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Investigating neural impairments in psychotic disorders using electroencephalography and cortical spheroids
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  • Published: 17 February 2026

Investigating neural impairments in psychotic disorders using electroencephalography and cortical spheroids

  • Denis Reis de Assis  ORCID: orcid.org/0000-0002-2984-02791,2,
  • Atle Bråthen Pentz1,
  • Jordi Requena Osete1,2,
  • Oleksandr Ievglevskyi1,
  • Matthieu Vandenberghe1,2,
  • Ibrahim Ahmed Akkouh1,2,
  • Tuomo Mäki-Marttunen3,4,
  • Erik G. Jönsson1,5,
  • Ole A. Andreassen1,
  • Srdjan Djurovic  ORCID: orcid.org/0000-0002-8140-80611,2,
  • Elena Kondratskaya  ORCID: orcid.org/0000-0001-5066-50681,2 na1 &
  • …
  • Torbjørn Elvsåshagen1,6,7 na1 

Translational Psychiatry , Article number:  (2026) Cite this article

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We are providing an unedited version of this manuscript to give early access to its findings. Before final publication, the manuscript will undergo further editing. Please note there may be errors present which affect the content, and all legal disclaimers apply.

Subjects

  • Bipolar disorder
  • Molecular neuroscience
  • Schizophrenia
  • Stem cells

Abstract

Synaptic dysfunction is a candidate mechanism in psychotic disorders, yet the precise underlying substrates remain elusive. We investigated how combining in vivo electroencephalography (EEG) and in vitro human cortical spheroid (hCS)-based methods can further our understanding of psychosis pathophysiology during fetal stages of neurodevelopment. Ten individuals with schizophrenia (SZ) or bipolar disorder (BD; 5 males and 5 females) and five controls (CTRL; 3 males and 2 females) underwent EEG assessments, including long-term potentiation (LTP)-like cortical plasticity and mismatch negativity (MMN). hCS were generated from induced pluripotent stem cells of all participants, and immunohistochemistry, Seahorse bioenergetics and patch-clamp recordings were performed. EEG-based LTP-like plasticity was reduced in individuals with SZ and BD. Basal respiration was decreased in BD hCS and VGLUT1 levels were reduced in both SZ and BD hCS. There was a positive association between EEG-based LTP-like plasticity and hCS basal respiration which survived correction. Our data provide further support for roles of mitochondrial and glutamatergic impairments in the synaptic dysfunction of psychosis and demonstrate the potential of combining EEG- and hCS-based methods for early development mechanistic studies of brain disorders.

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Data availability

De-identified data supporting the findings of this study are available from the corresponding author upon reasonable request. Access is subjected to approval by the relevant ethics committee and data protection regulations.

References

  1. Freedman R. Schizophrenia. N Engl J Med. 2003;349:1738–49.

    Google Scholar 

  2. Belmaker RH. Bipolar disorder. N Engl J Med. 2004;351:476–86.

    Google Scholar 

  3. Lopez AD, Murray CC. The global burden of disease, 1990-2020. Nat Med. 1998;4:1241–3.

    Google Scholar 

  4. PGC. Genomic dissection of bipolar disorder and schizophrenia, including 28 subphenotypes. Cell. 2018;173:1705–15.e1716.

    Google Scholar 

  5. Trubetskoy V, Pardiñas AF, Qi T, Panagiotaropoulou G, Awasthi S, Bigdeli TB, et al. Mapping genomic loci implicates genes and synaptic biology in schizophrenia. Nature. 2022;604:502–8.

    Google Scholar 

  6. Mullins N, Forstner AJ, O’Connell KS, Coombes B, Coleman JRI, Qiao Z, et al. Genome-wide association study of more than 40,000 bipolar disorder cases provides new insights into the underlying biology. Nat Genet. 2021.

  7. Luck SJ An Introduction to the Event-Related Potential Technique. The MIT Press: Cambridge, MA, 2005.

  8. Cavus I, Reinhart RM, Roach BJ, Gueorguieva R, Teyler TJ, Clapp WC, et al. Impaired visual cortical plasticity in schizophrenia. Biol Psychiatry. 2012;71:512–20.

    Google Scholar 

  9. Cooke SF, Bear MF. Stimulus-selective response plasticity in the visual cortex: an assay for the assessment of pathophysiology and treatment of cognitive impairment associated with psychiatric disorders. Biol Psychiatry. 2012;71:487–95.

