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. 2024 Jun 28;147(9):3032–3047. doi: 10.1093/brain/awae205

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© The Author(s) 2024. Published by Oxford University Press on behalf of the Guarantors of Brain.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Overlap between FTLD atrophy correlated genes and genes regulated by TDP-43. (A) Cryptic splicing (CS) genes are genes that incorporate novel intronic RNA into mature mRNA when TDP-43 is knocked down experimentally or depleted from diseased neuronal nuclei. (B) One hundred and forty-six genes were shared between cryptic splicing genes and genes correlating with atrophy in FTLD-TDP. This overlap did not reach significance (P = 0.11). (C) Eighty-eight genes were shared between cryptic splicing genes and genes correlating with atrophy in FTLD-tau, with this overlap being far from significant (P = 0.75). (D) TDP-43 binds to GU repeats located on the intronic portions of the pre-messenger RNA. GU repeats are ubiquitous among brain-expressed genes, we hence identified a set of 7792 genes with above-median GU repeat content, increasing the likelihood that these genes are regulated by TDP-43. (E) Genes (n = 4271) were shared between genes with above-median GU repeat content and genes correlating with atrophy in FTLD-TDP. This overlap was significant (P = 0.03). (F) Genes (n = 2875) were shared between genes with above-median GU repeat content and genes correlating with atrophy in FTLD-tau, with this overlap being not significant (P = 0.13). *P < 0.05. FTLD = frontotemporal lobar degeneration.