TY - JOUR AU - Mace, Jackson W. AU - Gadani, Sachin P. AU - Smith, Matthew D. AU - Galleguillos, Danny AU - Kang, Bong Gu AU - Roy, Milton AU - Liu, Meilian AU - Summers, Benjamin AU - Garton, Thomas AU - Gharagozloo, Marjan AU - Gill, Alexander J. AU - Pardo, Carlos A. AU - Sotirchos, Elias S. AU - Dawson, Valina L. AU - Dawson, Ted M. AU - Calabresi, Peter A. TI - Autoimmune neuroinflammation leads to neuronal death via MIF nuclease-mediated parthanatos JF - NATURE NEUROSCIENCE J2 - NAT NEUROSCI PY - 2026 PG - 39 SN - 1097-6256 DO - 10.1038/s41593-026-02201-7 UR - https://m2.mtmt.hu/api/publication/36994616 ID - 36994616 N1 - Funding Agency and Grant Number: U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) [R01NS041435, F31NS132520, NS065725]; U.S. Department of Defense (United States Department of Defense) [W81XWH2210819]; National Multiple Sclerosis Society (National MS Society) [FAN-2106-37832, TA-2407-43578, TA-2104-37423, FAN-2007-36944] Funding text: We thank H. W. (G.) Chen for his cover artwork submission and for working with J.W.M. to create the parthanatos cell death diagram. All other cartoons were created by J.W.M. with BioRender.com. This work was supported, in part, by grants from the National Institutes of Health (F31NS132520 to J.W.M.; R01NS041435 to P.A.C., AG085688, AG093848, NS065725 to T.M.D., V.L.D.), the Department of Defense (W81XWH2210819 to P.A.C.), the National MS Society (FAN-2106-37832, TA-2407-43578 to S.P.G.; FAN-2007-36944 to A.J.G.; TA-2104-37423 to M.G.) and gifts from the Sol and Lillian Goldman Foundation and the Fishman Family Foundation. J.W.M. was also supported by the Karen Toffler Charitable Trust (90105789). T.M.D. is the Leonard and Madlyn Abramson Professor in Neurodegenerative Diseases. P.A.C. was the Snyder-Granader Professor in Multiple Sclerosis. AB - Central nervous system inflammation is implicated in neurodegeneration across several disorders, including multiple sclerosis (MS). While marked therapeutic progress has been made in preventing relapses in MS, primary neuroprotection in this disease remains elusive. This, in part, is due to an incomplete understanding of the molecular pathways involved in immune-mediated neuronal death. Here we show that parthanatos, a recently described caspase-independent and DNA damage-induced cell death program, contributes to neuron death in the experimental autoimmune encephalomyelitis (EAE) mouse model of autoimmune neuroinflammation. We reveal that DNA damage increases in neurons during EAE, and that neurons are progressively lost over the disease course. Neurons in affected areas display intracellular hallmarks of the parthanatos cascade. Genetic or pharmacologic blockade of the final step in parthanatos, genomic fragmentation by macrophage migration inhibitory factor (MIF) nuclease, reduces neuron loss and disease severity. Transcriptomic characterization of neurons with and without MIF nuclease activity reveals parthanatos-dependent differences in response to EAE. Together, this work establishes parthanatos as a key mechanism of neuron cell death during neuroinflammation. LA - English DB - MTMT ER - TY - JOUR AU - Kim, Mujun AU - Suh, Boin AU - So, Sunhoi AU - Choi, Jung Wook AU - Hwang, Jaemin AU - Park, Juhee AU - Han, Jin-Hee TI - A septo-entorhinal GABAergic pathway that enables switching between episodic memories JF - NATURE NEUROSCIENCE J2 - NAT NEUROSCI PY - 2026 PG - 34 SN - 1097-6256 DO - 10.1038/s41593-026-02280-6 UR - https://m2.mtmt.hu/api/publication/37108073 ID - 37108073 N1 - Funding Agency and Grant Number: KAIST Jang Young Sil Fellow Program; This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MIST) (RS-2023-NR077269), and partly by Samsung Science and Technology Foundation Project SSTF-BA1801-10. Funding text: We thank all laboratory members for their helpful suggestions and constructive discussions. We thank the KAIST Bio-Core Center and the KAIST Analysis Center for Research Advancement for use of confocal microscopes and assistance in performing imaging experiments. We are grateful to E. Kim at KAIST for generously providing the Vgat-Cre transgenic mouse line and to G. Suh at KAIST for kindly sharing the calcium imaging device. This work was supported by the National Research Foundation of Korea (NRF) (RS-2023-NR077269 to J.