ArticleMolecular psychiatry2016
A2A adenosine receptor deletion is protective in a mouse model of Tauopathy.
Article in Molecular psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 87 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
87 citing papers in PubMed, 181 citations in OpenAlex.
- From danger to resolution: targeting purinergic signaling in CNS diseases.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026Review
- ENT1 inhibition links oligodendrocyte lipid metabolism to connectivity in tauopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Adenosine APharmaceuticals (Basel, Switzerland) · 2026Article
- Nonlinear kernel-based high-dimensional inference for set-based genetic association studies.Briefings in bioinformatics · 2026Article
- N-terminally acetylated Met11-Tau: a new pathological truncated Tau species with functional relevance in Alzheimer's disease.Translational neurodegeneration · 2026Article
- Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026Review
- Article
- Upregulation of adenosine AMolecular psychiatry · 2025Article
- Blockade of AGeroScience · 2025Article
- Cell redistribution of G quadruplex-structured DNA is associated with morphological changes of nuclei and nucleoli in neurons during tau pathology progression.Brain pathology (Zurich, Switzerland) · 2025Article
- Neuronal A2A receptor exacerbates synapse loss and memory deficits in APP/PS1 mice.Brain : a journal of neurology · 2024Article
- Feedback facilitation by adenosine APurinergic signalling · 2024Article
- Inhibition of the interaction between microglial adenosine 2A receptor and NLRP3 inflammasome attenuates neuroinflammation posttraumatic brain injury.CNS neuroscience & therapeutics · 2024Article
- Novel Development and Prospects in Pathogenesis, Diagnosis, and Therapy of Alzheimer's Disease.Journal of Alzheimer's disease reports · 2024Review
- Blockade of adenosine AAlzheimer's research & therapy · 2023Article
- Butyrate protects and synergizes with nicotine against iron- and manganese-induced toxicities in cell culture: Implications for neurodegenerative diseases.Research square · 2023Article
- Effect of caffeine in the intraventricular hemorrhage of the preterm newborn.Neural regeneration research · 2023Article
- Adenosine ABiomolecules · 2023Article
- Xanthine-Dopamine Hybrid Molecules as Multitarget Drugs with Potential for the Treatment of Neurodegenerative Diseases.Biomolecules · 2023Article
- Caffeine for Prevention of Alzheimer's Disease: Is the ABiomolecules · 2023Review
27 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedA2A adenosine receptor deletion is protective in a mouse model of Tauopathy.2016 · Mariciniak, E [Corrected to Marciniak, E]
Authors and funding
21 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Consumption of caffeine, a non-selective adenosine A2A receptor (A2AR) antagonist, reduces the risk of developing Alzheimer's disease (AD) in humans and mitigates both amyloid and Tau burden in transgenic mouse models. However, the impact of selective A2AR blockade on the progressive development of AD-related lesions and associated memory impairments has not been investigated. In the present study, we removed the gene encoding A2AR from THY-Tau22 mice and analysed the subsequent effects on both pathological (Tau phosphorylation and aggregation, neuro-inflammation) and functional impairments (spatial learning and memory, hippocampal plasticity, neurotransmitter profile). We found that deleting A2ARs protect from Tau pathology-induced deficits in terms of spatial memory and hippocampal long-term depression. These effects were concomitant with a normalization of the hippocampal glutamate/gamma-amino butyric acid ratio, together with a global reduction in neuro-inflammatory markers and a decrease in Tau hyperphosphorylation. Additionally, oral therapy using a specific A2AR antagonist (MSX-3) significantly improved memory and reduced Tau hyperphosphorylation in THY-Tau22 mice. By showing that A2AR genetic or pharmacological blockade improves the pathological phenotype in a Tau transgenic mouse model, the present data highlight A2A receptors as important molecular targets to consider against AD and Tauopathies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.