cells Clinical trials testing metabolic interventions (e.g., benfotiamine) Publications reveal expertise in: TCA cycle enzyme abnormalities Neurodegenerative biomarker discovery Calcium dyshomeostasis Metabolic-epigenetic crosstalk Neuroprotective strategies Animal models of oxidative stress Honors: ASN Award for Outstanding Young Investigator Three U.S. patents NIH Director’s Talk and other honorary lectureships Grants: Continuously funded by NIH/NIA grants (P01AG014930) for mitochondrial dysfunction research since 1999. Serves on Alzheimer’s Association and American Federation for Aging Research review panels.
Federico Salas-Lucia is an Assistant Professor in the Department of Medicine, Division of Endocrinology at the University of Chicago's Pritzker School of Medicine. His research integrates neurobiology and endocrinology to investigate thyroid hormone mechanisms in brain development and function, utilizing human iPSC-derived models, transgenic mice, and multi-omics approaches. His educational background includes a BS in Biology from the University of Alicante (2012), an MSc in Neuroscience from University Miguel Hernandez (2014), and a PhD in Neuroscience from the same institution (2018). Dr. Salas-Lucia's research focuses on intracellular mechanisms customizing thyroid hormone action during human brain development. His laboratory examines how thyroid hormones regulate bioenergetic processes supporting neurogenesis, with emphasis on mitochondrial function in neural progenitor cells and epigenetic regulation via DNA methylation. Using cutting-edge iPSC-derived cerebral organoids and advanced imaging, his work bridges molecular mechanisms to clinical correlations between maternal thyroid levels and neurodevelopmental outcomes. Current investigations include thyroid hormone transport via MCT8, deiodinase activity (DIO2/DIO3), and nuclear receptor signaling in neural cells. His publication portfolio since 2018 shows accelerating productivity, with 23 publications through 2025 (8 in 2023 alone). The research demonstrates strong thematic continuity in thyroid-brain interactions , evolving from foundational rodent studies to sophisticated human iPSC models. Recent work increasingly incorporates multi-omics approaches and addresses clinical implications for disorders like Allan-Herndon-Dudley syndrome and Alzheimer's disease. Emerging Group Leader Award, International Society for Neurochemistry (2025) As principal investigator of the Salas-Lucia Laboratory, he directs research on thyroid hormone signaling in neural development. His work receives significant attention, with publications referenced in clinical guidelines and covered by multiple news outlets. The laboratory maintains active collaborations with leading endocrinology researchers including Antonio Bianco and Samuel Refetoff, and participates in interdisciplinary networks exploring metabolic regulation and neurodevelopment. Current projects investigate epigenetic mechanisms in thyroid-mediated cortical development and therapeutic strategies for thyroid hormone transport disorders.
Professor Marcelo Rivolta is a Professor of Sensory Stem Cell Biology in the School of Biosciences at the University of Sheffield. His research focuses on developing stem cell-based therapies for hearing loss, with particular emphasis on regenerating damaged inner ear structures. His educational background includes an M.D. from the University of Córdoba, Argentina (1989) and a Ph.D. from the NIH in Bethesda, Maryland, USA and the University of Córdoba, Argentina (1992-1995). Professor Rivolta's research interests center on sensory stem cell biology and regenerative therapies for hearing loss. His laboratory has made key advances in stem cell technologies for potential hearing restoration therapies. They isolated stem cells from the human fetal cochlea and developed protocols to drive otic differentiation from human pluripotent stem cells. The group has demonstrated that hESC-derived otic progenitors can repair damaged cochlea in animal models, showing functional recovery as measured by auditory brainstem thresholds. Currently, they are exploring the combination of stem cells with cochlear implants to develop a "bionic ear" and using stem cells to create in vitro platforms for drug discovery. Professor Rivolta is part of Otostem, an international consortium with partners in Stanford, Harvard, Geneva, Uppsala, Tübigen and Marseille. His work has significant implications for the millions of people worldwide affected by hearing loss. His scientific awards and honors include: Trustee of the charity 'The Ear Foundation' Reviewer for leading scientific journals Reviewer for research proposals submitted to Action on Hearing Loss, Deafness Research UK, The Wellcome Trust, MRC, BBSRC and other funding bodies Invited speaker at numerous national and international meetings Professor Rivolta teaches Stem Cell Biology at both undergraduate (BMS382) and Masters (BMS6051, BMS6056) levels. He leads the Hearing Research Group at the University of Sheffield, which focuses on regenerative therapies for hearing loss using human stem cells. His laboratory works on developing protocols for otic differentiation from human pluripotent stem cells and testing these in animal models of hearing loss.
Agnete Kirkeby is an Associate Professor at the Department of Biomedical Sciences , University of Copenhagen, and leads the Kirkeby Lab under the reNEW research center. Her work focuses on human brain development and stem cell engineering. Research Interests : Understanding human neural cell development for regenerative therapies , drug screening , and Parkinson's disease treatment . Her lab uses stem cell differentiation and bioactive materials. Key Article Trends : Recent publications center on Stem cell-derived neuron therapies Neuroregeneration using diamond scaffolds Clinical translation of stem cell treatments External Roles : Group leader at Lund University. Conflicts of Interest : Owns Kirkeby Cell Therapy APS, consults for Novo Nordisk, and co-invents patents on neuron generation from stem cells.