    Google Scholar 

  10. Normann C, Schmitz D, Furmaier A, Doing C, Bach M. Long-term plasticity of visually evoked potentials in humans is altered in major depression. Biol Psychiatry. 2007;62:373–80.

    Google Scholar 

  11. Elvsåshagen T, Moberget T, Boen E, Boye B, Englin NO, Pedersen PO, et al. Evidence for impaired neocortical synaptic plasticity in bipolar II disorder. Biol Psychiatry. 2012;71:68–74.

    Google Scholar 

  12. Valstad M, Roelfs D, Slapo NB, Timpe CMF, Rai A, Matziorinis AM, et al. Evidence for reduced long-term potentiation-like visual cortical plasticity in schizophrenia and bipolar disorder. Schizophr Bull. 2021;47:1751–60.

    Google Scholar 

  13. Naatanen R, Alho K. Mismatch negativity-a unique measure of sensory processing in audition. Int J Neurosci. 1995;80:317–37.

    Google Scholar 

  14. Thiebes S, Leicht G, Curic S, Steinmann S, Polomac N, Andreou C, et al. Glutamatergic deficit and schizophrenia-like negative symptoms: new evidence from ketamine-induced mismatch negativity alterations in healthy male humans. J Psychiatry Neurosci. 2017;42:273–83.

    Google Scholar 

  15. Javitt DC, Steinschneider M, Schroeder CE, Arezzo JC. Role of cortical N-methyl-D-aspartate receptors in auditory sensory memory and mismatch negativity generation: implications for schizophrenia. Proc Natl Acad Sci USA. 1996;93:11962–7.

    Google Scholar 

  16. de Sousa RT, Machado-Vieira R, Zarate CA Jr, Manji HK. Targeting mitochondrially mediated plasticity to develop improved therapeutics for bipolar disorder. Expert Opin Ther Targets. 2014;18:1131–47.

    Google Scholar 

  17. Hermens DF, Chitty KM, Kaur M. Mismatch negativity in bipolar disorder: A neurophysiological biomarker of intermediate effect?. Schizophr Res. 2018;191:132–9.

    Google Scholar 

  18. Erickson MA, Ruffle A, Gold JM. A meta-analysis of mismatch negativity in schizophrenia: from clinical risk to disease specificity and progression. Biol Psychiatry. 2016;79:980–7.

    Google Scholar 

  19. Light GA, Swerdlow NR, Thomas ML, Calkins ME, Green MF, Greenwood TA, et al. Validation of mismatch negativity and P3a for use in multi-site studies of schizophrenia: characterization of demographic, clinical, cognitive, and functional correlates in COGS-2. Schizophr Res. 2015;163:63–72.

    Google Scholar 

  20. Rangaraju V, Calloway N, Ryan TA. Activity-driven local ATP synthesis is required for synaptic function. Cell. 2014;156:825–35.

    Google Scholar 

  21. Logothetis NK, Pauls J, Augath M, Trinath T, Oeltermann A. Neurophysiological investigation of the basis of the fMRI signal. Nature. 2001;412:150–7.

    Google Scholar 

  22. Magistretti PJ, Allaman I. A cellular perspective on brain energy metabolism and functional imaging. Neuron. 2015;86:883–901.

    Google Scholar 

  23. Pellerin L, Magistretti PJ. Sweet sixteen for ANLS. Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism. 2012;32:1152–66.

    Google Scholar 

  24. Du F, Cooper AJ, Thida T, Sehovic S, Lukas SE, Cohen BM, et al. In vivo evidence for cerebral bioenergetic abnormalities in schizophrenia measured using 31P magnetization transfer spectroscopy. JAMA Psychiatry. 2014;71:19–27.

    Google Scholar 

  25. Du F, Yuksel C, Chouinard VA, Huynh P, Ryan K, Cohen BM, et al. Abnormalities in high-energy phosphate metabolism in first-episode bipolar disorder measured using (31)P-magnetic resonance spectroscopy. Biol Psychiatry. 2018;84:797–802.

    Google Scholar 

  26. Sarnyai Z, Ben-Shachar D. Schizophrenia, a disease of impaired dynamic metabolic flexibility: A new mechanistic framework. Psychiatry Res. 2024;342:116220.

