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Epigenomic dissection of Alzheimer’s disease pinpoints causal variants and reveals epigenome erosion
Open accessAbstract
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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In the citing paper
“Recent single-cell studies of human AD revealed the links between DNA damage and epigenome erosion during disease progression77,78.”
From Single-cell parallel analysis of DNA damage and transcriptome reveals selective genome vulnerability (2025) · cites this paper as [78]
In the citing paper
“These work estimated damage burden by measuring chimeric gene fusions arose from DSBs.”
From Single-cell parallel analysis of DNA damage and transcriptome reveals selective genome vulnerability (2025) · cites this paper as [78]
In the citing paper
“Note the rs10792832-flanking peak (highlighted in the vertical yellow box) identified in our iMG is only present in brain microglia but not in other cell types.”
From PICALM Alzheimer’s risk allele causes aberrant lipid droplets in microglia (2025) · cites this paper as [24]
In the citing paper
“These severely affected donors had lower transcription and reduced chromatin accessibility that may correspond to senescent states97, or global epigenome dysregulation that is indicative of cell identity loss98.”
From Integrated multimodal cell atlas of Alzheimer’s disease (2024) · cites this paper as [98]
In the citing paper
“the accompanying manuscript by Xiong et al. describes widespread changes in cell-type specific chromatin accessibility within excitatory neurons in human AD samples which they term “epigenome erosion””
From Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration (2023) · cites this paper as [89]
In the citing paper
“This is strikingly similar to epigenome erosion, particularly in excitatory neurons and oligodendrocytes, characterized by the loss of cell-type specific chromatin accessibility profile reported in the companion manuscript89.”
From Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration (2023) · cites this paper as [89]
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Context-dependent regulatory variants in Alzheimer’s diseasePreprint
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“Patients with late-stage Alzheimer’s disease also display less identifiable cell-type-specific ATAC-seq signatures in CNS neurons and glia 170 , suggesting accelerated epigenetic erosion of cell-type-specific transcriptional programs.”
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“In particular, most AD-associated variants reside in intronic or intergenic regions, and their regulatory roles remain largely unexplored ( 13 ).”
Tau alters global gene expression affecting chromatin in the early stages of Alzheimer’s diseasePreprint
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“…should examine whether widespread DNA hypomethylation is coincident with promoter-specific DNA hypermethylation, akin to a cancer and aging epigenome ( 51 ), or associated with loss of H3K27me3 (and other marks) to mimic a state of epigenome erosion, recently observed in Alzheimer’s disease ( 52 ).”
Eyring, K. W., Liu, C., Elhajjaoui, N., Abuhanna, K. D., Zhang, Y., von Behren, Z., Eskin, E., Geschwind, D. H., & Luo, C. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.06.17.660162 · Cited by 2
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Abdelhady, G., Brull, O. R., He, J., Lin, M. K., Galván, A., Pfenning, A. R., Bostan, A. C., & Stauffer, W. R. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.11.16.688724 · Cited by 2
“This validation was successful: Alzheimer’s disease (AD) risk variants were exclusively enriched in microglia, 18,68,69 consistent with extensive evidence implicating microglia to be key cell mediators of neuroinflammation in the AD brain.”
Li, Y., Tan, Y. J., Chen, R., Zhou, X., Chen, Y., Huo, Y., Guo, X., Tiwari, A., Wen, Z., Zhong, X. Y., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2025.12.11.693589 · Cited by 2
“To assess the biological plausibility of inferred interactions, we used the gene-peak pairs reported in [40] as a reference for enrichment analysis.”
Genetic drivers of progression in Alzheimer’s disease are distinct from disease risk
Cohen, C. E., Fernandez, S., Yaman, U., Ehyaei, A. R., Kodosaki, E., Askarova, A., Porter, T., O’Brien, E., Study, A. I. B. A. L., Initiative, A. D. N., et al. (2026) · Alzheimer's Research & Therapy · doi:10.1186/s13195-026-02036-1 · Cited by 1
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Interpretable deep generative ensemble learning for single-cell omics with Hydra
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“To achieve this, we utilized our previously published single-cell multiome dataset that pro fi led the transcriptome and epigenome of the medial frontal cortex (MFC) region of the brain (Xiong et al, 2023).”
