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. 2024 Dec 12;272(1):58. doi: 10.1007/s00415-024-12822-2

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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. 2 — Neuropathology. Typical ALS pathology with (a) loss of motor neurons in the anterior horn of the spinal cord (H&E) and TDP-43-immunoreactive neuronal cytoplasmic inclusions in the spinal cord (b) and precentral gyrus (c). (d) The caudate nucleus revealed no signs of neurodegeneration by H&E. However, mild astrogliosis was detected by GFAP immunohistochemistry (e). PolyQ-immunoreactive neuronal intranuclear inclusions were present in the striatum (f) and frontal cortex (g)