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. 2021 Nov 20;13(1):26–46. doi: 10.1007/s13238-021-00888-x

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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/.

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Targeting PINK1 in the adult monkey brain caused neuronal loss without alteration in mitochondria. (A) Targeting PINK1 reduced NeuN expression in the AAV-PINK1 gRNA/Cas9-injected substantia nigra in the monkey brain. (B) In the PINK1 targeted substantia nigra, the survived neurons showed that mitochondrial labeling by TOM20 antibody is not different from the control neuron without PINK1 targeting. Scale bars: 10 μm. (C) Electron microscopy revealed degenerated cells in the substantia nigra injected with AAV-PINK1-gRNA/Cas9. Degenerated neurons show electron-dense cytoplasm, with no clear profiling or identifiable nuclear membrane (upper panel). Arrows indicate lysosomes, and stars indicate phagocytic vacuole-like structures. Mitochondrial morphology in degenerated neurons is not different from normal neurons in the control gRNA/Cas9-injected brain region (lower panel). Scale bars: 2 μm (upper panel), 0.5 μm (lower panel)