ReviewFrontiers in pharmacology2019
Exploring the Role of P2X Receptors in Alzheimer's Disease.
Review in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
17 citing papers in PubMed, 28 citations in OpenAlex.
- Are Hippocampal Hypoperfusion and ATP Depletion Prime Movers in the Genesis of Alzheimer's Disease? A Review of Recent Pertinent Observations from Molecular Biology.International journal of molecular sciences · 2025Review
- Cell Type-Specific Expression of Purinergic P2X Receptors in the Hypothalamus.International journal of molecular sciences · 2025Review
- Focus on P2X7R in microglia: its mechanism of action and therapeutic prospects in various neuropathic pain models.Frontiers in pharmacology · 2025Review
- Crosstalk between P2Y receptors and cyclooxygenase activity in inflammation and tissue repair.Purinergic signalling · 2024Review
- Next Generation Sequencing and Electromyography Reveal the Involvement of theCurrent issues in molecular biology · 2024Article
- 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
- The ATP-dependent Pathways and Human Diseases.Current medicinal chemistry · 2023Article
- Neuroprotective Properties of Eudesmin on a Cellular Model of Amyloid-β Peptide Toxicity.Journal of Alzheimer's disease : JAD · 2023Article
- Alternative Pharmacological Strategies for the Treatment of Alzheimer's Disease: Focus on Neuromodulator Function.Biomedicines · 2022Review
- Platelets and the Role of P2X Receptors in Nociception, Pain, Neuronal Toxicity and Thromboinflammation.International journal of molecular sciences · 2022Review
- Deciphering the role of PGC-1α in neurological disorders: from mitochondrial dysfunction to synaptic failure.Neural regeneration research · 2022Review
- Microglial Activation Modulated by P2X4R in Ischemia and Repercussions in Alzheimer's Disease.Frontiers in physiology · 2022Review
- Role of P2X4/NLRP3 Pathway-Mediated Neuroinflammation in Perioperative Neurocognitive Disorders.Mediators of inflammation · 2022Article
- Proteomics of autism and Alzheimer's mouse models reveal common alterations in mTOR signaling pathway.Translational psychiatry · 2021Article
- Implication of Neuronal Versus Microglial P2X4 Receptors in Central Nervous System Disorders.Neuroscience bulletin · 2020Review
- Amyloid Beta Peptide (AβJournal of clinical medicine · 2020Article
- P2X7 Receptor is Involved in Mitochondrial Dysfunction Induced by Extracellular Alpha Synuclein in Neuroblastoma SH-SY5Y Cells.International journal of molecular sciences · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several studies have pointed to soluble oligomers of beta amyloid peptide (SOAβ) as the principal neurotoxic agents responsible for the generation of synaptotoxic events that can explain the main symptoms of Alzheimer's disease (AD). Among the toxic features associated with SOAβ, one of the most notorious is the formation of a non-selective pore-like structure in the plasma membrane, which may partly explain the overload of intracellular Ca
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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.