A Single-Cell Omics Technical Guide for Advancing Neuropsychiatric Research
Casmey, K., Zimmermann, M., Xie, Y., Codeluppi-Arrowsmith, S. A., & Turecki, G. (2025) · Genes · doi:10.3390/genes16121394 · Cited by 3
“Single-cell multi-omic technologies that have been applied to the human postmortem brain include Chromium Epi Multiome ATAC + Gene Expression [132,137,161,167,168], snm3C-seq [156,171,172], snmC-seq3 [172], MUSIC [170], and snmCAT-seq/snmCT-seq [173,174] (Table 2).”
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“…global epigenome erosion was observed in late-stage Alzheimer's patients, whereby regions of the genome that were previously accessible become repressed, previously inaccessible regions become active, and the boundaries between euchromatic and heterochromatin are blurred (Xiong et al. 2023).”
Genetic evidence supports therapeutic modulation of progranulin levels in Alzheimer’s Disease
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“These large AD genetic studies have identified key AD risk genes as well as the strong impact of microglial inflammation and lipid metabolism on disease pathology, in addition to amyloid and Tau pathology [10, 16].”
Li, Z., Li, H., Zhang, S., Wang, X., Ji, X., Zhang, J., Hou, D., Fan, M., Liu, R., Xiang, Y., et al. (2026) · Pharmacological Research · doi:10.1016/j.phrs.2026.108137 · Cited by 1
A computational framework for epigenetic plasticity in memory
Delamare, G., Wagle, S., Gräff, J., & Clopath, C. (2026) · Brain · doi:10.1093/brain/awag094 · Cited by 1
“40-43 We simulated cognitive deficiency by decreasing the learning rate (see the ‘Materials and methods’ section), which mimics working memory impairments 44 and reduced cognitive flexibility, 45 thereby isolating the contribution of impaired potentiation without altering forgetting rates.”
Decoding neurodegeneration one cell at a time
Gautier, O., Nguyen, T. P., & Gitler, A. D. (2026) · Journal of Clinical Investigation · doi:10.1172/jci199841 · Cited by 3
Epigenetic Gene Networks Governing Immune State Transitions Across the Lifespan
Al-Ewaidat, O. A., & Naffaa, M. M. (2026) · Immunology · doi:10.1111/imm.70161 · Cited by 2
“Inflammation may persist without repair, antigen presentation may decline despite immune-cell presence, or injury signals may remain intact while reparative programs remain inaccessible [24, 25].”
Single-cell multiomics connects 3D genome and transcriptome alterations in Alzheimer’s disease
Zhang, Y., Lu, X., Kunisky, A. K., Alam, S., Tang, J., Zhang, R., Wang, S., Zhang, H. H., Baroudi, J. K., Ichcho, W., et al. (2026) · Science · doi:10.1126/science.adz1652 · Cited by 3
Personalized single-cell transcriptomics reveals molecular diversity in Alzheimer’s disease
Chandrashekar, P. B., Alatkar, S. A., Kalafut, N. C., Jin, T., Gupta, C., Burczak, R. C., Xiang, H., Liu, S., Li, A. Z., Hong, A., et al. (2026) · Nature Communications · doi:10.1038/s41467-026-72310-1 · Cited by 2
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Omics Approaches in Alzheimer’s Disease Research
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The brain cells linked to protection against dementia
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“Microglia-specific regulatory regions originating from human samples are strongly enriched for AD genetic risk 5,6,10,43 .”
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Epigenetic dysregulation in Alzheimer’s disease based on single-cell multi-omics
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Postnatal epigenome-mediated aging control and global trends
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Bioinformatics and Machine Learning-Based Screening of Key Genes in Alzheimer's Disease
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“While this observation strongly suggests a potential loss of epigenetic marks that effectuate silencing of the second X-chromosome 26 , further studies need to investigate causality and the sequence of events during disease development. iterating over all SNV position and haplotype options…”
BackgroundEpigenomic anomalies in induced pluripotent stem cells from Alzheimer’s disease casesPreprint
Flamier, A., Katbe, A., Serhani, D., Hamam, R., Hogan, R., Tavares, E. S., Héon, E., Hanna, R., & Bernier, G. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.08.29.610372
“A comparable phenomenon was described in AD neurons and glial cells in situ , as revealed using single-nuclei RNA-seq of late AD brains and referred to as epigenome erosion 14 .”
