Human Microglia Show Unique Transcriptional Changes in Alzheimer's Disease
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Abstract
Microglia, the innate immune cells of the brain, influence Alzheimer’s disease (AD) progression and are potential therapeutic targets. However, microglia exhibit diverse functions, the regulation of which is not fully understood, complicating therapeutics development. To better define the transcriptomic phenotypes and gene regulatory networks associated with AD, we enriched for microglia nuclei from 12 AD and 10 control human dorsolateral prefrontal cortices (7 males and 15 females, all aged >60 years) before single-nucleus RNA sequencing. Here we describe both established and previously unrecognized microglial molecular phenotypes, the inferred gene networks driving observed transcriptomic change, and apply trajectory analysis to reveal the putative relationships between microglial phenotypes. We identify microglial phenotypes more prevalent in AD cases compared with controls. Further, we describe the heterogeneity in microglia subclusters expressing homeostatic markers. Our study demonstrates that deep profiling of microglia in human AD brain can provide insight into microglial transcriptional changes associated with AD.
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This inflammatory cluster showed significant downregulation of INPP5D, IL-1β expression was significantly elevated, and this cluster was enriched for NLR signaling.
“While this cluster showed significant downregulation of INPP5D, IL-1β expression was significantly elevated, and this cluster was enriched for NLR signaling [175].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [175]
In Results, ‘Complexity of microglia states’ (page unavailable), the paper reports increased IL1β in cluster 6 relative to homeostatic microglia and enrichment for NLR signaling. It does not state that the IL1β increase was statistically significant, and a search for INPP5D found no support for its claimed significant downregulation. (LLM, conf=0.86)
Experimental — accuracy not yet measuredRegulatory networks of microglial transcription factors are specific to distinct microglial phenotypes observed in Alzheimer's disease, including the endolysosomal phenotype and inflammatory effector cluster.
“the regulatory networks of these transcription factors are specific to the distinct microglial phenotypes observed in Alzheimer's disease, including the endolysosomal phenotype and inflammatory effector cluster”
From Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease (2026) · cites this paper as [86]
A recent single-nucleus RNA sequencing profiling study of microglia from AD and non-AD brains identified an "inflammatory" cluster that was over-represented in the AD brains.
“Furthermore, a recent single-nucleus RNA sequencing profiling study of microglia from AD and non-AD brains identified an “inflammatory” cluster that was over-represented in the AD brains.”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [175]
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Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease
Kim, B., Wang, S. S., Kim, J. R., & Kim, J. (2026) · BioEssays · doi:10.1002/bies.70186
- Authors
- Prater, K. E., Green, K. J., Mamde, S., Sun, W., Cochoit, A., Smith, C. L., Chiou, K. L., Heath, L., Rose, S. E., Wiley, J., Keene, C. D., Kwon, R. Y., Snyder-Mackler, N., Blue, E. E., Logsdon, B., Young, J. E., Shojaie, A., Garden, G. A., & Jayadev, S.
- Affiliations
- University of Washington (US)
- Fred Hutch Cancer Center (US)
- Arizona State University (US)
- Sage Bionetworks (US)
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Jayadev, Suman
- ORCID
- Venue
- Nature Aging
- Published
- 2023-05-29
- Volume
- 3
- Issue
- 7
- Pages
- 894-907
- ISSN
- 2662-8465 (ISSN-L)
- PMC
- PMC10353942
- OpenAlex
- W4378714758
- Cited by
- 164
- References
- 35
- Citations by year
- 2026: 46 · 2025: 52 · 2024: 52 · 2023: 13 · 2022: 1
- FWCI
- 17.11
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Nature Aging (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc-nd)
- Research Square (acceptedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Health & Human Services | NIH | National Institute on Aging (RF1AG063540, P30AG066509, AG05136, 5T32-AG052354-02)
- Ellison Foundation, Weill Neurohub
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Single-cell and spatial transcriptomics
- Keywords
- microglia, Alzheimer's disease, microglial transcriptome, single-nucleus RNA sequencing, gene regulatory networks, microglial heterogeneity, microglial phenotype, dorsolateral prefrontal cortex, human brain
- MeSH terms
- Alzheimer Disease, Brain, Female, Humans, Male, Microglia, Gene Expression Profiling, Transcriptome
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