@article{MTMT:34760259, title = {Microglia-neuron interactions in schizophrenia}, url = {https://m2.mtmt.hu/api/publication/34760259}, author = {Hartmann, S.-M. and Heider, J. and Wüst, R. and Fallgatter, A.J. and Volkmer, H.}, doi = {10.3389/fncel.2024.1345349}, journal-iso = {FRONT CELL NEUROSCI}, journal = {FRONTIERS IN CELLULAR NEUROSCIENCE}, volume = {18}, unique-id = {34760259}, issn = {1662-5102}, abstract = {Multiple lines of evidence implicate increased neuroinflammation mediated by glial cells to play a key role in neurodevelopmental disorders such as schizophrenia. Microglia, which are the primary innate immune cells of the brain, are crucial for the refinement of the synaptic circuitry during early brain development by synaptic pruning and the regulation of synaptic plasticity during adulthood. Schizophrenia risk factors as genetics or environmental influences may further be linked to increased activation of microglia, an increase of pro-inflammatory cytokine levels and activation of the inflammasome resulting in an overall elevated neuroinflammatory state in patients. Synaptic loss, one of the central pathological hallmarks of schizophrenia, is believed to be due to excess removal of synapses by activated microglia, primarily affecting glutamatergic neurons. Therefore, it is crucial to investigate microglia-neuron interactions, which has been done by multiple studies focusing on post-mortem brain tissues, brain imaging, animal models and patient iPSC-derived 2D culture systems. In this review, we summarize the major findings in patients and in vivo and in vitro models in the context of neuron-microglia interactions in schizophrenia and secondly discuss the potential of anti-inflammatory treatments for the alleviation of positive, negative, and cognitive symptoms. Copyright © 2024 Hartmann, Heider, Wüst, Fallgatter and Volkmer.}, keywords = {Inflammation; SCHIZOPHRENIA; NEURON; Complement system; microglia; co-culture; synaptic pruning}, year = {2024}, eissn = {1662-5102} } @article{MTMT:34739873, title = {Unique pathways downstream of TLR-4 and TLR-7 activation: sex-dependent behavioural, cytokine, and metabolic consequences}, url = {https://m2.mtmt.hu/api/publication/34739873}, author = {Dunstan, I.K. and McLeod, R. and Radford-Smith, D.E. and Xiong, W. and Pate, T. and Probert, F. and Anthony, D.C.}, doi = {10.3389/fncel.2024.1345441}, journal-iso = {FRONT CELL NEUROSCI}, journal = {FRONTIERS IN CELLULAR NEUROSCIENCE}, volume = {18}, unique-id = {34739873}, issn = {1662-5102}, year = {2024}, eissn = {1662-5102} } @article{MTMT:34734240, title = {Neuropeptide Y receptor 1 and galanin receptor 2 (NPY1R-GALR2) interactions in the dentate gyrus and their relevance for neurogenesis and cognition}, url = {https://m2.mtmt.hu/api/publication/34734240}, author = {Beltran-Casanueva, R. and Hernández-García, A. and de, Amo García P. and Blanco-Reina, E. and Serrano-Castro, P. and García-Casares, N. and Fuxe, K. and Borroto-Escuela, D.O. and Narváez, M.