    Google Scholar 

  27. McCullumsmith RE, Clinton SM, Meador-Woodruff JH. Schizophrenia as a disorder of neuroplasticity. Int Rev Neurobiol. 2004;59:19–45. pp.

    Google Scholar 

  28. Hjelm BE, Rollins B, Mamdani F, Lauterborn JC, Kirov G, Lynch G, et al. Evidence of mitochondrial dysfunction within the complex genetic etiology of schizophrenia. Mol Neuropsychiatry. 2015;1:201–19.

    Google Scholar 

  29. Breen MS, Dobbyn A, Li Q, Roussos P, Hoffman GE, Stahl E, et al. Global landscape and genetic regulation of RNA editing in cortical samples from individuals with schizophrenia. Nat Neurosci. 2019;22:1402–12.

    Google Scholar 

  30. Manji H, Kato T, Di Prospero NA, Ness S, Beal MF, Krams M, et al. Impaired mitochondrial function in psychiatric disorders. Nat Rev Neurosci. 2012;13:293–307.

    Google Scholar 

  31. Lancaster MA, Knoblich JA. Organogenesis in a dish: modeling development and disease using organoid technologies. Science (New York, NY). 2014;345:1247125.

    Google Scholar 

  32. Lancaster MA, Renner M, Martin CA, Wenzel D, Bicknell LS, Hurles ME, et al. Cerebral organoids model human brain development and microcephaly. Nature. 2013;501:373–9.

    Google Scholar 

  33. Paşca AM, Sloan SA, Clarke LE, Tian Y, Makinson CD, Huber N, et al. Functional cortical neurons and astrocytes from human pluripotent stem cells in 3D culture. Nat Methods. 2015;12:671–8.

    Google Scholar 

  34. Quadrato G, Nguyen T, Macosko EZ, Sherwood JL, Min Yang S, Berger DR, et al. Cell diversity and network dynamics in photosensitive human brain organoids. Nature. 2017;545:48–53.

    Google Scholar 

  35. Akkouh IA, Ueland T, Szabo A, Hughes T, Smeland OB, Andreassen OA. et al. Longitudinal transcriptomic analysis of human cortical spheroids identifies axonal dysregulation in the prenatal brain as a mediator of genetic risk for schizophrenia. Biol Psychiatry. 2024;95:687–98.

    Google Scholar 

  36. Yang G, Ullah HMA, Parker E, Gorsi B, Libowitz M, Maguire C. et al. Neurite outgrowth deficits caused by rare PLXNB1 mutation in pediatric bipolar disorder. Mol Psychiatry. 2023;28:2525–39.

    Google Scholar 

  37. Osete JR, Akkouh IA, Ievglevskyi O, Vandenberghe M, de Assis DR, Ueland T, et al. Transcriptional and functional effects of lithium in bipolar disorder iPSC-derived cortical spheroids. Mol Psychiatry. 2023;28:3033–43.

    Google Scholar 

  38. Notaras M, Lodhi A, Dündar F, Collier P, Sayles NM, Tilgner H, et al. Schizophrenia is defined by cell-specific neuropathology and multiple neurodevelopmental mechanisms in patient-derived cerebral organoids. Mol Psychiatry. 2022;27:1416–34.

    Google Scholar 

  39. Kathuria A, Lopez-Lengowski K, Jagtap SS, McPhie D, Perlis RH, Cohen BM, et al. Transcriptomic landscape and functional characterization of induced pluripotent stem cell-derived cerebral organoids in schizophrenia. JAMA Psychiatry. 2020;77:745–54.

    Google Scholar 

  40. Stachowiak EK, Benson CA, Narla ST, Dimitri A, Chuye LEB, Dhiman S, et al. Cerebral organoids reveal early cortical maldevelopment in schizophrenia-computational anatomy and genomics, role of FGFR1. Transl Psychiatry. 2017;7:6.

    Google Scholar 

  41. Kathuria A, Lopez-Lengowski K, Vater M, McPhie D, Cohen BM, Karmacharya R. Transcriptome analysis and functional characterization of cerebral organoids in bipolar disorder. Genome Med. 2020;12:34.

