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@ARTICLE{Keane:153985,
author = {Keane, Lily and Antignano, Ignazio and Riechers,
Sean-Patrick and Zollinger, Raphael and Dumas, Anaelle A.
and Offermann, Nina and Bernis, Maria E. and Russ, Jenny and
Graelmann, Frederike and McCormick, Patrick Neil and Esser,
Julia and Tejera, Dario and Nagano, Ai and Wang, Jun and
Chelala, Claude and Biederbick, Yvonne and Halle, Annett and
Salomoni, Paolo and Heneka, Michael T. and Capasso, Melania},
title = {m{TOR}-dependent translation amplifies microglia priming in
aging mice},
journal = {The journal of clinical investigation},
volume = {131},
number = {1},
issn = {1558-8238},
address = {Ann Arbor, Mich.},
publisher = {ASCJ},
reportid = {DZNE-2021-00002},
pages = {e132727},
year = {2021},
abstract = {Microglia maintain homeostasis in the brain. However, with
age, they become primed and respond more strongly to
inflammatory stimuli. We show here that microglia from aged
mice had upregulated mTOR complex 1 signaling controlling
translation, as well as protein levels of inflammatory
mediators. Genetic ablation of mTOR signaling showed a dual
yet contrasting effect on microglia priming: it caused an
NF-κB–dependent upregulation of priming genes at the mRNA
level; however, mice displayed reduced cytokine protein
levels, diminished microglia activation, and milder sickness
behavior. The effect on translation was dependent on reduced
phosphorylation of 4EBP1, resulting in decreased binding of
eIF4E to eIF4G. Similar changes were present in aged human
microglia and in damage-associated microglia, indicating
that upregulation of mTOR-dependent translation is an
essential aspect of microglia priming in aging and
neurodegeneration.},
keywords = {Aging: genetics / Aging: metabolism / Animals / Eukaryotic
Initiation Factor-4E: genetics / Eukaryotic Initiation
Factor-4E: metabolism / Eukaryotic Initiation Factor-4G:
genetics / Eukaryotic Initiation Factor-4G: metabolism /
Humans / Mice / Mice, Transgenic / Microglia: enzymology /
NF-kappa B: genetics / NF-kappa B: metabolism /
Phosphorylation: genetics / Protein Biosynthesis / Signal
Transduction / TOR Serine-Threonine Kinases: genetics / TOR
Serine-Threonine Kinases: metabolism},
cin = {AG Capasso / AG Heneka ; AG Heneka / AG Salomoni / AG
Halle},
ddc = {610},
cid = {I:(DE-2719)1013033 / I:(DE-2719)1011303 /
I:(DE-2719)1013032 / I:(DE-2719)1013034},
pnm = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
(POF4-352) / 353 - Clinical and Health Care Research
(POF4-353)},
pid = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352 /
G:(DE-HGF)POF4-353},
experiment = {EXP:(DE-2719)IDAF-20190308 / EXP:(DE-2719)LMF-20190308},
typ = {PUB:(DE-HGF)16},
pmc = {pmc:PMC7773382},
pubmed = {pmid:33108356},
doi = {10.1172/JCI132727},
url = {https://pub.dzne.de/record/153985},
}