Cited by 206Alzheimer's disease research and treatmentsGenomics and Chromatin DynamicsEpigenetics and DNA Methylation

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Epigenomic dissection of Alzheimer’s disease pinpoints causal variants and reveals epigenome erosion

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Xiong, Xushen, James, Benjamin T., Boix, Carles A., Park, Yongjin P., Galani, Kyriaki, Victor, Matheus B., Sun, Na, Hou, Lei, Ho, Li-Lun, Mantero, Julio, Scannail, Aine Ni, Dileep, Vishnu, Dong, Weixiu, Mathys, Hansruedi, Bennett, David A., Tsai, Li-Huei, Kellis, Manolis·2023·Cell

DOI 10.1016/j.cell.2023.08.040PMC PMC10782612

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Abstract

Recent work has identified dozens of non-coding loci for Alzheimer's disease (AD) risk, but their mechanisms and AD transcriptional regulatory circuitry are poorly understood. Here, we profile epigenomic and transcriptomic landscapes of 850,000 nuclei from prefrontal cortexes of 92 individuals with and without AD to build a map of the brain regulome, including epigenomic profiles, transcriptional regulators, co-accessibility modules, and peak-to-gene links in a cell-type-specific manner. We develop methods for multimodal integration and detecting regulatory modules using peak-to-gene linking. We show AD risk loci are enriched in microglial enhancers and for specific TFs including SPI1, ELF2, and RUNX1. We detect 9,628 cell-type-specific ATAC-QTL loci, which we integrate alongside peak-to-gene links to prioritize AD variant regulatory circuits. We report differential accessibility of regulatory modules in late AD in glia and in early AD in neurons. Strikingly, late-stage AD brains show global epigenome dysregulation indicative of epigenome erosion and cell identity loss.

