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Title: Overactivity of neuronal adenosine A2A receptors accelerates neurodegeneration

Journal Article · · Brain
ORCiD logo [1]
  1. Center for Neurosciences and Cell Biology and Faculty of Medicine, University of Coimbra, Portugal

This scientific commentary refers to ‘Exacerbation of C1q dysregulation, synaptic loss and memory deficits in tau pathology linked to neuronal adenosine A2A receptors’, by Carvalho et al. (doi:10.1093/brain/awz288).

Sponsoring Organization:
USDOE Office of Nuclear Energy (NE), Nuclear Fuel Cycle and Supply Chain
OSTI ID:
1572438
Journal Information:
Brain, Journal Name: Brain Journal Issue: 11 Vol. 142; ISSN 0006-8950
Publisher:
Oxford University PressCopyright Statement
Country of Publication:
United Kingdom
Language:
English

References (10)

The physiological effects of caffeine on synaptic transmission and plasticity in the mouse hippocampus selectively depend on adenosine A1 and A2A receptors journal August 2019
Blockade of adenosine A 2A receptors recovers early deficits of memory and plasticity in the triple transgenic mouse model of Alzheimer's disease journal September 2018
A complement–microglial axis drives synapse loss during virus-induced memory impairment journal June 2016
Exacerbation of C1q dysregulation, synaptic loss and memory deficits in tau pathology linked to neuronal adenosine A2A receptor journal October 2019
How does adenosine control neuronal dysfunction and neurodegeneration? journal August 2016
Interindividual Differences in Caffeine Metabolism and Factors Driving Caffeine Consumption journal March 2018
Alzheimer's Disease Is a Synaptic Failure journal October 2002
Neuronal Adenosine A2A Receptors Are Critical Mediators of Neurodegeneration Triggered by Convulsions journal November 2018
Caffeine Intake and Dementia: Systematic Review and Meta-Analysis journal April 2010
Beneficial Effect of a Selective Adenosine A2A Receptor Antagonist in the APPswe/PS1dE9 Mouse Model of Alzheimer’s Disease journal July 2018