ArticleMolecular neurobiology2014
Loss of P2Y₂ nucleotide receptors enhances early pathology in the TgCRND8 mouse model of Alzheimer's disease.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 56 citations in OpenAlex.
- The role of natural polyphenols in purinergic signaling: from molecular mechanisms to physiological implications.Purinergic signalling · 2026Review
- Inhibition of the P2Y2 Receptor Promotes Facial Nerve Function by Enhancing Neuron Autophagy.Current neuropharmacology · 2026Article
- 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
- Pharmacological interaction and immune response of purinergic receptors in therapeutic modulation.Purinergic signalling · 2024Review
- P2X7 receptor inhibition ameliorates ubiquitin-proteasome system dysfunction associated with Alzheimer's disease.Alzheimer's research & therapy · 2023Article
- Therapeutic potential for P2YPurinergic signalling · 2023Review
- 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 role of efferocytosis in neuro-degenerative diseases.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Review
- Glial Purinergic Signaling in Neurodegeneration.Frontiers in neurology · 2021Review
- Antagonistic Roles of P2X7 and P2Y2 Receptors in Neurodegenerative Diseases.Frontiers in pharmacology · 2021Article
- Exercise training ameliorates cerebrovascular dysfunction in a murine model of Alzheimer's disease: role of the P2Y2 receptor and endoplasmic reticulum stress.American journal of physiology. Heart and circulatory physiology · 2020Article
- Blood Transcriptome Response to Environmental Metal Exposure Reveals Potential Biological Processes Related to Alzheimer's Disease.Frontiers in public health · 2020Article
- P2 Receptors as Therapeutic Targets in the Salivary Gland: From Physiology to Dysfunction.Frontiers in pharmacology · 2020Review
- Review
- Microglia in Alzheimer Disease: Well-Known Targets and New Opportunities.Frontiers in aging neuroscience · 2019Review
- Role of purinergic receptors in the Alzheimer's disease.Purinergic signalling · 2018Review
- P2YOral diseases · 2018Article
- The Role of Macrophages in Neuroinflammatory and Neurodegenerative Pathways of Alzheimer's Disease, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis: Pathogenetic Cellular Effectors and Potential Therapeutic Targets.International journal of molecular sciences · 2018Review
- Importance of GPCR-Mediated Microglial Activation in Alzheimer's Disease.Frontiers in cellular neuroscience · 2018Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Neuroinflammation is a prominent feature in Alzheimer's disease (AD) and activation of the brain's innate immune system, particularly microglia, has been postulated to both retard and accelerate AD progression. Recent studies indicate that the G protein-coupled P2Y2 nucleotide receptor (P2Y2R) is an important regulator of innate immunity by assisting in the recruitment of monocytes to injured tissue, neutrophils to bacterial infections and eosinophils to allergen-infected lungs. In this study, we investigated the role of the P2Y2R in progression of an AD-like phenotype in the TgCRND8 mouse model that expresses Swedish and Indiana mutations in amyloid precursor protein (APP). Our results indicate that P2Y 2 R expression is upregulated in TgCRND8 mouse brain within 10 weeks of age and then decreases after 25 weeks of age, as compared to littermate controls expressing low levels of the P2Y 2 R. TgCRND8 mice with homozygous P2Y 2 R deletion survive less than 5 weeks, whereas mice with heterozygous P2Y 2 R deletion survive for 12 weeks, a time point when TgCRND8 mice are fully viable. Heterozygous P2Y 2 R deletion in TgCRND8 mice increased β-amyloid (Aβ) plaque load and soluble Aβ1-42 levels in the cerebral cortex and hippocampus, decreased the expression of the microglial marker CD11b in these brain regions and caused neurological deficits within 10 weeks of age, as compared to age-matched TgCRND8 mice. These findings suggest that the P2Y2R is important for the recruitment and activation of microglial cells in the TgCRND8 mouse brain and that the P2Y2R may regulate neuroprotective mechanisms through microglia-mediated clearance of Aβ that when lost can accelerate the onset of an AD-like phenotype in the TgCRND8 mouse.
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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.