}, doi = {10.3389/fncel.2024.1323986}, journal-iso = {FRONT CELL NEUROSCI}, journal = {FRONTIERS IN CELLULAR NEUROSCIENCE}, volume = {18}, unique-id = {34734240}, issn = {1662-5102}, abstract = {Introduction: This study may unveil novel insights into the interactions between neuropeptide Y receptor 1 (NPY1R) and galanin receptor 2 (GALR2), in the dentate gyrus of the dorsal hippocampus, shedding light on their role in neurogenesis and cognitive functions. Existing literature highlights the potential of these interactions in enhancing learning and memory, yet detailed mechanisms remain underexplored. Methods: Utilizing intracerebroventricular injections of GALR2 and NPY1R agonists in Sprague-Dawley male rats, we examined neurogenesis via markers PCNA and DCX, and memory consolidation through the object-in-place task over a three-week period. Results: Significant increases in NPY1R-GALR2 co-localization and neuroblast proliferation were observed, alongside enhanced memory consolidation. These findings suggest a synergistic effect of NPY1R and GALR2 activation on cognitive functions. Discussion: Our findings may foster the development of novel heterobivalent or multitargeting drugs, affecting NPY1R-GALR2 interaction, and suggest a future pharmacogical strategy for improving learning and memory found in many brain diseases. Further research is encouraged to explore these mechanisms in pathological models. Copyright © 2024 Beltran-Casanueva, Hernández-García, de Amo García, Blanco-Reina, Serrano-Castro, García-Casares, Fuxe, Borroto-Escuela and Narváez.}, keywords = {Male; MEMORY; hippocampus; ARTICLE; controlled study; nonhuman; animal tissue; animal model; animal experiment; cell proliferation; learning; brain cortex; cognition; spatial memory; dentate gyrus; outcome assessment; unclassified drug; PENTOBARBITAL; ASTROCYTE; nervous system development; antibody labeling; neuroblast; Dorsal hippocampus; galanin receptor 2; Synergistic effect; cognitive enhancement; behavior assessment; neuropeptide Y receptor; rat; Neuronal proliferation; GALR2 agonist; neurogenic enhancement; NPY1R agonist; spatial memory performance; Galanin receptor 2 agonist M1145; GALR2 Antagonist M871; NPY1R receptor agonist Leu31; NPY1R receptor agonist Pro34; object in place task}, year = {2024}, eissn = {1662-5102} } @article{MTMT:34679229, title = {Editorial: Targeting neuron-non-neuronal interactions at the neurovascular unit in stroke and neurodegenerative disease models}, url = {https://m2.mtmt.hu/api/publication/34679229}, author = {Li, Changxiang and Liu, Yang and Liu, Jian and Xu, Xiaoyu}, doi = {10.3389/fncel.2024.1353281}, journal-iso = {FRONT CELL NEUROSCI}, journal = {FRONTIERS IN CELLULAR NEUROSCIENCE}, volume = {18}, unique-id = {34679229}, issn = {1662-5102}, keywords = {MECHANISMS; stroke; treatment; NEURODEGENERATIVE DISEASE; Neurovascular unit; neuron-non-neuronal cells interactions}, year = {2024}, eissn = {1662-5102} } @article{MTMT:34675646, title = {A combinatory genetic strategy for targeting neurogliaform neurons in the mouse basolateral amygdala}, url = {https://m2.mtmt.hu/api/publication/34675646}, author = {Ozsvar, Attila and Sieburg, Meike Claudia and Sietam, Monica Dahlstrup and Hou, Wen-Hsien and Capogna, Marco}, doi = {10.3389/fncel.2024.1254460}, journal-iso = {FRONT CELL NEUROSCI}, journal = {FRONTIERS IN CELLULAR NEUROSCIENCE}, volume = {18}, unique-id = {34675646}, issn = {1662-5102}, keywords = {optogenetics; GABAERGIC INTERNEURONS; neurogliaform cell; basolateral amygdala (BLA); neuron-derived neurotrophic factor (NDNF); retroaxonal barrage firing}, year = {2024}, eissn = {1662-5102} } @article{MTMT:34664747, title = {Utilizing hiPSC-derived oligodendrocytes to study myelin pathophysiology in neuropsychiatric and neurodegenerative disorders.