    Google Scholar 

  42. Simonsen C, Sundet K, Vaskinn A, Birkenaes AB, Engh JA, Faerden A, et al. Neurocognitive dysfunction in bipolar and schizophrenia spectrum disorders depends on history of psychosis rather than diagnostic group. Schizophr Bull. 2011;37:73–83.

    Google Scholar 

  43. Pentz AB, O’Connel KS, van Jole O, Timpe CMF, Slapo NB, Melle I, et al. Mismatch negativity and polygenic risk scores for schizophrenia and bipolar disorder. Schizophr Res. 2024;264:314–26.

    Google Scholar 

  44. Delorme A, Makeig S. EEGLAB: an open-source toolbox for analysis of single trial EEG dynamics. J Neurosci Methods. 2004;134:139–121.

    Google Scholar 

  45. Bigdely-Shamlo N, Mullen T, Kothe C, Su KM, Robbins KA. The PREP pipeline: standardized preprocessing for large-scale EEG analysis. Front Neuroinform. 2015;9:16.

    Google Scholar 

  46. Pion-Tonachini L, Kreutz-Delgado K, Makeig S. ICLabel: An automated electroencephalographic independent component classifier, dataset, and website. Neuroimage. 2019;198:181–97.

    Google Scholar 

  47. Valstad M, Moberget T, Roelfs D, Slapo NB, Timpe CMF, Beck D, et al. Experience-dependent modulation of the visual evoked potential: Testing effect sizes, retention over time, and associations with age in 415 healthy individuals. Neuroimage. 2020;223:117302.

    Google Scholar 

  48. Garrido MI, Friston KJ, Kiebel SJ, Stephan KE, Baldeweg T, Kilner JM. The functional anatomy of the MMN: a DCM study of the roving paradigm. Neuroimage. 2008;42:936–44.

    Google Scholar 

  49. Baldeweg T, Klugman A, Gruzelier J, Hirsch SR. Mismatch negativity potentials and cognitive impairment in schizophrenia. Schizophr Res. 2004;69:203–17.

    Google Scholar 

  50. Yoon SJ, Elahi LS, Pașca AM, Marton RM, Gordon A, Revah O, et al. Reliability of human cortical organoid generation. Nat Methods. 2019;16:75–8.

    Google Scholar 

  51. Pentz AB, Timpe CMF, Normann EM, Slapo NB, Melle I, Lagerberg TV, et al. Mismatch negativity in schizophrenia spectrum and bipolar disorders: Group and sex differences and associations with symptom severity. Schizophr Res. 2023;261:80–93.

    Google Scholar 

  52. Moriyama Y, Yamamoto A. Glutamatergic chemical transmission: look! Here, there, and anywhere. J Biochem. 2004;135:155–63.

    Google Scholar 

  53. Wilson NR, Kang J, Hueske EV, Leung T, Varoqui H, Murnick JG, et al. Presynaptic regulation of quantal size by the vesicular glutamate transporter VGLUT1. J Neurosci. 2005;25:6221–34.

    Google Scholar 

  54. Liguz-Lecznar M, Skangiel-Kramska J. Vesicular glutamate transporters (VGLUTs): the three musketeers of glutamatergic system. Acta Neurobiol Exp (Wars). 2007;67:207–18.

    Google Scholar 

  55. Balschun D, Moechars D, Callaerts-Vegh Z, Vermaercke B, Van Acker N, Andries L, et al. Vesicular glutamate transporter VGLUT1 has a role in hippocampal long-term potentiation and spatial reversal learning. Cereb Cortex. 2010;20:684–93.

    Google Scholar 

  56. Berry CT, Sceniak MP, Zhou L, Sabo SL. Developmental up-regulation of vesicular glutamate transporter-1 promotes neocortical presynaptic terminal development. PLoS ONE. 2012;7:e50911.

    Google Scholar 

  57. Smith RE, Haroutunian V, Davis KL, Meador-Woodruff JH. Vesicular glutamate transporter transcript expression in the thalamus in schizophrenia. Neuroreport. 2001;12:2885–7.

    Google Scholar 

  58. Oni-Orisan A, Kristiansen LV, Haroutunian V, Meador-Woodruff JH, McCullumsmith RE. Altered Vesicular Glutamate Transporter Expression in the Anterior Cingulate Cortex in Schizophrenia. Biol Psychiatry. 2008;63:766–75.

