Exacerbation of C1q dysregulation, synaptic loss and memory deficits in tau pathology linked to neuronal adenosine A2A receptor.


Journal

Brain : a journal of neurology
ISSN: 1460-2156
Titre abrégé: Brain
Pays: England
ID NLM: 0372537

Informations de publication

Date de publication:
01 11 2019
Historique:
received: 19 03 2019
revised: 24 07 2019
accepted: 26 07 2019
pubmed: 11 10 2019
medline: 27 5 2020
entrez: 11 10 2019
Statut: ppublish

Résumé

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.

Identifiants

pubmed: 31599329
pii: 5584878
doi: 10.1093/brain/awz288
pmc: PMC6821333
doi:

Substances chimiques

ADORA2A protein, human 0
Adora2a protein, mouse 0
MAPT protein, human 0
Receptor, Adenosine A2A 0
tau Proteins 0
Complement C1q 80295-33-6

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

3636-3654

Commentaires et corrections

Type : CommentIn

Informations de copyright

© The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain.

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Auteurs

Kevin Carvalho (K)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.

Emilie Faivre (E)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.

Marie J Pietrowski (MJ)

German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.

Xavier Marques (X)

Institut du Fer à Moulin, Inserm UMR-S 1270, Sorbonne Université, F, Paris, France.

Victoria Gomez-Murcia (V)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.

Aude Deleau (A)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.

Vincent Huin (V)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.

Jan N Hansen (JN)

German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.

Stanislav Kozlov (S)

German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.

Clément Danis (C)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.
University of Lille, CNRS UMR8576, Unité de Glycobiologie Structurale et Fonctionnelle, LabEx DISTALZ, Lille, F Lille, France.

Mariana Temido-Ferreira (M)

Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Universidade de Lisboa, Lisbon, Portugal.

Joana E Coelho (JE)

Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Universidade de Lisboa, Lisbon, Portugal.

Céline Mériaux (C)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.

Sabiha Eddarkaoui (S)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.

Stéphanie Le Gras (SL)

CNRS, Inserm, UMR 7104, GenomEast Platform, Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg, F Illkirch, France.

Mélanie Dumoulin (M)

University of Lille, F Lille, France.

Lucrezia Cellai (L)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.

Isabelle Landrieu (I)

University of Lille, CNRS UMR8576, Unité de Glycobiologie Structurale et Fonctionnelle, LabEx DISTALZ, Lille, F Lille, France.

Yijuang Chern (Y)

Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.

Malika Hamdane (M)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.

Luc Buée (L)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.

Anne-Laurence Boutillier (AL)

Laboratoire de Neuroscience Cognitives et Adaptatives (LNCA), CNRS UMR 7364, Université de Strasbourg, F Strasbourg, France.

Sabine Levi (S)

Institut du Fer à Moulin, Inserm UMR-S 1270, Sorbonne Université, F, Paris, France.

Annett Halle (A)

German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.
Institute of Neuropathology, University of Bonn Medical Center, Bonn, Germany.

Luisa V Lopes (LV)

Instituto de Medicina Molecular, Faculdade de Medicina de Lisboa, Universidade de Lisboa, Lisbon, Portugal.

David Blum (D)

University of Lille, Inserm, CHU Lille, UMR-S 1172 - JPArc, LabEx DISTALZ, F Lille, France.

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