}, url = {https://m2.mtmt.hu/api/publication/34664747}, author = {Shim, Gina and Romero-Morales, Alejandra I. and Sripathy, Srinidhi R. and Maher, Brady J.}, doi = {10.3389/fncel.2023.1322813}, journal-iso = {FRONT CELL NEUROSCI}, journal = {FRONTIERS IN CELLULAR NEUROSCIENCE}, volume = {17}, unique-id = {34664747}, issn = {1662-5102}, keywords = {Stem Cells; OLIGODENDROCYTES; myelination; NEURODEGENERATIVE DISEASE; Neuropsychiatric Disease; neural organoids}, year = {2024}, eissn = {1662-5102} } @article{MTMT:34650284, title = {Non-invasive in vivo imaging of brain and retinal microglia in neurodegenerative diseases}, url = {https://m2.mtmt.hu/api/publication/34650284}, author = {Etebar, Fazeleh and Harkin, Damien G. and White, Anthony R. and Dando, Samantha J.}, doi = {10.3389/fncel.2024.1355557}, journal-iso = {FRONT CELL NEUROSCI}, journal = {FRONTIERS IN CELLULAR NEUROSCIENCE}, volume = {18}, unique-id = {34650284}, issn = {1662-5102}, keywords = {MULTIPLE SCLEROSIS; Alzheimer's disease; positron emission tomography; microglia; optical coherence tomography; ADAPTIVE OPTICS; confocal scanning laser ophthalmoscopy; non-invasive in vivo imaging}, year = {2024}, eissn = {1662-5102} } @article{MTMT:34650017, title = {Human iPSC-derived retinal organoids develop robust Alzheimer's disease neuropathology}, url = {https://m2.mtmt.hu/api/publication/34650017}, author = {James, Ethan and Vielle, Anne and Cusato, Karen and Li, Helen and Lee, Byoungin and Parween, Shama and Howell, Anna and Johnson, Noah R. and Chial, Heidi J. and Potter, Huntington and Vergara, M. Natalia}, doi = {10.3389/fncel.2024.1340448}, journal-iso = {FRONT CELL NEUROSCI}, journal = {FRONTIERS IN CELLULAR NEUROSCIENCE}, volume = {18}, unique-id = {34650017}, issn = {1662-5102}, keywords = {Alzheimer's disease; Retina; Disease modeling; Organoid; hiPSC}, year = {2024}, eissn = {1662-5102} } @article{MTMT:34638422, title = {Neuronal dysfunction and gene modulation by non-coding RNA in Parkinson's disease and synucleinopathies}, url = {https://m2.mtmt.hu/api/publication/34638422}, author = {Meccariello, Rosaria and Bellenchi, Gian Carlo and Pulcrano, Salvatore and D'Addario, Sebastian Luca and Tafuri, Domenico and Mercuri, Nicola B. and Guatteo, Ezia}, doi = {10.3389/fncel.2023.1328269}, journal-iso = {FRONT CELL NEUROSCI}, journal = {FRONTIERS IN CELLULAR NEUROSCIENCE}, volume = {17}, unique-id = {34638422}, issn = {1662-5102}, keywords = {ALPHA-SYNUCLEIN; DOPAMINE NEURONS; Parkinson's disease; miRNA; LncRNA; NCRNA; synucleinopathy; circRNA}, year = {2024}, eissn = {1662-5102} } @article{MTMT:34635096, title = {Exploring the memory: existing activity-dependent tools to tag and manipulate engram cells}, url = {https://m2.mtmt.hu/api/publication/34635096}, author = {Pang, Bo and Wu, Xiaoyan and Chen, Hailun and Yan, Yiwen and Du, Zibo and Yu, Zihan and Yang, Xiai and Wang, Wanshan and Lu, Kangrong}, doi = {10.3389/fncel.2023.1279032}, journal-iso = {FRONT CELL NEUROSCI}, journal = {FRONTIERS IN CELLULAR NEUROSCIENCE}, volume = {17}, unique-id = {34635096}, issn = {1662-5102}, keywords = {MEMORY; Neuronal activity; engram cells; Activity-dependent tools; genetic strategy}, year = {2024}, eissn = {1662-5102} }