Loss of P2Y nucleotide receptors enhances early pathology in the TgCRND8 mouse model of Alzheimer's disease
Molecular Neurobiology, ISSN: 1559-1182, Vol: 49, Issue: 2, Page: 1031-1042
2014
- 48Citations
- 64Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations48
- Citation Indexes48
- 48
- CrossRef40
- Captures64
- Readers64
- 64
Article Description
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 P2Y nucleotide receptor (P2YR) 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 P2YR 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 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 P2YR. TgCRND8 mice with homozygous P2YR deletion survive less than 5 weeks, whereas mice with heterozygous P2YR deletion survive for 12 weeks, a time point when TgCRND8 mice are fully viable. Heterozygous P2YR deletion in TgCRND8 mice increased β-amyloid (Aβ) plaque load and soluble Aβ 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 P2YR is important for the recruitment and activation of microglial cells in the TgCRND8 mouse brain and that the P2YR 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. © 2013 Springer Science+Business Media.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84896547142&origin=inward; http://dx.doi.org/10.1007/s12035-013-8577-5; http://www.ncbi.nlm.nih.gov/pubmed/24193664; http://link.springer.com/10.1007/s12035-013-8577-5; https://dx.doi.org/10.1007/s12035-013-8577-5; https://link.springer.com/article/10.1007/s12035-013-8577-5
Springer Science and Business Media LLC
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