Details

Autor(en) / Beteiligte

• Faivre, Emilie
• Coelho, Joana E.
• Zornbach, Katja
• Malik, Enas
• Baqi, Younis
• Schneider, Marion
• Cellai, Lucrezia
• Carvalho, Kevin
• Sebda, Shéhérazade
• Figeac, Martin
• Eddarkaoui, Sabiha
• Caillierez, Raphaëlle
• Chern, Yijuang
• Heneka, Michael
• Sergeant, Nicolas
• Müller, Christa E.
• Halle, Annett
• Buée, Luc
• Lopes, Luisa V.
• Blum, David

Titel

Beneficial Effect of a Selective Adenosine A2A Receptor Antagonist in the APPswe/PS1dE9 Mouse Model of Alzheimer’s Disease

Ist Teil von

• Frontiers in molecular neuroscience, 2018-07, Vol.11, p.235-235

Ort / Verlag

Lausanne: Frontiers Research Foundation

Erscheinungsjahr

2018

Quelle

EZB Electronic Journals Library

Beschreibungen/Notizen

• Consumption of caffeine, a non-selective adenosine A2A receptor (A2AR) antagonist, reduces the risk of developing Alzheimer’s disease (AD) and mitigates both amyloid and Tau lesions in transgenic mouse models of the disease. While short-term treatment with A2AR antagonists have been shown to alleviate cognitive deficits in mouse models of amyloidogenesis, impact of a chronic and long-term treatment on the development of amyloid burden, associated neuroinflammation and memory deficits has never been assessed. In the present study, we have evaluated the effect of a 6-month treatment of APPsw/PS1dE9 mice with the potent and selective A2AR antagonist MSX-3 from 3 to 9-10 months of age. At completion of the treatment, we found that the MSX-3 treatment prevented the development of memory deficits in APP/PS1dE9 mice, without significantly altering hippocampal and cortical gene expressions. Interestingly, MSX-3 treatment led to a significant decrease of A1-42 levels in the cortex of APP/PS1dE9 animals, while A1-40 increased, thereby strongly affecting the A1-42/A1-40 ratio. Together, these data support the idea that A2AR blockade is of therapeutic value for Alzheimer’s disease.