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Alzheimer's disease: from molecular pathways to therapies
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“Analysis of the epigenomic and transcriptomic landscapes of 850,000 nuclei from the prefrontal cortex of 92 individuals with and without AD revealed widespread epi-genomic dysregulation in the brains of late-stage AD patients [242].”
Revolutionizing Alzheimer’s Detection: Immune-Related Gene Biomarkers as Non-Invasive Predictors
Abed, S., Ebrahimi, A., Fattahi, F., Khaniani, M. S., & Derakhshan, S. M. (2025) · Molecular Neurobiology · doi:10.1007/s12035-025-04970-x · Cited by 8
“While the influence of environmental factors on AD is undeniable, genetics has garnered increased interest recently due to the finding of many genetic and epigenetic anomalies associated with AD [5].”
Cognitive rejuvenation through partial reprogramming of engram cells
Berdugo‐Vega, G., Sierra, C., Astori, S., Calati, V., Orsat, J., Scoglio, M. J., Sandi, C., & Gräff, J. (2026) · Neuron · doi:10.1016/j.neuron.2025.11.028 · Cited by 9
Simultaneous isolation of intact brain cells and cell-specific extracellular vesicles from cryopreserved Alzheimer’s disease cortex
Melnik, M., Miyoshi, E., Ma, R., Corrada, M. M., Kawas, C. H., Bohannan, R. C., Caraway, C. A., Miller, C. A., Hinman, J. D., John, V., et al. (2024) · Journal of Neuroscience Methods · doi:10.1016/j.jneumeth.2024.110137 · Cited by 8
GWAS highlights the neuronal contribution to multiple sclerosis susceptibilityPreprint
Zeng, L., Khan, A., Lama, T. D., Chitnis, T., Weiner, H. L., Wang, G., Fujita, M., Zipp, F., Taga, M. F., Kiryluk, K., et al. (2024) · medRxiv · doi:10.1101/2024.12.04.24318500 · Cited by 11
“Reviewing reference epigenomic profiles ( 70 ), we found that most of our top prioritized variants ( Figure 5 and Supplementary Table S7 ) are not located in segments of open chromatin in the cell types implicated by the eQTL analyses.”
Functional insight into East Asian–specific genetic risk loci for Alzheimer's disease
Cho, M., Chaudhuri, S., Liu, S., Park, T., Huang, Y.-N., Rosewood, T. J., Bice, P. J., Saykin, A. J., Won, H., & Nho, K. T. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14553 · Cited by 6
SPI1 affects Aβ1–42-induced microglia-mediated neuroinflammation by transcriptionally regulating FOSL2 expression
Du, J., & An, Z. (2025) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2025.578650 · Cited by 7
Single Cell Sequencing Technology and Its Application in Alzheimer’s Disease
Han, Y., Huang, C., Pan, Y., & Gu, X. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230861 · Cited by 7
GoFCards: an integrated database and analytic platform for gain of function variants in humans
Zhao, W., Tao, Y., Xiong, J., Liu, L., Wang, Z., Shao, C., Shang, L., Hu, Y., Xu, Y., Su, Y., et al. (2024) · Nucleic Acids Research · doi:10.1093/nar/gkae1079 · Cited by 7
Interpretation of Neurodegenerative GWAS Risk Alleles in Microglia and their Interplay with Other Cell Types
Holtman, I. R., Glass, C. K., & Nott, A. (2024) · Advances in neurobiology · doi:10.1007/978-3-031-55529-9_29 · Cited by 6
Massive changes in gene expression and their cause(s) can be a unifying principle in the pathobiology of Alzheimer's disease
Coleman, P. D., Delvaux, E., Kordower, J. H., Boehringer, A. V., & Huseby, C. J. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.14555 · Cited by 7
“The relationship between the epigenome and gene expression in AD received added evidence in the recent data from Xiong et al., 41 which showed a close correspondence between chromatin accessibility and geneexpression.”
Monitoring of single-nucleus chromatin landscape of ischemic stroke in mouse cerebral cortex across time
Zhang, R., Guo, S., Zhou, J., Lin, X., Wang, Y., Wang, Y., Li, M., Zhao, K., Bao, W., Shui, K., et al. (2025) · Scientific Data · doi:10.1038/s41597-025-04367-4 · Cited by 6
“The coordination between chromatin structure and transcription plays a crucial role in gene regulation, influencing processes from embryonic development to the progression of disease 7,8 .”
fSuSiE enables fine-mapping of QTLs from genome-scale molecular profilesPreprint
Denault, W. R. P., Sun, H. H., Carbonetto, P. S., Liu, A., Jager, P. L. D., Bennett, D., Wang, G., & Stephens, M. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.08.17.670732 · Cited by 8
Redox-sensitive high mobility group box 1 (HMGB1) protein is a multipotent regulator in the pathogenesis of Alzheimer's disease
Salminen, A. (2026) · Neurochemistry International · doi:10.1016/j.neuint.2026.106115 · Cited by 5
Genome-wide association analyses highlight the neuronal contribution to multiple sclerosis susceptibility