BackgroundCell-type-specific mapping of enhancers and target genes from single-cell multimodal dataPreprint
Su, C., Lee, D., Jin, P. K., & Zhang, J. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.09.24.614814
“We focused on the three abundant brain cell types as in Figure 3C and did not include astrocytes and microglia due to the limited number of cells from these two cell types in the second dataset [33].”
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“This coordinated remodeling is not only limited to development, but is also important for neuronal reprogramming 38 and disease 39,40 .”
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“…regulatory mechanisms, large-scale single-cell transcriptomic and epigenomic pro fi ling studies have begun to characterize widespread remodeling of cis-regulatory elements and transcription factor (TF) programs in vulnerable brain cell types in AD and related tauopathies 10,17,18,28 – 33 .”
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Brain Region-Specific Epigenomic Reorganization and Altered Cell States in Alzheimer’s DiseasePreprint
Wang, W., Berube, P., Yang, B., Castanon, R., Bartlett, A., Komandur, K., Nery, J. R., Barragan, C., Kenworthy, M., Valadon, C., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.29.678849
Sun, X., Wu, L., Orr, T. C., Heck, A., Young, K., Dunaway, N., Navarro, J. C., Beechem, J., & Orr, M. E. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.11.19.689127
Liu, A., Jager, P. L. D., Bennett, D. A. A., Wang, G., & Denault, W. R. P. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.11.25.690439
“Chromatin accessibility profiles were obtained from six major brain cell types previously profiled in 92 donors from dorsolateral prefrontal cortex [29], including astrocytes (Ast), excitatory neurons (Exc), inhibitory neurons (Inh), microglia (Mic), oligodendrocytes (Oli), and oligodendrocyte…”
InfluentialKelsey, M. M. G., Chongtham, A., LaCava, J., Taylor, M. S., Boeke, J. D., Gage, F. H., Seluanov, A., Gorbunova, V. A., Pereira, A. C., & Sedivy, J. M. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2025.12.12.693943 · Cited by 1
The ‘vulnerability code’: Is cell identity the architect of its own decay?
Bai, D., Cao, Z., & Zhu, C. (2025) · Clinical and Translational Medicine · doi:10.1002/ctm2.70555
“…correlations between elevated DNA damage, the gradual decline of the epigenetic landscape and the development of age-related neurodegenerative disorders, 7,8 indicating that an imbalance between DNA repair mechanisms and epigenetic stability may contribute to neuronal aging and disease progression.”
Zhang, J., Mao, Y., & Rao, J. (2024) · Figshare · doi:10.6084/m9.figshare.26754694
Zhang, J., Mao, Y., & Rao, J. (2024) · Figshare · doi:10.6084/m9.figshare.26754697
Pelletier, A., Tuck, T., & Julia, T. C. W. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.01.02.697432
“Xiong et al. 29 ROSMAP snATAC-seq fragment files (syn52335505) have been processed using Signac 30 .”
InfluentialMouse models to interrogate the developmental pathogenesis of Huntington's disease
Altun, Y., Yan, S., Zheng, K., Molero, A. E., & Mehler, M. F. (2026) · Journal of Huntington s Disease · doi:10.1177/18796397251412135 · Cited by 1
Huang, Z., Liu, W., Zhang, Y., Zha, B., Wang, P., & Yang, J. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2025.1708008
Modeling Late-Onset Sporadic Alzheimer’s Disease Using Patient-Derived Cells: A Review
Katbe, A., Diagne, I., & Bernier, G. (2026) · Neurology International · doi:10.3390/neurolint18010017
Ren, Y., Hu, M., Yang, L., Pieper, A. A., Cummings, J. L., & Cheng, F. (2026) · Genome Research · doi:10.1101/gr.280436.125
Z-RNA-ZBP1 axis drives Tau-mediated neurodegenerationPreprint
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) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.02.16.706067
“Xiong et al. established a single-cell epigenomic atlas of the prefrontal cortex (PFC) and demonstrated progressive epigenetic erosion in late-stage Alzheimer’s disease (AD) patients 37 .”
