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. 2023 May 13;14:2765. doi: 10.1038/s41467-023-38374-z

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© The Author(s) 2023

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — A Integration of five female-specific EAML candidates involved in cell-cycle/DNA repair with genes predominantly dysregulated in female AD brains and cell cycle genes known to accumulate in AD neurons. B positive correlation of gene expression and neuropathologic features for some of the genes in the module shown in (A). C graphs representing longitudinal analyses of neuronal dysfunction assessed as speed of the animals as a function of age (days) for the indicated alleles. Blue corresponds to negative (healthy) controls expressing a non-targeting hp-RNA. Purple shows the performance of β42/ non-targeting and grey the performance of tau/ non-targeting hp-RNA diseased animals. Green or red show the performance of animals carrying the allele indicated on top and either expressing β42 (green) or tau (red) paneuronally. Knockdown of the Drosophila homologs of three of the EAML female-specific candidates (ANLN, POLD1, WDHD1) results in amelioration of the neurodegenerative phenotypes. Knockdown of the Drosophila homolog of BRCA1 also ameliorates neuronal dysfunction (specific alleles used are indicated in Supplementary Data 2). Each graph shows the fit curve of the third-degree polynomial regression (dark line) and the confidence intervals for the same regression (shaded). All experiments shown are statistically significantly different p < 0.05 (exact p values are shown in Supplementary Data 2) when analyzed using non-linear random mixed effects model ANOVA. Four replicates of ten animals each per genotype were used for these experiments.