%0 Journal Article %@ 1662-5099 %A Francistiová Linda %A Bianchi Carolina %A Di Lauro Caterina %A Sebastián-Serrano Álvaro %A Diego-García, de Laura %A Kobolák Julianna %A Dinnyés András %A Diaz-Hernández Miguel %A Állatélettani Tanszék SZIE / MKK / BTI ÁT [2020-], %A MTMT Központi kezelésű szerzők [1994-], %A Sejtbiológiai és Molekuláris Medicina Tanszék SZTE / TTIK / BI [2016-], %D 2020 %F publicatio:21164 %J FRONTIERS IN MOLECULAR NEUROSCIENCE %P Terjedelem: 14 p-Azonosító: 94 %T The Role of P2X7 Receptor in Alzheimer’s Disease %U http://publicatio.bibl.u-szeged.hu/21164/ %V 13 %X Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease characterized by a progressive cognitive decline associated with global brain damage. Initially, intracellular paired helical filaments composed by hyperphosphorylated tau and extracellular deposits of amyloid-β (Aβ) were postulated as the causing factors of the synaptic dysfunction, neuroinflammation, oxidative stress, and neuronal death, detected in AD patients. Therefore, the vast majority of clinical trials were focused on targeting Aβ and tau directly, but no effective treatment has been reported so far. Consequently, only palliative treatments are currently available for AD patients. Over recent years, several studies have suggested the involvement of the purinergic receptor P2X7 (P2X7R), a plasma membrane ionotropic ATP-gated receptor, in the AD brain pathology. In this line, altered expression levels and function of P2X7R were found both in AD patients and AD mouse models. Consequently, genetic depletion or pharmacological inhibition of P2X7R ameliorated the hallmarks and symptoms of different AD mouse models. In this review, we provide an overview of the current knowledge about the role of the P2X7R in AD. © Copyright © 2020 Francistiová, Bianchi, Di Lauro, Sebastián-Serrano, de Diego-García, Kobolák, Dinnyés and Díaz-Hernández. %Z BioTalentum Ltd, Gödöllõ, Hungary Szent István University, Gödöllõ, Hungary Department of Biochemistry and Molecular Biology, Veterinary School, Complutense University of Madrid, Madrid, Spain Instituto de Investigación Sanitaria del Hospital Clínico San Carlos, Madrid, Spain HCEMM-USZ StemCell Research Group, University of Szeged, Szeged, Hungary Export Date: 4 August 2020 Correspondence Address: Díaz-Hernández, M.; Department of Biochemistry and Molecular Biology, Veterinary School, Complutense University of Madrid, Instituto de Investigación Sanitaria del Hospital Clínico San CarlosSpain; email: migueldiaz@ucm.es Funding details: RTI2018-095753-B-I00 Funding details: 739593 Funding details: 766124 Funding text 1: Funding. This project has received funding from the European Union?s Horizon 2020 Research and Innovation Program under the Marie Sk?odowska-Curie Grant Agreement No. 766124. The project has received funding from the EU?s Horizon 2020 Research and Innovation Program under Grant Agreement No. 739593. Spanish Ministry of Economy and Competitiveness RTI2018-095753-B-I00 (to MD-H).