Gojani, E. G., Farzin, H., Sutherland, R. J., & Mohajerani, M. H. (2026) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2026.106619
Rewiring of 3D Enhancer-Promoter Interactome Underlies Diabetic Endothelial DysfunctionPreprint
Jiang, L., Yang, X., Zhou, R., Zheng, S., Li, Y., Tan, N., Pauklin, S., Sadayappan, S., Zhang, C., Hong, W., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.03.03.709273
Huang, C., Han, Y., He, J., Ma, W., Chen, Y., Dong, Z., Cheng, X., Lu, C., & Gu, X. (2026) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-25-00789
Fukui, M., Kaise, T., Masaki, T., Sakamoto, T., & Kageyama, R. (2026) · Cell Reports · doi:10.1016/j.celrep.2026.117250
Washer, S. J., Frith, M., Cowan, E., Dempster, E. L., Mill, J. S., & Farrow, S. L. (2026) · Trends in Neurosciences · doi:10.1016/j.tins.2026.03.004
Shapira, Y., Noack, F., Vangelisti, S., Chong, F., Lifshitz, A., Tanay, A., & Bonev, B. (2026) · Genes & Development · doi:10.1101/gad.353090.125
“This coordinated remodeling is not only limited to development but also important for neuronal re-programming (Pereira et al. 2024) and disease (Dileep et al. 2023; Xiong et al. 2023).”
Mercer, T. J., Dániel, B., Fredrickson, C., Le, D., Lee, S., Kulkarni, V. V., Hou, X., Fiesel, F. C., Ngu, H., Jung, M., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.04.24.719390 · Cited by 1
Dissecting Alzheimer’s disease heterogeneity by cross-trait polygenic predictionPreprint
Li, W. F., Mohammed, N., Bennett, D. A. A., Kellis, M., & Tanigawa, Y. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.05.15.725551
A Multi-Context Regulome-Wide Association Atlas for Genetic Studies of Aging Brain DisordersPreprint
Liu, C., Wang, A., Sun, H. H., Luo, K., Qian, S., Li, Y., Nachun, D. C., He, X., Jager, P. L. D., Bennett, D. A. A., et al. (2026) · medRxiv · doi:10.64898/2026.05.15.26353329
A large-scale single cell map of primary and conditional regulatory variation in the human brainPreprint
Lee, S., Hamdan, Z., Huntress, S. S., Yang, A., & Guo, M. H. (2026) · medRxiv · doi:10.64898/2026.05.30.26354534
Rogers, B. B., Anderson, A. G., Rodríguez-Nunez, I., Bartley, S. C., Johnston, S. Q., Taylor, J. W., Meadows, S. K., Newberry, K. M., Myers, R., & Cochran, J. N. (2026) · iScience · doi:10.1016/j.isci.2026.116412 · Cited by 1
Ngo, J. C., Xu, Y., Olah, M., & Sher, F. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.06.30.735672
“To determine the relevance of migration-regulating WRC subunits in the human brain, we examined their expression in published single-nucleus RNA-sequencing datasets [20, 54] (Fig.”
Ferroptosis-related biomarkers for diagnosis and mechanistic insights into Alzheimer’s disease
Zhao, M., Sui, X., Li, J. S., Wang, Q., Sun, Y. M., Zheng, H., & Li, B. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1857642
Zhang, X., Zhuang, D., Lai, C., Zheng, C., Soh, Z. D., Wagner, S. K., Cai, V. Y., Yang, Z., Wang, S., Geng, X., et al. (2026) · Progress in Retinal and Eye Research · doi:10.1016/j.preteyeres.2026.101504
Cytoplasmic DNA Sensing Links LINE-1 Expression to Neuronal Senescence in Alzheimer’s DiseasePreprint
Herdy, J. R., Taylor, E. E., Karbacher, L., Borgogno, O., Traxler, L., Lagerwall, J., Huynh, V. A., Lefterova, Z. V., Kang, A., Tosat‐Bitrián, C., et al. (2026) · SSRN Electronic Journal · doi:10.64898/2026.07.27.740588 · Cited by 2
“Indeed, we have previously reported widespread chromatin decompaction and dedifferentiation as hallmarks of the AD iN epigenome 20,61 .”
