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. 2024 Jul 27;81(1):316. doi: 10.1007/s00018-024-05335-8

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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. 4 — Load of CNVs in sALS patients compared to neurological control samples. Panel A: sALS patients show a higher load of CNVs in ALS-related genes (Definitive, Moderate, Strong and Clinical Modifier) compared to controls (p-value = 0,02, unpaired t-test two tailed); Panel B: sALS patients show a higher load of CNVs in Definitive ALS genes compared to controls (p-value = 0,03, unpaired t-test two tailed); Panel C: sALS patients show a higher total length of CNVs in Definitive ALS genes compared to controls (p-value = 0,03, unpaired t-test two tailed)