-H.H.), the KAIST Jang Young Sil Fellow Program (A0801026001 to M.K.) and partly by the Samsung Science and Technology Foundation Project (SSTF-BA1801-10 to J.-H.H.). AB - New experiences are integrated with existing knowledge to update memory, which is essential for survival in a dynamic environment. Despite this updating, the brain can still access previous memories to guide appropriate behavior. How the brain organizes the retrieval of old and new memories remains unknown. Here we demonstrate a flexible memory switching mechanism in male mice, mediated by medial septum (MS) GABAergic neurons projecting to the medial entorhinal cortex (MEC). This neuronal subset was specifically recruited during retrieval after updating, and inactivation of their projections to the MEC reversed the updated behaviors-indicating a behavioral switch to previous memories-and induced a switch in CA1 population activity patterns back to the pre-update pattern. After updating, the duration of the 'online' state correlated with memory performance. Together, these findings reveal a neural switch mechanism mediated by the septo-entorhinal GABAergic pathway that organizes memory retrieval to enable updating. LA - English DB - MTMT ER - TY - JOUR AU - Toker, Daniel AU - Zheng, Zhong Sheng AU - Thum, Jasmine A. AU - Guang, Jing AU - Annen, Jitka AU - Miyamoto, Hiroyuki AU - Yamakawa, Kazuhiro AU - Vespa, Paul M. AU - Laureys, Steven AU - Schnakers, Caroline AU - Bari, Ausaf A. AU - Hudson, Andrew AU - Pouratian, Nader AU - Monti, Martin M. TI - Adversarial AI reveals mechanisms and treatments for disorders of consciousness JF - NATURE NEUROSCIENCE J2 - NAT NEUROSCI VL - 29 PY - 2026 IS - 4 PG - 28 SN - 1097-6256 DO - 10.1038/s41593-026-02220-4 UR - https://m2.mtmt.hu/api/publication/37072954 ID - 37072954 N1 - Funding Agency and Grant Number: Canada Excellence Research Chairs, Government of Canada (Canada Excellence Research Chairs Program); United States Department of Defense | United States Army | Army Medical Command | Congressionally Directed Medical Research Programs (CDMRP) [HT9425-24-1-1081]; Belgian National Fund for Scientific Research | Fonds pour la Formation la Recherche dans l'Industrie et dans l'Agriculture (Training Fund for Research in Industry and Agriculture); U.S. Department of Health & Human Services | National Institutes of Health (NIH) [R01 GM135420] Funding text: We thank D. Mateos for providing MEG data from a human patient with epilepsy who experienced absence seizures. We also thank M. Johnson for help with deterministic tractography. This work was supported by the National Institutes of Health (NIH grant R01 GM135420), the Department of Defense Congressionally Directed Medical Research Programs (DoD CDMRP grant HT9425-24-1-1081), the Brain Injury Research Center at UCLA, the Fund for Scientific Research-Flanders (FWO), the Canada Excellence Research Chair in Neuroplasticity, the Belgian National Fund for Scientific Research, the Fund Generet of the King Baudouin Foundation, the European Foundation for Biomedical Research, and the Foundation for Research and Rehabilitation of Neurodegenerative Diseases. AB - Understanding disorders of consciousness (DOC) remains one of the most challenging problems in neuroscience, hindered by the lack of experimental models for probing mechanisms or testing interventions. Here, to address this, we introduce a generative adversarial artificial intelligence (AI) framework that pits deep neural networks-trained to detect consciousness across more than 680,000 ten-second neuroelectrophysiology samples and validated on 565 patients, healthy volunteers and animals-against interpretable, machine learning-driven neural field models. This adversarial architecture produces biologically realistic simulations of both conscious and comatose brains that recapitulate empirical neurophysiological features across humans, monkeys, rats and bats. Without explicit