Zeng, L., Khan, A., Fitzgerald, K. C., Lama, T., Chen, J., Li, R., Harroud, A., Compston, A., Sawcer, S. J., Kermode, A. G., et al. (2026) · Nature Genetics · doi:10.1038/s41588-026-02731-7 · Cited by 5
“Review of reference epigenomic profiles 66 showed that many prioritized variants (Fig.”
The role of astrocytes in Alzheimer’s disease: a bibliometric analysis
An, X., He, J., Bi, B., Wu, G., Xu, J., Yu, W., & Ren, Z. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1481748 · Cited by 5
The China Brain Multi-omics Atlas Project (CBMAP)
Zhou, D., Zhou, Y., Sun, Z., Ji, F., Zhang, D., Wang, Q., Ruan, Y., Wang, Y., Zhu, Y., Sun, X., et al. (2025) · Molecular Psychiatry · doi:10.1038/s41380-025-03250-3 · Cited by 6
“…has analyzed the genomes, epigenomes, transcriptomes, and proteomes of hundreds of human brain tissue samples, primarily from individuals of European ancestry, thereby creating a multi-omics atlas mainly focused on understanding the etiology of Alzheimer ’ s disease (AD) [10, 11, 13, 16 – 18].”
Single-cell sequencing: accurate disease detection
Wang, X., Li, N., Wang, W., & Liu, B. (2025) · Clinical & Translational Oncology · doi:10.1007/s12094-025-04007-8 · Cited by 6
“On September 28, 2023, the team of Professor Li Huei Tsai of Massachusetts Institute of Technology published three research papers related to AD in the journal Cell, analyzing the pathogenesis of AD from multiple perspectives from the cellular, genetic and mechanism levels [72–74].”
Single‐cell digital twins identify drug targets and repurposable medicine in Alzheimer’s disease
Ren, Y., Hu, M., Li, Y. E., Pieper, A. A., Cummings, J. L., & Cheng, F. (2025) · Alzheimer s & Dementia · doi:10.1002/alz70859_102982 · Cited by 4
ACSS2 upregulation enhances neuronal resilience to aging and tau-associated neurodegeneration
Pourshafie, N., Alexander, D. C., Xu, H. W., Yang, K., Donahue, G., Lei, X., Zhang, S., Shcherbakova, O., Hogan, C., Gilbert, M., et al. (2026) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2503834122 · Cited by 4
Central amygdala single-nucleus atlas reveals chromatin and gene transcription dynamics in human alcohol use disorder
Lee, C.-Y., Hwang, A., McRiley, D., Lee, J., Thibodeau, G., Duman, C. H., Zhang, X., Škarica, M., Coudriet, J. M., Xu, S., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-68351-1 · Cited by 5
Impacts of host genetics on gut microbiome composition in Alzheimer’s disease
Liu, J., Cao, J., Jia, L., Gan, Z., Zhao, X., Yang, A., Lai, S., Chen, F., Yang, Y. T., & Zhao, X.-M. (2026) · Microbiome · doi:10.1186/s40168-026-02342-8 · Cited by 4
“To investigate the differential expression patterns of the ES-Ana-associated genes in AD brains, we leveraged a recently published snRNA-seq dataset of prefrontal cortex samples from 15 late-stage AD and 48 non-AD individuals [100].”
Dysfunction of the neurovascular unit as a temporal driver in Alzheimer’s pathogenesis
Wang, L., Han, L., & Liu, S. (2026) · Translational Neurodegeneration · doi:10.1186/s40035-026-00548-2 · Cited by 6
“Microglia play a key role in the onset and progression of AD [79, 80].”
Tau aggregates cause reactivation of transposable DNA elements, leading to Z-RNA–ZBP1-mediated neuronal death
Liu, W., Wu, S.-A., Zhang, B.-X., Guo, S., Li, L., Sun, W., Xiong, X., Nan, J., Wu, J., Zeng, L., et al. (2026) · Nature Neuroscience · doi:10.1038/s41593-026-02299-9 · Cited by 4
Regression convolutional neural network models implicate peripheral immune regulatory variants in the predisposition to Alzheimer’s disease
Ramamurthy, E., Agarwal, S., Toong, N., Sestili, H. H., Kaplow, I. M., Chen, Z., Phan, B. N., & Pfenning, A. R. (2024) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1012356 · Cited by 4
The chromatin conformation landscape of Alzheimer’s diseasePreprint
Nativio, R., Lan, Y., Donahue, G. D., Shcherbakova, O., Barnett, N., Titus, K., Chandrashekar, H., Phillips‐Cremins, J. E., Bonini, N. M., & Berger, S. L. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.04.09.588722 · Cited by 5
“To understand the changes that may occur to the genome with disease, our work 8,9 and others 10–13 has focused on epigenetic status of the brain in Alzheimer’s.”
Background
A Reproducibility Focused Meta-Analysis Method for Single-Cell Transcriptomic Case-Control Studies Uncovers Robust Differentially Expressed GenesPreprint
Nakatsuka, N. J., Adler, D. I., Jiang, L., Hartman, A., Cheng, E., Klann, E., & Satija, R. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.10.15.618577 · Cited by 4
Early microglial priming in Alzheimer’s disease revealed by ME-seqPreprint
Zhu, B., Ghosh, A., Wang, Z., Liao, Z., Appiah, M. G., Li, J., Zhang, M., Tullio, F. D., Kurowski, A., Fullard, J. F., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.01.30.702946 · Cited by 4