Mark Zylka serves as the W.R. Kenan, Jr. Distinguished Professor in the Department of Cell Biology and Physiology at the UNC School of Medicine, University of North Carolina at Chapel Hill. He directs a research laboratory focused on neurodevelopmental disorders and pain mechanisms, with affiliations at the UNC Neuroscience Center and support from multiple NIH institutes. His research spans autism etiology , Angelman syndrome , chronic pain pathways , and environmental neurotoxicology . The lab employs CRISPR/Cas gene editing, AAV vectors, single-cell RNA-seq, and behavioral analysis to investigate molecular mechanisms underlying neurodevelopmental disorders and pain sensation. Recent work emphasizes environmental chemical impacts on neurodevelopment and gene therapy approaches for autism-related conditions. Publications from 2023-2025 reveal strong trends in CRISPR-based therapeutics for Angelman syndrome, environmental chemical screening for neurodevelopmental risks, and computational pain assessment tools . Key interdisciplinary fields include neurogenetics, molecular toxicology, and translational neuroscience with emphasis on Wnt signaling pathways and epigenetic regulation. Scientific Awards: Rita Allen Foundation Award Alfred P. Sloan Foundation Fellowship Searles Scholars Program Whitehall Foundation Grant Ester A. & Joseph Klingenstein Fund Award Brain & Behavior Research Foundation Grant Laboratory funding demonstrates exceptional grant acquisition across federal and private sources. Major support comes from NIH/NIEHS, NIH/NIMH, NIH/NINDS, Rett Syndrome Research Trust, Angelman Syndrome Foundation, Autism Speaks, and Simons Foundation. The lab maintains active collaborations through the UNC Neuroscience Center and NC TraCS institute, with recent focus on developing PainFace software for standardized pain assessment and CRISPR-based therapies for neurogenetic disorders.
Edor Kabashi is a leading researcher in translational neuroscience, specializing in genetic causes of neurological disorders such as Developmental and Epileptic Encephalopathy (DEE), Spinal Muscular Atrophy (SMA), Amyotrophic Lateral Sclerosis (ALS), and Frontotemporal Dementia (FTD). His team at the Imagine Institute (Necker Hospital site) develops advanced cellular and zebrafish models to elucidate disease mechanisms and accelerate therapeutic validation. Key research areas include iPSC-derived neurons, drug screening platforms, and genomic sequencing analysis. Collaborations span national/international networks with institutions like ANR and pharmaceutical partners. Expertise: Genetic epilepsy, neurodegeneration, translational drug development Techniques: CRISPR gene editing, induced pluripotent stem cells, high-throughput screening Current projects focus on fast-tracking neuroprotective compounds into clinical trials, leveraging state-of-the-art platforms such as transcriptomic/proteomic analysis and advanced imaging. Actively recruiting postdocs and PhD candidates with expertise in zebrafish models, molecular genetics, and bioinformatics.
Masatoshi Suzuki is a Professor in the Biomedical Engineering department at the University of Wisconsin-Madison, with an additional affiliation in the School of Veterinary Medicine. His research focuses on applying stem cell technology to model and treat neuromuscular and musculoskeletal disorders , particularly amyotrophic lateral sclerosis (ALS) , through growth factor delivery and advanced imaging techniques. PhD (1999, The University of Tokyo, Japan) DVM (1995, The Ministry of Agriculture and Fishery, Japan) BS (1995, The University of Tokyo, Japan in Veterinary Medicine) Suzuki's work spans basic and translational studies using human neural progenitor cells, mesenchymal stem cells, and pluripotent stem cells. His lab has pioneered strategies for stem cell-based ALS therapy , including growth factor delivery systems and in vitro neuromuscular junction models . He also develops non-invasive imaging approaches to monitor stem cell dynamics in the central nervous system. Research trends in his publications reveal a focus on stem cell technology for neuromuscular diseases, ALS pathology , muscle progenitor isolation , and imaging methodologies . His lab has contributed to understanding sex-specific differences in ALS progression and macrophage-mediated inflammation in disease models. The Suzuki Lab team includes lab manager Samantha Robertson (PhD Genetics), undergraduate assistants Elizabeth Altman (Genetics and Genomics) and Adam Eckardt (Biochemistry), and research assistant Clarisse Rebancos (DVM Candidate). The lab collaborates with funding partners such as the University of Wisconsin-Madison and the School of Veterinary Medicine.