    Google Scholar 

  59. Gilabert-Juan J, Varea E, Guirado R, Blasco-Ibáñez JM, Crespo C, Nácher J. Alterations in the expression of PSA-NCAM and synaptic proteins in the dorsolateral prefrontal cortex of psychiatric disorder patients. Neurosci Lett. 2012;530:97–102.

    Google Scholar 

  60. Eastwood SL, Harrison PJ. Decreased expression of vesicular glutamate transporter 1 and complexin II mRNAs in schizophrenia: further evidence for a synaptic pathology affecting glutamate neurons. Schizophr Res. 2005;73:159–72.

    Google Scholar 

  61. Uezato A, Meador-Woodruff JH, McCullumsmith RE. Vesicular glutamate transporter mRNA expression in the medial temporal lobe in major depressive disorder, bipolar disorder, and schizophrenia. Bipolar Disord. 2009;11:711–25.

    Google Scholar 

  62. Schoonover KE, Miller NE, Fish KN, Lewis DA. Scaling of smaller pyramidal neuron size and lower energy production in schizophrenia. Neurobiol Dis. 2024;191:106394.

    Google Scholar 

  63. Ni P, Noh H, Park GH, Shao Z, Guan Y, Park JM, et al. iPSC-derived homogeneous populations of developing schizophrenia cortical interneurons have compromised mitochondrial function. Mol Psychiatry. 2020;25:2873–88.

    Google Scholar 

  64. Kathuria A, Lopez-Lengowski K, McPhie D, Cohen BM, Karmacharya R. Disease-specific differences in gene expression, mitochondrial function and mitochondria-endoplasmic reticulum interactions in iPSC-derived cerebral organoids and cortical neurons in schizophrenia and bipolar disorder. Discover mental health. 2023;3:8.

    Google Scholar 

  65. Sullivan CR, Mielnik CA, Funk A, O’Donovan SM, Bentea E, Pletnikov M, et al. Measurement of lactate levels in postmortem brain, iPSCs, and animal models of schizophrenia. Sci Rep. 2019;9:5087.

    Google Scholar 

  66. Sakaguchi H, Ozaki Y, Ashida T, Matsubara T, Oishi N, Kihara S, et al. Self-organized synchronous calcium transients in a cultured human neural network derived from cerebral organoids. Stem Cell Reports. 2019;13:458–73.

    Google Scholar 

  67. Trujillo CA, Gao R, Negraes PD, Gu J, Buchanan J, Preissl S, et al. Complex oscillatory waves emerging from cortical organoids model early human brain network development. Cell Stem Cell. 2019;25:558–69.e557.

    Google Scholar 

  68. Pekkurnaz G, Wang X. Mitochondrial heterogeneity and homeostasis through the lens of a neuron. Nature Metabolism. 2022;4:802–12.

    Google Scholar 

  69. Inan M, Zhao M, Manuszak M, Karakaya C, Rajadhyaksha AM, Pickel VM, et al. Energy deficit in parvalbumin neurons leads to circuit dysfunction, impaired sensory gating and social disability. Neurobiol Dis. 2016;93:35–46.

    Google Scholar 

  70. Robicsek O, Ene HM, Karry R, Ytzhaki O, Asor E, McPhie D, et al. Isolated mitochondria transfer improves neuronal differentiation of schizophrenia-derived induced pluripotent stem cells and rescues deficits in a rat model of the disorder. Schizophr Bull. 2018;44:432–42.

    Google Scholar 

  71. Spooner RK, Taylor BK, Ahmad IM, Dyball KN, Emanuel K, Fox HS, et al. Neural oscillatory activity serving sensorimotor control is predicted by superoxide-sensitive mitochondrial redox environments. Proc Natl Acad Sci USA. 2021;118:e2104569118.

    Google Scholar 

  72. Birnbaum R, Weinberger DR. Genetic insights into the neurodevelopmental origins of schizophrenia. Nat Rev Neurosci. 2017;18:727–40.

    Google Scholar 

  73. Kloiber S, Rosenblat JD, Husain MI, Ortiz A, Berk M, Quevedo J, et al. Neurodevelopmental pathways in bipolar disorder. Neurosci Biobehav Rev. 2020;112:213–26.

    Google Scholar 

  74. Chung DW, Geramita MA, Lewis DA. Synaptic variability and cortical gamma oscillation power in schizophrenia. Am J Psychiatry. 2022;179:277–87.

