Neuropathological correlates and genetic architecture of microglial activation in elderly human brain
Abstract
Microglia, the resident immune cells of the brain, have important roles in brain health. However, little is known about the regulation and consequences of microglial activation in the aging human brain. Here we report that the proportion of morphologically activated microglia (PAM) in postmortem cortical tissue is strongly associated with ß-amyloid, tau-related neuropathology, and the rate of cognitive decline. Effect sizes for PAM measures are substantial, comparable to that of APOE e4, the strongest genetic risk factor for Alzheimer's disease, and mediation models support an upstream role for microglial activation in Alzheimer's disease via accumulation of tau. Further, we identify a common variant (rs2997325) influencing PAM that also affects in vivo microglial activation measured by [11C]-PBR28 PET in an independent cohort. Thus, our analyses begin to uncover pathways regulating resident neuroinflammation and identify overlaps of PAM's genetic architecture with those of Alzheimer's disease and several other traits.
- Authors:
-
[2];
[4];
[3];
[1]
- Columbia Univ. Medical Center, New York, NY (United States); Broad Inst. of MIT and Harvard, Cambridge, MA (United States)
- Columbia Univ. Medical Center, New York, NY (United States)
- Indiana Univ. School of Medicine, Indianapolis, IN (United States)
- Pacific Northwest National Lab. (PNNL), Richland, WA (United States)
- Rush Univ. Medical Center, Chicago, IL (United States)
- Publication Date:
- Research Org.:
- Pacific Northwest National Laboratory (PNNL), Richland, WA (United States)
- Sponsoring Org.:
- USDOE
- OSTI Identifier:
- 1591798
- Report Number(s):
- PNNL-SA-147570
Journal ID: ISSN 2041-1723
- Grant/Contract Number:
- AC05-76RL01830; P30AG10161; R01AG15819; R01AG17917; R01AG30146; R01NS084965; R01AG048015; U01AG046152; R01LM012535; R03AG054936
- Resource Type:
- Accepted Manuscript
- Journal Name:
- Nature Communications
- Additional Journal Information:
- Journal Volume: 10; Journal Issue: 1; Journal ID: ISSN 2041-1723
- Publisher:
- Nature Publishing Group
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 59 BASIC BIOLOGICAL SCIENCES; microglial; neuropathological; genetic architecture
Citation Formats
Felsky, Daniel, Roostaei, Tina, Nho, Kwangsik, Risacher, Shannon L., Bradshaw, Elizabeth M., Petyuk, Vlad A., Schneider, Julie A., Saykin, Andrew, Bennett, David A., and De Jager, Philip L. Neuropathological correlates and genetic architecture of microglial activation in elderly human brain. United States: N. p., 2019.
Web. doi:10.1038/s41467-018-08279-3.
Felsky, Daniel, Roostaei, Tina, Nho, Kwangsik, Risacher, Shannon L., Bradshaw, Elizabeth M., Petyuk, Vlad A., Schneider, Julie A., Saykin, Andrew, Bennett, David A., & De Jager, Philip L. Neuropathological correlates and genetic architecture of microglial activation in elderly human brain. United States. https://doi.org/10.1038/s41467-018-08279-3
Felsky, Daniel, Roostaei, Tina, Nho, Kwangsik, Risacher, Shannon L., Bradshaw, Elizabeth M., Petyuk, Vlad A., Schneider, Julie A., Saykin, Andrew, Bennett, David A., and De Jager, Philip L. Thu .
"Neuropathological correlates and genetic architecture of microglial activation in elderly human brain". United States. https://doi.org/10.1038/s41467-018-08279-3. https://www.osti.gov/servlets/purl/1591798.
@article{osti_1591798,
title = {Neuropathological correlates and genetic architecture of microglial activation in elderly human brain},
author = {Felsky, Daniel and Roostaei, Tina and Nho, Kwangsik and Risacher, Shannon L. and Bradshaw, Elizabeth M. and Petyuk, Vlad A. and Schneider, Julie A. and Saykin, Andrew and Bennett, David A. and De Jager, Philip L.},
abstractNote = {Microglia, the resident immune cells of the brain, have important roles in brain health. However, little is known about the regulation and consequences of microglial activation in the aging human brain. Here we report that the proportion of morphologically activated microglia (PAM) in postmortem cortical tissue is strongly associated with ß-amyloid, tau-related neuropathology, and the rate of cognitive decline. Effect sizes for PAM measures are substantial, comparable to that of APOE e4, the strongest genetic risk factor for Alzheimer's disease, and mediation models support an upstream role for microglial activation in Alzheimer's disease via accumulation of tau. Further, we identify a common variant (rs2997325) influencing PAM that also affects in vivo microglial activation measured by [11C]-PBR28 PET in an independent cohort. Thus, our analyses begin to uncover pathways regulating resident neuroinflammation and identify overlaps of PAM's genetic architecture with those of Alzheimer's disease and several other traits.},
doi = {10.1038/s41467-018-08279-3},
journal = {Nature Communications},
number = 1,
volume = 10,
place = {United States},
year = {Thu Jan 24 00:00:00 EST 2019},
month = {Thu Jan 24 00:00:00 EST 2019}
}
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