programming, the AI model retrodicts known DOC responses to brain stimulation and generates testable predictions about the mechanisms of unconsciousness. Two such predictions are validated here: selective disruption of the basal ganglia indirect pathway, supported by diffusion magnetic resonance imaging in 51 patients with DOC, and increased cortical inhibitory-to-inhibitory synaptic coupling, supported by RNA sequencing of resected brain tissue from 6 human patients with coma and a rat stroke model. The model also identifies high-frequency stimulation of the subthalamic nucleus as a promising intervention for DOC, supported by electrophysiological data from human patients. This work introduces an AI framework for causal inference and therapeutic discovery in consciousness research, as well as in complex systems more broadly. LA - English DB - MTMT ER - TY - JOUR AU - Thiagarajan, Tara C. AU - Vianney, Sr John-Mary AU - Swaminathan, Shailender AU - Newson, Jennifer Jane AU - Parameshwaran, Dhanya AU - Subramaniyam, Narayan Puthanmadam TI - Building scalable neuroimaging programs across diverse human environments JF - NATURE NEUROSCIENCE J2 - NAT NEUROSCI VL - 29 PY - 2026 IS - 4 SP - 767 EP - 771 PG - 5 SN - 1097-6256 DO - 10.1038/s41593-026-02215-1 UR - https://m2.mtmt.hu/api/publication/37091025 ID - 37091025 N1 - Funding Agency and Grant Number: This work was supported by funding from Sapien Labs, USA and the Sapien Labs Foundation, India. dName This work was supported by funding from Sapien Labs, USA and the Sapien Labs Foundation, India. Funding text: This work was supported by funding from Sapien Labs, USA and the Sapien Labs Foundation, India. LA - English DB - MTMT ER - TY - JOUR AU - Magee, Jeffrey C. TI - Behavioral timescale synaptic plasticity: properties, elements and functions JF - NATURE NEUROSCIENCE J2 - NAT NEUROSCI VL - 29 PY - 2026 IS - 3 SP - 520 EP - 534 PG - 15 SN - 1097-6256 DO - 10.1038/s41593-026-02214-2 UR - https://m2.mtmt.hu/api/publication/37008584 ID - 37008584 N1 - Funding Agency and Grant Number: Cullen Foundation [na]; Howard Hughes Medical Institute (HHMI) [na] Funding text: I thank M. Harnett for the pyramidal neuron image in Fig. 1, all members of the Magee lab for useful discussions, R. Chitwood and S. Vaidya for help with the manuscript, and C. Grienberger, A. Losonczy, S. Romani and S. R. Williams for comments on the manuscript. This work was supported by the Howard Hughes Medical Institute and the Cullen Foundation. AB - Understanding how brains learn and remember remains among the most important challenges in science. Recent studies in the hippocampus implicate a new form of synaptic plasticity, named behavioral timescale synaptic plasticity (BTSP), in the generation of experience-based learning and memory. BTSP is a strong, bidirectional type of plasticity that affects synaptic weights over many seconds of time. It is induced by single dendritic plateau potentials, as opposed to many action potentials, and is thus capable of producing new place cells in one trial. Plateau potential initiation is controlled, at least in part, by local feedback inhibition and an instructive input from a higher-order brain region that potentially links the plasticity to current experience. The new credit assignment procedure in BTSP provides a nonstandard mechanism for memory storage and retrieval that could mitigate the need for widespread synapse stabilization. In addition, it may allow hippocampal networks both to form memories of specific behavioral episodes and to generalize on the basis of past episodes. Finally, recent BTSP investigations could provide a basis for future explorations into how brains learn and remember, ranging from the systems and cognitive levels down to the basic biochemical building blocks of learning and memory. LA - English DB - MTMT ER - TY - JOUR AU - Gonzalez-Gallego, Judit AU - Todorov-Volgyi, Katalin AU - Muller, Stephan A. AU - Antesberger, Sophie AU - Todorov, Mihail Ivilinov AU - Malik, Rainer AU - Grimalt-Mirada, Rita AU - Goncalves, Carolina Cardoso AU - Schifferer, Martina AU - Kislinger, Georg