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. 2021 Sep 7;21(4):681–714. doi: 10.1007/s12311-021-01320-0

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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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Fig. 1 — Putative mechanisms underlying synaptic dysfunction in C9orf72-ALS/FTD. A schematic detailing the role of the hexanucleotide expansion, (G₄C₂)_n, of the C9orf72 gene in driving synaptic, axonal and dendritic dysfunction. This operates through the three main pathogenic mechanisms implicated in C9-ALS/FTD which are haploinsufficiency of the C9orf72 protein and the accumulation of RNA foci and dipeptide repeats (DPRs). Abbreviations: p53, tumour protein p53; RAN, repeat-associated non-AUG; Ca²⁺, calcium ions; mRNP, messenger ribonucleoprotein; RNA, ribonucleic acid