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. 2024 Mar 11;15:2180. doi: 10.1038/s41467-024-46592-2

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — Network showing the gene overlap size between different gene modules and upstream transcriptional regulators. Cellular expression pattern of KDM1A immunoreactivity (IR) assessed in TLE-HS, FCD IIb, and TSC (n = 3 biological replicates per cohorts, n = 2 technical replicates). a The ridgeplots showed the distribution of gene modules coexpression (R²) for epilepsy and control cohorts within the energy metabolism regulome. Statistical significance of differential coexpression was assessed using a two-sided permutation test (TSC.10.u p-value = 3.9 × 10⁻², FCD2b.7.u p-value = 1.46 × 10⁻²). b Energy metabolism network highlighting the differentially coexpressed gene modules. KMD1A/LSD1 was predicted as common transcriptional regulator showing activation effect on FCD2b.12.u, TSC.7.u, and mTOR.5.u. c Cellular expression of KDM1A IR in TLE-HS, FCD IIb, and TSC. Panels 1–11: IHC of KDM1A. Panels 1–2: In control hippocampus, KDM1A expression was restricted to neuronal cells; KDM1A was not detectable in GFAP-positive cells (astrocytes); Panel 1: Nuclear expression in granule cell layer (gcl; arrows) of the dentate gyrus (DG); Panel 2: Nuclear expression in hilar neurons (arrows). Panels 3–4: In TLE-HS, KDM1A nuclear expression in both neurons (arrows) and astroglial cells (arrowheads). KDM1A expression in a NeuN positive neuron (insert in 2 in panel 4). Absence of KDM1A expression in HLA-DR positive cells (microglia/macrophages; insert 3 in panel 4). Panels 5–6: In control cortex, KDM1A expression was restricted to neuronal cells (insert in panel 5: high-magnification of a positive neuron); KDM1A was not detectable in GFAP-positive cells. Panels 7–9: In FCD IIb, KDM1A IR was observed in dysplastic neurons (arrows) and GFAP-positive cells (arrowheads; insert 1 in panel 7), including GFAP-positive balloon cells (asterisk). KDM1A expression in a NeuN positive dysplastic neuron (insert 2 in panel 7). Absence of KDM1A expression in HLA-DR positive cells (microglia/macrophages; panel 9). Panels 10–11: In TSC, KDM1A IR was observed in dysplastic neurons (arrows) and GFAP-positive cells (arrowheads), including giant cells (asterisks). Absence of KDM1A expression in HLA-DR positive cells (microglia/macrophages; insert 1 in panel 11). KDM1A expression in a NeuN dysplastic neuron (insert 2 in panel 11). Scale bars: 50 µm. FCD focal cortical dysplasia, GFAP glial fibrillary acidic protein, HLA human leukocyte antigen, TLE-HS temporal lobe epilepsy with hippocampal sclerosis, TSC tuberous sclerosis complex. Source data are provided as a Source Data file.