AU - Weisheit, Isabel AU - Lindner, Barbara AU - Crusius, Dennis AU - Kroeger, Joseph AU - Borri, Mila AU - Erturk, Ali AU - Nelson, Mark AU - Misgeld, Thomas AU - Lichtenthaler, Stefan F. AU - Dichgans, Martin AU - Paquet, Dominik TI - A fully iPS-cell-derived 3D model of the human blood-brain barrier for exploring neurovascular disease mechanisms and therapeutic interventions JF - NATURE NEUROSCIENCE J2 - NAT NEUROSCI VL - 29 PY - 2026 IS - 2 SP - 479 EP - 492 PG - 14 SN - 1097-6256 DO - 10.1038/s41593-025-02123-w UR - https://m2.mtmt.hu/api/publication/36795316 ID - 36795316 N1 - Funding Agency and Grant Number: Deutsche Forschungsgemeinschaft (German Research Foundation) [EXC 2145 SyNergy, ID 390857198, SFB TRR 274/2 2024 - 408885537 project Z01, Mi 694/9-1 A03-ID 428663564 FOR Immunostroke, DI 722/13-1; DI 722/16-1, BE 6169/1-1]; Fondation Leducq [BRENDA]; EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) [SVDs@target, No 666881] Funding text: Open access funding provided by Ludwig-Maximilians-Universitat Munchen. LA - English DB - MTMT ER - TY - JOUR AU - Bhambri, Aksheev AU - Thai, Phu AU - Wei, Songtao AU - Bae, Han-Gyu AU - Reynolds, Payton AU - Barbosa, Daniela AU - Sharma, Tripti AU - Yu, Ze AU - Xing, Chao AU - Kim, Jun Hee AU - Yu, Guoqiang AU - Sun, Lu O. TI - Genetic targeting of premyelinating oligodendrocytes reveals activity-dependent myelination mechanisms JF - NATURE NEUROSCIENCE J2 - NAT NEUROSCI VL - 29 PY - 2026 IS - 1 PG - 41 SN - 1097-6256 DO - 10.1038/s41593-025-02110-1 UR - https://m2.mtmt.hu/api/publication/37003312 ID - 37003312 N1 - Funding Agency and Grant Number: Chan Zuckerberg Initiative, Ben Barres Early Career Acceleration Award, Klingstein Simons Foundation Fellowship for Neuroscience Funding text: We thank the members of the Sun laboratory for assistance and discussions. This work was supported by the UT Southwestern Endowed Scholarship (L.O.S.), the Chan Zuckerberg Initiative Ben Barres Early Career Acceleration Award (L.O.S.), the Klingenstein-Simons Foundation Fellowship Award in Neuroscience (L.O.S.) and National Institutes of Health grants U19NS123719 (G.Y.) and R01 DC018797 (J.H.K.). L.O.S. is a Southwestern Medical Foundation Scholar in Biomedical Research. AB - To myelinate axons, oligodendrocyte precursor cells (OPCs) must stop dividing and differentiate into premyelinating oligodendrocytes (preOLs), a transient cell stage during myelination that is often stalled at human demyelinating lesions. PreOLs extend processes, surveying nearby axons to begin ensheathment. The lack of genetic tools to visualize and manipulate preOLs has hindered their in-depth study. Here we present a CreERT2 knockin mouse line that enables genetic labeling, lineage tracing, manipulation and multimodal profiling of preOL subsets across the central nervous system. Genetically labeled preOLs are postmitotic, with distinct morphology and unique transcriptomic, epigenetic and electrophysiological features. PreOL lineage tracing revealed spatiotemporal dynamics of oligodendrogenesis across the mouse brain. Moreover, fate mapping of preOLs under sensory deprivation revealed that neuronal activity influences preOLs within a narrow maturation window, promoting their survival and successful integration. Together, our work presents a genetic tool to study preOL biology and axon-oligodendrocyte interactions in health and disease. LA - English DB - MTMT ER - TY - JOUR AU - Groos, Dominik AU - Reuss, Anna Maria AU - Rupprecht, Peter AU - Stachniak, Tevye AU - Lewis, Christopher AU - Han, Shuting AU - Roggenbach, Adrian AU - Sturman, Oliver AU - Sych, Yaroslav AU - Wieckhorst, Martin AU - Bohacek, Johannes AU - Karayannis, Theofanis AU - Aguzzi, Adriano AU - Helmchen, Fritjof TI - A distinct hypothalamus-habenula circuit governs risk preference JF - NATURE NEUROSCIENCE J2 - NAT NEUROSCI PY - 2025 PG - 34 SN - 1097-6256 DO - 10.1038/s41593-024-01856-4 UR - https://m2.mtmt.hu/api/publication/35754625 ID - 35754625 LA - English DB - MTMT ER - TY - JOUR AU - Vega-Zuniga, T AU - Sumser, A AU - Symonova, O AU - Koppensteiner, P AU - Schmidt, FH AU - Joesch, M