Chugh, S., Shim, H., & McCarthy, D. J. (2026) · Genome biology · doi:10.1186/s13059-026-04199-4
“We benchmarked these simulations against a publicly available Alzheimer’s disease dataset [18], at the time of writing the only open-access scATAC-seq resource that includes both genotype and cell-type-resolved accessibility data across individuals.”
InfluentialReduced expression of Brain Expressed X-linked genes in Alzheimer's disease
Li, L., Kenner, E., Wan, L., Yan, Z., & Feng, J. (2026) · Journal of Alzheimer s Disease · doi:10.1177/13872877261471446
“Four scRNA-seq datasets from three independent studies 33,37,38 for a total of 192 controls and AD patients were analyzed (Figure 4A-D for each dataset).”
scCotag: Prior-Informed Co-Optimal Transport for Robust Single-Cell Multi-Omics Integration
Li, Y., Tan, Y., Chen, R., Zhou, X., Chen, Y., Huo, Y., Guo, X., Tiwari, A., Wen, Z., Zhong, X. Y., et al. (2026) · ACM SIGKDD Conference on Knowledge Discovery and Data Mining (KDD) · doi:10.1145/3770855.3818921
“To assess the biological plausibility of inferred interactions, we used the interactions reported in [51] as a reference for enrichment analysis.”
InfluentialAlzweiri, M. H., Agha, A. S. A. A., Qinna, N. A., AlDabet, G., Khassawna, T. E., & Aburjai, T. A. (2026) · Biomedicines · doi:10.3390/biomedicines14081823
“Crucially, most common-risk variants act through non-coding regulatory elements with strong cell-type specificity, embedding fragility directly into regulatory connectivity, especially within microglial enhancer landscapes [48,64].”
Multimodal brain cell atlas across the adult macaque lifespan
Zhang, X., Lai, G., Guo, X., Ma, W., Yuan, Y., Zhang, H., Zhang, B., Fan, P., Liu, X., Guo, P., et al. (2026) · Cell · doi:10.1016/j.cell.2026.07.045
Cell type-resolved chromatin accessibility clocks for brain agingPreprint
Yu, P. Z., Yu, D., Yao, X., & Noble, W. S. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.08.22.746439
Coordinated dysregulation of modular gene activity in human neuropathologiesPreprint
Kang, G., & Oldham, M. C. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.08.25.747130
Morgans, W. G., Sharrocks, A. D., & Iqbal, M. (2026) · NAR Genomics and Bioinformatics · doi:10.1093/nargab/lqag104 · Cited by 2
“Another recently published paper [ 45 ] identified SPI1 and ELF2 as two TFs with the most enriched motifs at Alzheimer’s genetic risk loci, although it is worth noting these TFs bind similar DNA motifs.”
Niñerola, S., del Blanco, B., Cangonja, M., Paraíso‐Luna, J., Miozzo, F., Torres-Raves, P., Lipiński, M., Santos-Pereira, J. M., & Barco, Á. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.08.28.747502
“Moreover, chromatin accessibility and multi-omic studies have identified losses of accessibility at neuronal regulatory elements linked to synaptic and identity-associated genes (Leng et al., 2021; Xiong et al., 2023).”
Beyond Bulk: Cell‐Type‐Resolved Epigenomics as the Path Forward in Alzheimer's Disease Research
Cañizares-Moscato, L., Ruiz-Iglesias, J., Isoler‐Alcaráz, J., & Palomer, E. (2026) · European Journal of Neuroscience · doi:10.1111/ejn.70683
“…current evidence is largely correlative; direct tests of causality will depend on experimental manipulations that either exacerbate or restore epigenomic identity in defined cell types and assess the consequent effects on neuronal function and behaviour (Liu et al. 2025; Xiong et al. 2023).”
Influential
Metadata
- 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
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2023-09
- Volume
- 186
- Issue
- 20
- Pages
- 4422-4437.e21
- ISSN
- 0092-8674 (ISSN-L)
- 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
- 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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