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. 2020 Nov 26;52(11):1787–1797. doi: 10.1038/s12276-020-00522-6

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Expression changes are mainly temporal by relative preservation of their spatial identity. Substantial expression changes are detected in the sixth and seventh decades of human life. The directions of gene expression changes during adult aging tend to be opposite those occurring during fetal development. Throughout multiple brain regions, age-dependent transcriptomic changes include decreased synaptic function and increased immunity. It is worth noting that synaptic aging occurs even prior to neuronal loss. Decreased synaptic function underlies increased expression of repressor element-1-silencing transcription factor (REST) and decreased expression of the tumor protein 73 (TP73) gene. Increased immune responses are accompanied by upregulation of microglial genes and complement component 1q A (C1QA) and downregulation of genes encoding immunosuppressive factors, including C-X3-C motif chemokine receptor 1 (CX3CR1).