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| 001 | 144978 | ||
| 005 | 20240321221016.0 | ||
| 024 | 7 | _ | |a 10.1093/brain/awz288 |2 doi |
| 024 | 7 | _ | |a pmid:31599329 |2 pmid |
| 024 | 7 | _ | |a pmc:PMC6821333 |2 pmc |
| 024 | 7 | _ | |a 0006-8950 |2 ISSN |
| 024 | 7 | _ | |a 1460-2156 |2 ISSN |
| 024 | 7 | _ | |a altmetric:68171037 |2 altmetric |
| 037 | _ | _ | |a DZNE-2020-00342 |
| 041 | _ | _ | |a English |
| 082 | _ | _ | |a 610 |
| 100 | 1 | _ | |a Carvalho, Kevin |b 0 |
| 245 | _ | _ | |a Exacerbation of C1q dysregulation, synaptic loss and memory deficits in tau pathology linked to neuronal adenosine A2A receptor. |
| 260 | _ | _ | |a Oxford |c 2019 |b Oxford Univ. Press |
| 264 | _ | 1 | |3 online |2 Crossref |b Oxford University Press (OUP) |c 2019-10-10 |
| 264 | _ | 1 | |3 print |2 Crossref |b Oxford University Press (OUP) |c 2019-11-01 |
| 336 | 7 | _ | |a article |2 DRIVER |
| 336 | 7 | _ | |a Output Types/Journal article |2 DataCite |
| 336 | 7 | _ | |a Journal Article |b journal |m journal |0 PUB:(DE-HGF)16 |s 1599485640_15686 |2 PUB:(DE-HGF) |
| 336 | 7 | _ | |a ARTICLE |2 BibTeX |
| 336 | 7 | _ | |a JOURNAL_ARTICLE |2 ORCID |
| 336 | 7 | _ | |a Journal Article |0 0 |2 EndNote |
| 520 | _ | _ | |a Accumulating data support the role of tau pathology in cognitive decline in ageing and Alzheimer's disease, but underlying mechanisms remain ill-defined. Interestingly, ageing and Alzheimer's disease have been associated with an abnormal upregulation of adenosine A2A receptor (A2AR), a fine tuner of synaptic plasticity. However, the link between A2AR signalling and tau pathology has remained largely unexplored. In the present study, we report for the first time a significant upregulation of A2AR in patients suffering from frontotemporal lobar degeneration with the MAPT P301L mutation. To model these alterations, we induced neuronal A2AR upregulation in a tauopathy mouse model (THY-Tau22) using a new conditional strain allowing forebrain overexpression of the receptor. We found that neuronal A2AR upregulation increases tau hyperphosphorylation, potentiating the onset of tau-induced memory deficits. This detrimental effect was linked to a singular microglial signature as revealed by RNA sequencing analysis. In particular, we found that A2AR overexpression in THY-Tau22 mice led to the hippocampal upregulation of C1q complement protein-also observed in patients with frontotemporal lobar degeneration-and correlated with the loss of glutamatergic synapses, likely underlying the observed memory deficits. These data reveal a key impact of overactive neuronal A2AR in the onset of synaptic loss in tauopathies, paving the way for new therapeutic approaches. |
| 536 | _ | _ | |a 342 - Disease Mechanisms and Model Systems (POF3-342) |0 G:(DE-HGF)POF3-342 |c POF3-342 |f POF III |x 0 |
| 542 | _ | _ | |i 2019-10-10 |2 Crossref |u http://creativecommons.org/licenses/by-nc/4.0/ |
| 588 | _ | _ | |a Dataset connected to CrossRef, PubMed, |
