ReviewBiology of the cell2015
P2Y receptors in Alzheimer's disease.
Review in Biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 42 citations in OpenAlex.
- Experimental Models and Translational Strategies in Neuroprotective Drug Development with Emphasis on Alzheimer's Disease.Molecules (Basel, Switzerland) · 2026Review
- Microglial purinergic signaling in Alzheimer's disease.Purinergic signalling · 2025Review
- Extracellular Vesicles and Purinergic Signaling in Alzheimer's Disease-Joining Forces for Novel Therapeutic Approach.Brain sciences · 2025Review
- P2Y1 receptor in Alzheimer's disease.Neural regeneration research · 2025Article
- Age-related changes in P2Y receptor signalling in mouse cochlear supporting cells.The Journal of physiology · 2023Article
- The ATP-dependent Pathways and Human Diseases.Current medicinal chemistry · 2023Article
- Astrocytes as a Therapeutic Target in Alzheimer's Disease-Comprehensive Review and Recent Developments.International journal of molecular sciences · 2022Review
- Identification of Therapeutic Targets for Amyotrophic Lateral Sclerosis Using PandaOmics - An AI-Enabled Biological Target Discovery Platform.Frontiers in aging neuroscience · 2022Article
- Dysregulation of Astrocyte-Neuronal Communication in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Phosphoinositides: Roles in the Development of Microglial-Mediated Neuroinflammation and Neurodegeneration.Frontiers in cellular neuroscience · 2021Review
- NeuroinflammatoryFrontiers in pharmacology · 2021Review
- State-of-the-Art: Inflammatory and Metabolic Markers in Mood Disorders.Life (Basel, Switzerland) · 2020Review
- Blood Transcriptome Response to Environmental Metal Exposure Reveals Potential Biological Processes Related to Alzheimer's Disease.Frontiers in public health · 2020Article
- Role of purinergic receptors in the Alzheimer's disease.Purinergic signalling · 2018Review
- Small Molecules Enhance Scaffold-Based Bone Grafts via Purinergic Receptor Signaling in Stem Cells.International journal of molecular sciences · 2018Review
- Association of cerebrovascular dysfunction with the development of Alzheimer's disease-like pathology in OXYS rats.BMC genomics · 2018Article
- Importance of GPCR-Mediated Microglial Activation in Alzheimer's Disease.Frontiers in cellular neuroscience · 2018Review
- Microglia P2Y6 receptor is related to Parkinson's disease through neuroinflammatory process.Journal of neuroinflammation · 2017Article
- Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017Review
- Roles of extracellular nucleotides and P2 receptors in ectodomain shedding.Cellular and molecular life sciences : CMLS · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is the most common cause of dementia, affecting more than 10% of people over the age of 65. Age is the greatest risk factor for AD, although a combination of genetic, lifestyle and environmental factors also contribute to disease development. Common features of AD are the formation of plaques composed of beta-amyloid peptides (Aβ) and neuronal death in brain regions involved in learning and memory. Although Aβ is neurotoxic, the primary mechanisms by which Aβ affects AD development remain uncertain and controversial. Mouse models overexpressing amyloid precursor protein and Aβ have revealed that Aβ has potent effects on neuroinflammation and cerebral blood flow that contribute to AD progression. Therefore, it is important to consider how endogenous signalling in the brain responds to Aβ and contributes to AD pathology. In recent years, Aβ has been shown to affect ATP release from brain and blood cells and alter the expression of G protein-coupled P2Y receptors that respond to ATP and other nucleotides. Accumulating evidence reveals a prominent role for P2Y receptors in AD pathology, including Aβ production and elimination, neuroinflammation, neuronal function and cerebral blood flow.
Indexed as
Identifiers
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.