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Genetic overlap between Alzheimer’s disease and immune-mediated diseases: an atlas of shared genetic determinants and biological convergence

Molecular Psychiatry (2024)Cite this article

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Abstract

The occurrence of immune disease comorbidities in Alzheimer’s disease (AD) has been observed in both epidemiological and molecular studies, suggesting a neuroinflammatory basis in AD. However, their shared genetic components have not been systematically studied. Here, we composed an atlas of the shared genetic associations between 11 immune-mediated diseases and AD by analyzing genome-wide association studies (GWAS) summary statistics. Our results unveiled a significant genetic overlap between AD and 11 individual immune-mediated diseases despite negligible genetic correlations, suggesting a complex shared genetic architecture distributed across the genome. The shared loci between AD and immune-mediated diseases implicated several genes, including GRAMD1B, FUT2, ADAMTS4, HBEGF, WNT3, TSPAN14, DHODH, ABCB9, and TNIP1, all of which are protein-coding genes and thus potential drug targets. Top biological pathways enriched with these identified shared genes were related to the immune system and cell adhesion. In addition, in silico single-cell analyses showed enrichment of immune and brain cells, including neurons and microglia. In summary, our results suggest a genetic relationship between AD and the 11 immune-mediated diseases, pinpointing the existence of a shared however non-causal genetic basis. These identified protein-coding genes have the potential to serve as a novel path to therapeutic interventions for both AD and immune-mediated diseases and their comorbidities.

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Fig. 1
Fig. 2: Genetic overlap between AD and 11 immune-mediated diseases using MiXeR software.
Fig. 3: Conditional quantile-quantile plots of nominal vs. empirical -log10 p-values in AD below the standard genome-wide association study threshold of p < 5 × 10−8 as a function of significance of association with immune-mediated diseases at the level of -log10 p-values of 1, 2, or 3, corresponding to p = 0.1, p = 0.01, and p = 0.001, respectively.
Fig. 4: A circular dendrogram showing the shared genes between AD (center circle) and each of eleven specific immune-mediated diseases (first circle), resulting in eleven pairs.

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Data availability

All the GWAS summary statistics data used in this study are publicly available to download from https://www.ebi.ac.uk/gwas/home and https://atlas.ctglab.nl/.

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Acknowledgements

We thank those investigators who generated and shared the genetic datasets used in the present study.

Funding

This research was partially supported by National Institutes of Health grants awarded to ZZ (R01LM012806, R01LM012806-07S1, R03AG077191, and U01AG079847). We thanked the resource support from Cancer Prevention and Research Institute of Texas (CPRIT RP180734). OAA is supported by the Research Council of Norway (#324499, #324252, #223273), South-East Norway Health Authority (2022-073), KG Jebsen Stiftelsen, Norwegian Health Association (#22731), and EU Horizon 2020 (# 847776). The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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Author notes

  1. These authors contributed equally: Nitesh Enduru, Brisa S. Fernandes.

Authors and Affiliations

  1. Center for Precision Health, McWilliams School of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX, USA

    Nitesh Enduru, Brisa S. Fernandes, Yulin Dai & Zhongming Zhao

  2. Department of Epidemiology, Human Genetics and Environmental Sciences, School of Public Health, The University of Texas Health Science Center at Houston, Houston, TX, USA

    Nitesh Enduru & Zhongming Zhao

  3. Norwegian Centre for Mental Disorders Research (NORMENT), Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway

    Shahram Bahrami & Ole A. Andreassen

  4. KG Jebsen Centre for Neurodevelopmental Disorders, University of Oslo, Oslo, Norway

    Shahram Bahrami & Ole A. Andreassen

  5. Faillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, USA

    Zhongming Zhao

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Contributions

NE, BSF, YD, and ZZ designed the study and collected the data. NE, SB, and YD performed the analyses. NE, BSF, OAA, and SB contributed to the literature search. NE, BSF, YD, and ZZ drafted the initial manuscript and all the authors contributed to data interpretation and manuscript writing.

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Correspondence to Zhongming Zhao.

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OAA is a consultant to Cortechs.ai, and has received speaker’s honoraria from Lundbeck, Janssen and Sunovion. NE, BSF, SB, YD, and ZZ have nothing to disclose.

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Enduru, N., Fernandes, B.S., Bahrami, S. et al. Genetic overlap between Alzheimer’s disease and immune-mediated diseases: an atlas of shared genetic determinants and biological convergence. Mol Psychiatry (2024). https://doi.org/10.1038/s41380-024-02510-y

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