| 650 | _ | 7 | |a ADORA2A protein, human |2 NLM Chemicals |
| 650 | _ | 7 | |a Adora2a protein, mouse |2 NLM Chemicals |
| 650 | _ | 7 | |a MAPT protein, human |2 NLM Chemicals |
| 650 | _ | 7 | |a Receptor, Adenosine A2A |2 NLM Chemicals |
| 650 | _ | 7 | |a tau Proteins |2 NLM Chemicals |
| 650 | _ | 7 | |a Complement C1q |0 80295-33-6 |2 NLM Chemicals |
| 650 | _ | 2 | |a Animals |2 MeSH |
| 650 | _ | 2 | |a Autopsy |2 MeSH |
| 650 | _ | 2 | |a Complement C1q: metabolism |2 MeSH |
| 650 | _ | 2 | |a Frontotemporal Lobar Degeneration: genetics |2 MeSH |
| 650 | _ | 2 | |a Frontotemporal Lobar Degeneration: metabolism |2 MeSH |
| 650 | _ | 2 | |a Hippocampus: metabolism |2 MeSH |
| 650 | _ | 2 | |a Hippocampus: pathology |2 MeSH |
| 650 | _ | 2 | |a Humans |2 MeSH |
| 650 | _ | 2 | |a Memory Disorders: etiology |2 MeSH |
| 650 | _ | 2 | |a Memory Disorders: psychology |2 MeSH |
| 650 | _ | 2 | |a Mice |2 MeSH |
| 650 | _ | 2 | |a Mice, Transgenic |2 MeSH |
| 650 | _ | 2 | |a Mutation |2 MeSH |
| 650 | _ | 2 | |a Neurons: metabolism |2 MeSH |
| 650 | _ | 2 | |a Receptor, Adenosine A2A: genetics |2 MeSH |
| 650 | _ | 2 | |a Receptor, Adenosine A2A: metabolism |2 MeSH |
| 650 | _ | 2 | |a Spatial Learning |2 MeSH |
| 650 | _ | 2 | |a Synapses: pathology |2 MeSH |
| 650 | _ | 2 | |a Tauopathies: genetics |2 MeSH |
| 650 | _ | 2 | |a Tauopathies: pathology |2 MeSH |
| 650 | _ | 2 | |a Tauopathies: psychology |2 MeSH |
| 650 | _ | 2 | |a tau Proteins: genetics |2 MeSH |
| 700 | 1 | _ | |a Faivre, Emilie |b 1 |
| 700 | 1 | _ | |a Pietrowski, Marie J |0 P:(DE-2719)2812560 |b 2 |u dzne |
| 700 | 1 | _ | |a Marques, Xavier |b 3 |
| 700 | 1 | _ | |a Gomez-Murcia, Victoria |b 4 |
| 700 | 1 | _ | |a Deleau, Aude |b 5 |
| 700 | 1 | _ | |a Huin, Vincent |b 6 |
| 700 | 1 | _ | |a Hansen, Jan N |0 P:(DE-2719)2812073 |b 7 |u dzne |
| 700 | 1 | _ | |a Kozlov, Stanislav |0 P:(DE-2719)2812648 |b 8 |u dzne |
| 700 | 1 | _ | |a Danis, Clément |b 9 |
| 700 | 1 | _ | |a Temido-Ferreira, Mariana |b 10 |
| 700 | 1 | _ | |a Coelho, Joana E |b 11 |
| 700 | 1 | _ | |a Mériaux, Céline |b 12 |
| 700 | 1 | _ | |a Eddarkaoui, Sabiha |b 13 |
| 700 | 1 | _ | |a Gras, Stéphanie Le |b 14 |
| 700 | 1 | _ | |a Dumoulin, Mélanie |b 15 |
| 700 | 1 | _ | |a Cellai, Lucrezia |b 16 |
| 700 | 1 | _ | |a Bank, NeuroCEB Brain |b 17 |e Collaboration Author |
| 700 | 1 | _ | |a Landrieu, Isabelle |b 18 |
| 700 | 1 | _ | |a Chern, Yijuang |b 19 |
| 700 | 1 | _ | |a Hamdane, Malika |b 20 |
| 700 | 1 | _ | |a Buée, Luc |b 21 |
| 700 | 1 | _ | |a Boutillier, Anne-Laurence |b 22 |
| 700 | 1 | _ | |a Levi, Sabine |b 23 |
| 700 | 1 | _ | |a Halle, Annett |0 P:(DE-2719)2812038 |b 24 |u dzne |
| 700 | 1 | _ | |a Lopes, Luisa V |b 25 |
| 700 | 1 | _ | |a Blum, David |0 P:(DE-HGF)0 |b 26 |e Corresponding author |
| 773 | 1 | 8 | |a 10.1093/brain/awz288 |b : Oxford University Press (OUP), 2019-10-10 |n 11 |p 3636-3654 |3 journal-article |2 Crossref |t Brain |v 142 |y 2019 |x 0006-8950 |
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