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. 2024 Apr 1;15:2823. doi: 10.1038/s41467-024-47028-7

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© The Author(s) 2024

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 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. 2 — A Experimental outline for comparative analysis of CIBOP-based proteomics of PV-INs and Camk2a excitatory neurons from the mouse cortex by label-free quantitation MS analyses. 1851 proteins were quantified above negative samples in either PV-INs or Camk2a neurons. B DEA comparing PV-CIBOP (n = 3) and Camk2a-CIBOP (n = 6) cortex proteomes identified proteins >3-fold differential enrichment (signature proteins of each neuronal class), which were then hierarchically clustered. Top proteins (based on fold-change) are shown alongside the heatmap. C GSEA of PV-IN (blue) and Camk2a (red) signature proteins identified over-represented terms (GO, KEGG, Wikipathways, Reactome, Pathway commons) for PV-IN and Camk2a neurons. X-axis represents enrichment Z score for a given term, and Y-axis represents level of statistical significance of enrichment (Fisher exact test). Size of each data point indicates the number of protein IDs in that enrichment term. D Volcano plot representation of PV-IN and Camk2a neuron signature proteins which have known genetic risk associations in Alzheimer’s disease (AD) and Parkinson’s disease (PD) based on MAGMA. Some proteins have shared genetic risk associations with AD and PD (Y-axis: Camk2a-CIBOP vs. PV-IN-CIBOP unpaired two-tailed T-test *p < 0.05). E Protein-protein interaction network (STRING) of AD-associated MAGMA risk genes with differential enrichment in PV-INs and Camk2a neurons. Clusters of mitochondrial, synaptic vesicle and endocytosis related proteins were revealed in PV-IN AD MAGMA risk genes. F Enrichment of PWAS-identified proteins associated with cognitive slope in PV-enriched and Camk2a-enriched proteomic signatures. Cognitive slope was estimated in ROSMAP cases. Positive slope indicates cognitive stability or resilience while a negative slope indicates cognitive decline. Proteins positively correlated with cognitive slope are referred to as pro-resilience proteins while those negative correlated with cognitive slope are anti-resilience proteins. Enrichment of pro-resilience and anti-resilience proteins in PV-enriched and Camk2a-enriched proteins identified by CIBOP was assessed after weighting based on strength of association between proteins and cognitive slope. FDR 5% threshold is shown. Also see Supplementary Fig. 4 and Supplementary Data 2 for related analyses and datasets. Image was created using BioRender.com.