ArticleNeuromolecular medicine2009
Amyloid-beta induces a caspase-mediated cleavage of P2X4 to promote purinotoxicity.
Article in Neuromolecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 53 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
- Microglial purinergic signaling in Alzheimer's disease.Purinergic signalling · 2025Review
- Species Differences of P2X4 Receptor Modulators.ACS pharmacology & translational science · 2025Article
- Preparation and preliminary evaluation of a tritium-labeled allosteric P2X4 receptor antagonist.Purinergic signalling · 2024Article
- Implications of COVID-19 in Parkinson's disease: the purinergic system in a therapeutic-target perspective to diminish neurodegeneration.Purinergic signalling · 2024Review
- Comorbidity Genes of Alzheimer's Disease and Type 2 Diabetes Associated with Memory and Cognitive Function.International journal of molecular sciences · 2024Review
- Action of the Purinergic and Cholinergic Anti-inflammatory Pathways on Oxidative Stress in Patients with Alzheimer's Disease in the Context of the COVID-19 Pandemic.Neuroscience · 2023Review
- P2X4 signalling contributes to hyperactivity but not pain sensitization comorbidity in a mouse model of attention deficit/hyperactivity disorder.Frontiers in pharmacology · 2023Article
- Modulation of P2XPhysiological reports · 2022Article
- Microglial Activation Modulated by P2X4R in Ischemia and Repercussions in Alzheimer's Disease.Frontiers in physiology · 2022Review
- Review
- Evans Blue Might Produce Pathologically Activated Neuroprotective Effects via the Inhibition of the P2X4R/p38 Signaling Pathway.Cellular and molecular neurobiology · 2021Article
- Increased surface P2X4 receptor regulates anxiety and memory in P2X4 internalization-defective knock-in mice.Molecular psychiatry · 2021Article
- Phosphoinositides: Roles in the Development of Microglial-Mediated Neuroinflammation and Neurodegeneration.Frontiers in cellular neuroscience · 2021Review
- Implication of Neuronal Versus Microglial P2X4 Receptors in Central Nervous System Disorders.Neuroscience bulletin · 2020Review
- Contribution of P2X4 Receptors to CNS Function and Pathophysiology.International journal of molecular sciences · 2020Review
- Calcium-Handling Defects and Neurodegenerative Disease.Cold Spring Harbor perspectives in biology · 2020Review
- The P2X7 Receptor: Central Hub of Brain Diseases.Frontiers in molecular neuroscience · 2020Review
- Exploring the Role of P2X Receptors in Alzheimer's Disease.Frontiers in pharmacology · 2019Review
- Microglia in Alzheimer Disease: Well-Known Targets and New Opportunities.Frontiers in aging neuroscience · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
Overproduction of the beta-amyloid fragment 1-42 (A beta(1-42)) is thought to contribute to synaptic dysfunction and neuronal death in Alzheimer's disease. Mounting evidence suggests that purinergic receptors play critical roles in synaptic plasticity and neuronal survival, but the potential involvement of these receptors in A beta(1-42)-induced synaptic dysfunction and neuronal death has not been addressed. Here we report that A beta(1-42) promoted accumulation of the calcium-permeable purinergic receptor P2X4 in neurons. We also report evidence that A beta(1-42) induced a caspase-3-mediated cleavage of the receptor that slowed channel closure times and prevented agonist-induced internalization of the receptor. Molecular interference to reduce the expression of P2X4 in primary rodent neurons attenuated A beta(1-42)-induced neuronal death while induced expression of P2X4 in a neuronal cell line that does not normally express P2-receptors enhanced the toxic effect of A beta(1-42). Together these findings suggest that A beta(1-42)-induced synaptic dysfunction and neuronal death may involve perturbations in P2X4 purinergic receptors.
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What OpenQuestion holds
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.