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. 2021 Dec 18;16:83. doi: 10.1186/s13024-021-00501-z

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© The Author(s) 2021

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 4 — Representative images of histopathology of Lewy body disease. A, B, F-H hematoxylin and eosin staining, C-E immunohistochemistry for α-synuclein (NACP antibody). A, C Brainstem type Lewy body in the substantia nigra. B, D cortical type Lewy body (arrow) in the superior temporal cortex. E Lewy neurites in the CA2 sector of the hippocampus. F-G Lewy body disease shows neuronal loss with extracellular neuromelanin pigment in the substantia nigra (F), while it is minimum in a control case (G). H Spongiform change in the entorhinal cortex. Scale 100 μm in (A, B, and H); 50 μm in (C); 20 μm in (D-G, and I)