A transcriptomic atlas of aged human microglia

Marta Olah, Ellis Patrick, Alexandra-Chloe Villani, Jishu Xu, Charles C. White, Katie J. Ryan, Paul Piehowski, Alifiya Kapasi, Parham Nejad, Maria Cimpean, Sarah Connor, Christina J. Yung, Michael Frangieh, Allison McHenry, Wassim Elyaman, Vlad Petyuk, Julie A. Schneider, David A. Bennett, Philip L. De Jager () and Elizabeth M. Bradshaw ()
Additional contact information
Marta Olah: Columbia University Medical Center
Ellis Patrick: The University of Sydney
Alexandra-Chloe Villani: Broad Institute
Jishu Xu: Broad Institute
Charles C. White: Broad Institute
Katie J. Ryan: Harvard Medical School
Paul Piehowski: Pacific Northwest National Laboratory
Alifiya Kapasi: Pacific Northwest National Laboratory
Parham Nejad: Broad Institute
Maria Cimpean: Harvard Medical School
Sarah Connor: Columbia University Medical Center
Christina J. Yung: Columbia University Medical Center
Michael Frangieh: Harvard Medical School
Allison McHenry: Harvard Medical School
Wassim Elyaman: Columbia University Medical Center
Vlad Petyuk: Pacific Northwest National Laboratory
Julie A. Schneider: Rush University Medical Center
David A. Bennett: Rush University Medical Center
Philip L. De Jager: Columbia University Medical Center
Elizabeth M. Bradshaw: Columbia University Medical Center

Nature Communications, 2018, vol. 9, issue 1, 1-8

Abstract: Abstract With a rapidly aging global human population, finding a cure for late onset neurodegenerative diseases has become an urgent enterprise. However, these efforts are hindered by the lack of understanding of what constitutes the phenotype of aged human microglia—the cell type that has been strongly implicated by genetic studies in the pathogenesis of age-related neurodegenerative disease. Here, we establish the set of genes that is preferentially expressed by microglia in the aged human brain. This HuMi_Aged gene set captures a unique phenotype, which we confirm at the protein level. Furthermore, we find this gene set to be enriched in susceptibility genes for Alzheimer’s disease and multiple sclerosis, to be increased with advancing age, and to be reduced by the protective APOEε2 haplotype. APOEε4 has no effect. These findings confirm the existence of an aging-related microglial phenotype in the aged human brain and its involvement in the pathological processes associated with brain aging.

Date: 2018
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DOI: 10.1038/s41467-018-02926-5

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