TI - A thalamic hub-and-spoke network enables visual perception during action by coordinating visuomotor dynamics JF - NATURE NEUROSCIENCE J2 - NAT NEUROSCI VL - 10 PY - 2025 SN - 1097-6256 DO - 10.1038/s41593-025-01874-w UR - https://m2.mtmt.hu/api/publication/35803616 ID - 35803616 LA - English DB - MTMT ER - TY - JOUR AU - Butola, Tanvi AU - Hernandez-Frausto, Melissa AU - Blankvoort, Stefan AU - Flatset, Marcus Sandbukt AU - Peng, Lulu AU - Hairston, Ariel AU - Johnson, Cara Deanne AU - Elmaleh, Margot AU - Amilcar, Amanda AU - Hussain, Fabliha AU - Clopath, Claudia AU - Kentros, Clifford AU - Basu, Jayeeta TI - Hippocampus shapes entorhinal cortical output through a direct feedback circuit JF - NATURE NEUROSCIENCE J2 - NAT NEUROSCI PY - 2025 PG - 41 SN - 1097-6256 DO - 10.1038/s41593-025-01883-9 UR - https://m2.mtmt.hu/api/publication/35819713 ID - 35819713 N1 - Funding Agency and Grant Number: U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) [1R01NS109362-01]; NIH NINDS [NINDS 1RM1NS132981]; NIH [23AARFD-1026841]; Alzheimer's Association; Parekh Center for Interdisciplinary Neurology (PCIN) Pilot Research Grant, Mathers Charitable Foundation Investigator Award; Klingenstein Fund-Simons Foundation Fellowship Award in Neuroscience, Alfred P. Sloan Research Fellowship; Whitehall Research Grant; American Epilepsy Society Junior Investigator Award; Blas Frangione Young Investigator Research Grant, New York University Whitehead Fellowship; Leon Levy Foundation Award [1R01NS109994]; NIH BRAIN INITIATIVE grant; Leon Levy Foundation postdoctoral fellowship; FACES Award (Finding A Cure for Epilepsy & Seizures award) by New York University Langone Health and Comprehensive Epilepsy Center; Collaborative and Research Pilot Project Award; CTSI (Clinical and Translational Science Institute) by New York University Langone Health [P30 AG066512]; REC Scholar Program of NYU Alzheimer's Disease Research Center (ADRC); Irene & Eric Simon (IES) Brain Research Foundation [3R01MH122391-04S1]; NIH NIMH Diversity Supplement Funding text: This work was supported by the following grants to J.B.: NIH NINDS 1R01NS109362-01, NIH NIMH 3R01MH122391, NIH NINDS 1RM1NS132981, Alzheimer's Association AARGD-NTF-23-1151101, Parekh Center for Interdisciplinary Neurology (PCIN) Pilot Research Grant, Mathers Charitable Foundation Investigator Award, McKnight Scholar Award in Neuroscience, Klingenstein Fund-Simons Foundation Fellowship Award in Neuroscience, Alfred P. Sloan Research Fellowship, Whitehall Research Grant, American Epilepsy Society Junior Investigator Award, Blas Frangione Young Investigator Research Grant, New York University Whitehead Fellowship for Junior Faculty in Biomedical and Biological Sciences and Leon Levy Foundation Award. The collaborative effort was supported by NIH BRAIN INITIATIVE grant 1R01NS109994 to J.B., C.C. and C.K. T.B. was supported by Leon Levy Foundation postdoctoral fellowship, FACES Award (Finding A Cure for Epilepsy & Seizures award) by New York University Langone Health and Comprehensive Epilepsy Center, and Collaborative and Research Pilot Project Award, CTSI (Clinical and Translational Science Institute) by New York University Langone Health. M.H.-F. was supported by REC Scholar Program of NYU Alzheimer's Disease Research Center (ADRC) P30 AG066512, and the Alzheimer's Association grant 23AARFD-1026841 fellowship. A.H. was supported by an Irene & Eric Simon (IES) Brain Research Foundation grant. C.D.J. was supported by NIH NIMH Diversity Supplement 3R01MH122391-04S1. F.H. was supported by McKnight Endowment Fund for Neuroscience Mathew Pecot Award for Training Underrepresented Minority Students. We thank R. Froemke, M. Long, D. Lin, O. Bilash, V. Robert and R. Tsien for helpful discussion on earlier versions of the paper. We thank A. Mar and C. Denny for their advice on freely moving behavior analysis and interpretation of results. We thank M. Dufour and S. Sundar for their input and technical support during the early stages of the project, and J. Moore for input and support on the in vivo imaging data analysis. LA - English DB - MTMT ER -