“Sai Ma sai.ma2@mssm.edu; Nan Yang nan.yang1@mssm.edu; Ka Lung Cheung kalung.cheung@mssm.edu Lead contact: Sai Ma sai.ma2@mssm.edu Graphic abstract”
WIMOAD: Weighted Integration of Multi-Omics Data with Meta Learning for Alzheimer’s Disease Diagnosis
Xiao, H., Wang, J., & Wan, S. (2024) · doi:10.1101/2024.09.25.614862 · Cited by 6
Tau mediates the reshaping of the transcriptional landscape toward intermediate Alzheimer’s disease stages
Siano, G., Varisco, M., Terrigno, M., Wang, C., Scarlatti, A., Iannone, V., Groth, M., Galas, M., Hoozemans, J. J. M., Cellerino, A., et al. (2025) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2024.1459573 · Cited by 5
“92 (Zerbino et al., 2018)) with Tophat v2.”
Bone-Derived Factors: Regulating Brain and Treating Alzheimer’s Disease
Guan, Q., Cao, Y., Zou, J., & Zhang, L. (2025) · Biology · doi:10.3390/biology14091112 · Cited by 3
“AD risk loci are significantly enriched in microglial enhancer regions (e.g., binding pockets of SPI1, ELF2, and RUNX1), with late-stage AD exhibiting epigenomic erosion that leads to loss of cellular identity [247].”
Age‐Associated Transcriptomic and Epigenetic Alterations in Mouse Hippocampus
Bilgic, M., Obata, R., Panfil, V., Zhu, Z., Saeki, M., Gotoh, Y., & Kishi, Y. (2025) · Aging Cell · doi:10.1111/acel.70233 · Cited by 5
“Many studies identified the specific molecular state of microglia, immune residents in the brain, in normal aging and in AD conditions in mice and humans (Li et al. 2023; Xiong et al. 2023; Sun et al. 2023; Lopes et al. 2022).”
Epigenomic alterations and neural development anomalies in induced pluripotent stem cells from sporadic Alzheimer's disease
Flamier, A., Katbe, A., Serhani, D., Hamam, R., Hogan, R., Tavares, E., Héon, E., Hanna, R., & Bernier, G. (2025) · Development · doi:10.1242/dev.204910 · Cited by 3
Multiomic single nuclei profiling the mouse hippocampus reveals that ACSS2 confers neuronal resilience to tauopathy
Egervári, G., Alexander, D. C., Huang, H., Donahue, G., Hogan, C., Mendoza, M. R., Xu, H. W., Lee, V., Garcia, B. A., Bonini, N. M., et al. (2026) · Alzheimer s & Dementia · doi:10.1002/alz.70998 · Cited by 3
FAM134B-mediated ER-phagy degrades APP and suppresses Alzheimer’s disease pathology
Zhang, Y., Sun, J., Cai, Y., Xu, Z., Li, X., Wei, W., Liu, P., Sun, Q., Wang, Z.-H., & Cui, Y. (2026) · The EMBO Journal · doi:10.1038/s44318-026-00818-9 · Cited by 3
“For ATAC-seq enrichment analysis of cortical tissue from AD cases in the Synapse database (dataset syn52293424 (Xiong et al, 2023)), data were processed using the Seurat, SingleCellExperiment, and GenomicRanges R packages.”
Omics-driven strategies for identifying biomarkers in Alzheimer’s disease
Khan, Y., Rekha, A., Ballal, S., Maharana, L., Maqbool, M., Goyal, K., Mishra, R., Uniyal, P., Alam, P., Aljarba, T. M., et al. (2026) · Metabolic Brain Disease · doi:10.1007/s11011-026-01873-1 · Cited by 3
“The late AD human brains exhibited widespread epigenomic mis-regulation with erosion of enhancers and loss of cell identity (Xiong et al. 2023).”
ReCIDE: robust estimation of cell type proportions by integrating single-reference-based deconvolutions
Li, M., Su, Y., Gao, Y., & Tian, W. (2024) · Briefings in Bioinformatics · doi:10.1093/bib/bbae422 · Cited by 3
Genetic architecture of postpartum psychosis: from common to rare genetic variation
Jung, S., Caballero, M., Kępińska, A. P., Smout, S., Munk‐Olsen, T., Robakis, T. K., Bergink, V., & Mahjani, B. (2026) · Molecular Psychiatry · doi:10.1038/s41380-026-03637-w · Cited by 3
The impact of genetic variability on Alzheimer’s therapies: obstacles for pharmacogenetic progress
Cacabelos, R., Martínez-Iglesias, O. A., Cacabelos, N., Carrera, J., Rodríguez, D., & Naidoo, V. (2025) · Expert Opinion on Drug Metabolism & Toxicology · doi:10.1080/17425255.2024.2433626 · Cited by 4
Single-cell multiplex chromatin and RNA interactions in aging human brainPreprint
Wen, X., Luo, Z., Zhao, W., Calandrelli, R., Nguyen, T. C., Wan, X., Richard, J. L. C., & Zhong, S. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.06.28.546457 · Cited by 3
“These data are reminiscent of the recent report on the association of a global epigenome dysregulation and AD 43 .”
Single-nucleus multiomics reveals the disrupted regulatory programs in three brain regions of sporadic early-onset Alzheimer's diseasePreprint
Zhao, Z., Liu, A., Citu, C., Enduru, N., Chen, X., Manuel, A. M., Sinha, T., Gorski, D., Fernandes, B. S., Yu, M., et al. (2024) · Research Square · doi:10.21203/rs.3.rs-4622123/v1 · Cited by 3
Leveraging genomic large language models to enhance causal genotype-brain-clinical pathways in Alzheimer’s diseasePreprint
Liu, Q., Zeng, W., Hongtu Zhu, B., Li, L., Wong, W. H., & Initiative, A. D. N. (2024) · medRxiv · doi:10.1101/2024.10.03.24314824 · Cited by 3