    Google Scholar 

  75. Van Derveer AB, Bastos G, Ferrell AD, Gallimore CG, Greene ML, Holmes JT, et al. A role for somatostatin-positive interneurons in neuro-oscillatory and information processing deficits in schizophrenia. Schizophr Bull. 2021;47:1385–98.

    Google Scholar 

  76. Dienel SJ, Fish KN, Lewis DA The nature of prefrontal cortical GABA neuron alterations in schizophrenia: markedly lower somatostatin and parvalbumin gene expression without missing neurons. The American journal of psychiatry 2023: 180:495-507.

  77. Javitt DC, Kantrowitz JT. The glutamate/N-methyl-d-aspartate receptor (NMDAR) model of schizophrenia at 35: On the path from syndrome to disease. Schizophr Res. 2022;242:56–61.

    Google Scholar 

  78. Booker SA, Wyllie DJA. NMDA receptor function in inhibitory neurons. Neuropharmacology. 2021;196:108609.

    Google Scholar 

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Acknowledgements

The research leading to these results has received funding from the South-Eastern Norway Regional Health Authority (#2018094, #2022087), EU’s Horizon Psych-STRATA project (#101057454), and the Research Council of Norway (#223273, #248828, #274359, #295679). D.R.A. has received funding from the European Union’s Horizon 2020 Research and Innovation Programme under the Marie Skłodowska-Curie Grant Agreement No 801133. We acknowledge the Norwegian Core Facility for Human Pluripotent Stem Cells Research Centre for the reprogramming of iPSC and for the use of their LSM700 confocal microscope.

Author information

Author notes

  1. These authors contributed equally: Elena Kondratskaya, Torbjørn Elvsåshagen.

Authors and Affiliations

  1. Center for Precision Psychiatry Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, and Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway

    Denis Reis de Assis, Atle Bråthen Pentz, Jordi Requena Osete, Oleksandr Ievglevskyi, Matthieu Vandenberghe, Ibrahim Ahmed Akkouh, Erik G. Jönsson, Ole A. Andreassen, Srdjan Djurovic, Elena Kondratskaya & Torbjørn Elvsåshagen

  2. Department of Medical Genetics, Oslo University Hospital, Oslo, Norway

    Denis Reis de Assis, Jordi Requena Osete, Matthieu Vandenberghe, Ibrahim Ahmed Akkouh, Srdjan Djurovic & Elena Kondratskaya

  3. Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland

    Tuomo Mäki-Marttunen

  4. Department of Biosciences, University of Oslo, Oslo, Norway

    Tuomo Mäki-Marttunen

  5. Centre for Psychiatric Research, Department of Clinical Neuroscience, Karolinska Institutet & Stockholm Health Care Sciences, Stockholm Region, Stockholm, Sweden

    Erik G. Jönsson

  6. Department of Neurology, Oslo University Hospital, Oslo, Norway

    Torbjørn Elvsåshagen

  7. Department of Behavioural Medicine, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway

    Torbjørn Elvsåshagen

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Contributions

Conceived and designed the analysis, DRA., SD, and TE; Collected the data, EK, DRA, ABP, JRO, OI, and MV Performed the analysis, EK, DRA, ABP, OI, JRO and MV; Writing and editing of the paper, DRA, ABP, JRO, OI, IAA, TMM, EGJ, OAA, SD, EK, TE; Supervision and funding acquisition, TE, SD and OAA All authors have read and agreed to the published version of the manuscript.

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Correspondence to Denis Reis de Assis.

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Competing interests

TE is a consultant to Sumitomo Pharma America and received speaker’s honoraria from Lundbeck and Janssen Cilag. OAA is a consultant to HealthLytix and received speaker’s honoraria from Lundbeck. The other authors declare no conflict of interest.

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Reis de Assis, D., Pentz, A.B., Requena Osete, J. et al. Investigating neural impairments in psychotic disorders using electroencephalography and cortical spheroids. Transl Psychiatry (2026). https://doi.org/10.1038/s41398-026-03863-4

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  • Received: 11 May 2025

  • Revised: 10 December 2025

  • Accepted: 28 January 2026

  • Published: 17 February 2026

  • DOI: https://doi.org/10.1038/s41398-026-03863-4

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