Caleb Webber is a Researcher at the Department of Physiology, Anatomy and Genetics, University of Oxford. He is actively engaged in collaborative research through the Genetics of Cognitive Dysfunction (Gencodys) Consortium and the IMI StemBANCC consortium, where he leads the Data Interpretation package. Education: PhD in 2003 from the European Bioinformatics Institute and the Department of Genetics, Cambridge University His research focuses on understanding the genetic basis of diseases, particularly the role of copy number variations (CNVs) in neurodevelopmental and neurodegenerative disorders such as autism and Parkinson's disease. Using computational biology and genomics approaches, he investigates gene clustering, functional interactions, and therapeutic targets related to these conditions. The recent publications highlight his work in genetics, neuroscience, and computational biology, with a focus on CNVs in autism, iPSC-derived neuronal models for Parkinson's disease, and the application of omics studies to understand disease mechanisms. He is affiliated with the Oxford Parkinson's Disease Centre and contributes to large-scale international research initiatives.
James L. Salzer is a Professor in both the Department of Neuroscience and Physiology and the Department of Neurology at NYU Grossman School of Medicine, New York University. He is a principal investigator at the Salzer Lab within the NYU Langone Health Neuroscience Institute, where he leads cutting-edge research on axon-glial interactions and myelination. Dr. Salzer earned his MD and PhD from Washington University in St. Louis, establishing a strong foundation in both clinical medicine and basic science research. His research centers on the molecular and cellular mechanisms underlying myelination, demyelination, and remyelination in the central and peripheral nervous systems. Key interests include the role of glial cells in organizing axonal electrogenic domains such as nodes of Ranvier and the axon initial segment, the signaling pathways (including Sonic hedgehog and Gli1) regulating neural stem cell repair, and the interplay between microglia and neural stem cells during injury and repair. His work has significant implications for understanding and treating multiple sclerosis and other demyelinating diseases. His recent publications, spanning high-impact journals such as Cold Spring Harbor Perspectives in Biology , Developmental Cell , and The Journal of Neuroscience , reflect a strong focus on Schwann cell biology, glial-axon signaling, and regenerative mechanisms in myelin disorders. The articles highlight advanced techniques including live imaging, transcriptomics, and electron microscopy, demonstrating a multidisciplinary approach to neuroscience. Dr. Salzer mentors a dynamic research team comprising PhD and MD/PhD students, postdoctoral researchers, and research associates, fostering the next generation of neuroscientists. His lab receives support from major research grants, enabling extensive studies using transgenic mouse models, cocultures, and advanced imaging to dissect the biology of myelinated axons. The Salzer Lab is actively involved in both fundamental discovery and translational research, aiming to develop therapeutic strategies for promoting nerve repair in demyelinating conditions. His work integrates molecular, cellular, and systems-level approaches to understand how neural circuits are assembled and maintained.
Professor Ioanna Sandvig is a leading academic at the Norwegian University of Science and Technology (NTNU) , where she serves as group leader of the Integrative Neuroscience Group within the Department of Neuromedicine and Movement Science. She is also President of the Norwegian Neuroscience Society (NNS) and actively participates in international societies including the Federation of European Neuroscience Societies (FENS), Society for Neuroscience (SfN), ALBA Network, and Clinical-Academic Group for Alzheimer's Disease. Research Interests : Her group investigates neuroplasticity mechanisms in CNS damage and repair , focusing on structure-function relationships in biological neural networks under healthy and pathological conditions. They integrate in vivo , in vitro , and computational models to identify adaptive/maladaptive plasticity in neurodegenerative diseases like ALS and Alzheimer's. The research combines connectomics , transcriptional analysis , and geometric network modeling to decode network behaviors. Scientific Contributions : Recent publications explore topics including synaptic transcript dysregulation in ALS, functional complexity of 3D-engineered networks, and platinum microelectrode technologies. Her work demonstrates interdisciplinary approaches bridging neuroscience , bioengineering , and computational systems . Scientific Recognition : President, Norwegian Neuroscience Society (2024) Member, Federation of European Neuroscience Societies Member, Society for Neuroscience Member, ALBA Network Member, Clinical-Academic Group for Alzheimer's Disease Laboratory & Collaborations : The Integrative Neuroscience Group collaborates across NTNU's neuroscience departments and clinical institutions, developing tools for neuroplasticity analysis and contributing to preclinical disease modeling.
Giulia Bernardini is an Associate Professor at the Department of Biotechnology, Chemistry and Pharmacy, University of Siena. She teaches Applied and Clinical Biochemistry in the Pharmacy program and maintains regular office hours at the Polo Scientifico San Miniato. Her research focuses on rare diseases like Alkaptonuria and Lesch-Nyhan Disease , with emphasis on biochemical pathways, proteomics, and in vitro modeling. Email: giulia.bernardini@unisi.it Phone: +39 0577 235792 Webex Virtual Room: Join Here Her recent work explores omics technologies in rare disease research, enzyme inhibition for novel therapeutics, and computational workflows targeting metabolic disorders. Publications highlight collaborations with international consortia like the DevelopAKUre project. Key research areas include: Homogentisic acid pathophysiology in Alkaptonuria Purine salvage pathway defects Induced pluripotent stem cell modeling 4-Hydroxyphenylpyruvate Dioxygenase (HPPD) inhibition Inflammatory/oxidative stress biomarkers Proteomic profiling of rare diseases