Authors: Xiong, X., James, B. T., Boix, C. A., Park, Y. P., Galani, K., Victor, M. B., Sun, N., Hou, L., Ho, L.-L., Mantero, J., Scannail, A. N., Dileep, V., Dong, W., Mathys, H., Bennett, D. A., Tsai, L.-H., & Kellis, M.
Affiliations: MIT Computer Science and Artificial Intelligence Laboratory (US)
Broad Institute (US)
Massachusetts Institute of Technology (US)
University of California San Diego (US)
University of Pittsburgh (US)
Rush University Medical Center (US)
Corresponding author: Tsai, Li-Huei
Kellis, Manolis
ORCID: Xiong, Xushen
James, Benjamin T.
Boix, Carles A.
Park, Yongjin P.
Victor, Matheus B.
Sun, Na
Mantero, Julio
Dileep, Vishnu
Dong, Weixiu
Mathys, Hansruedi
Bennett, David A.
Tsai, Li-Huei
Kellis, Manolis
Venue: Cell
Publisher: Elsevier BV
Published: 2023-09
Volume: 186
Issue: 20
Pages: 4422-4437.e21
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/j.cell.2023.08.040
PMC: PMC10782612
OpenAlex: W4387142583
Cited by: 205
References: 86
Citations by year: 2026: 70 · 2025: 72 · 2024: 51 · 2023: 11
FWCI: 36.23
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by-nc-nd/4.0/ (vor)
Locations: Cell (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
PubMed Central (acceptedVersion, other-oa)
Funders: Cure Alzheimer's Fund
National Institutes of Health (AG062377, P30AG10161, NS110453, U01AG46152, AG058002, MH119509, R01AG57473, U01AG61356, AG054012, NS127187, R01AG17917, P30AG72975, AG062335, NS115064, HG008155, MH109978, DA053631, R01AG15819, AG067151, AG074003, AG081017, AG077227, NS129032)
Russian Science Foundation
National Science Foundation (1745302)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords: Alzheimer's disease, prefrontal cortex, PU.1, RUNX1, chromatin accessibility, glial cells, neurons
MeSH terms: Epigenome, Alzheimer Disease, Brain, Gene Expression Regulation, Humans, Genome-Wide Association Study, Epigenomics

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Epigenomic dissection of Alzheimer’s disease pinpoints causal variants and reveals epigenome erosion

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