Loss of P2Y2 Nucleotide Receptors Enhances Early Pathology in the TgCRND8 Mouse Model of Alzheimer's Disease
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 2 nucleotide receptor (P...
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Published in | Molecular neurobiology Vol. 49; no. 2; pp. 1031 - 1042 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Boston
Springer US
01.04.2014
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Subjects | |
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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 P2Y
2
nucleotide receptor (P2Y
2
R) 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 P2Y
2
R 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 Aβ
1–42
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 P2Y
2
R is important for the recruitment and activation of microglial cells in the TgCRND8 mouse brain and that the P2Y
2
R 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. |
---|---|
AbstractList | 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
2
nucleotide receptor (P2Y
2
R) 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 P2Y
2
R 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 Aβ
1-42
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 P2Y
2
R is important for the recruitment and activation of microglial cells in the TgCRND8 mouse brain and that the P2Y
2
R 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. 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 2 nucleotide receptor (P2Y 2 R) 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 P2Y 2 R 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 Aβ 1–42 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 P2Y 2 R is important for the recruitment and activation of microglial cells in the TgCRND8 mouse brain and that the P2Y 2 R 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. 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. |
Author | Camden, Jean M. Weisman, Gary A. Ajit, Deepa Thebeau, Christina N. Sun, Grace Y. Erb, Laurie Miller, Douglas C. Petris, Michael J. El-Sayed, Farid G. Woods, Lucas T. Greeson, Glen W. |
AuthorAffiliation | 4 Interdisciplinary Neurosciences Program, University of Missouri, Columbia, Missouri, USA 1 Department of Biochemistry, University of Missouri, Columbia, Missouri, USA 3 Department of Pathology and Anatomical Sciences, University of Missouri School of Medicine, Columbia, Missouri, USA 2 Department of Nutritional Sciences and Exercise Physiology, University of Missouri, Columbia, Missouri, USA |
AuthorAffiliation_xml | – name: 2 Department of Nutritional Sciences and Exercise Physiology, University of Missouri, Columbia, Missouri, USA – name: 3 Department of Pathology and Anatomical Sciences, University of Missouri School of Medicine, Columbia, Missouri, USA – name: 1 Department of Biochemistry, University of Missouri, Columbia, Missouri, USA – name: 4 Interdisciplinary Neurosciences Program, University of Missouri, Columbia, Missouri, USA |
Author_xml | – sequence: 1 givenname: Deepa surname: Ajit fullname: Ajit, Deepa organization: Department of Biochemistry, University of Missouri – sequence: 2 givenname: Lucas T. surname: Woods fullname: Woods, Lucas T. organization: Department of Biochemistry, University of Missouri – sequence: 3 givenname: Jean M. surname: Camden fullname: Camden, Jean M. organization: Department of Biochemistry, University of Missouri – sequence: 4 givenname: Christina N. surname: Thebeau fullname: Thebeau, Christina N. organization: Department of Biochemistry, University of Missouri – sequence: 5 givenname: Farid G. surname: El-Sayed fullname: El-Sayed, Farid G. organization: Department of Biochemistry, University of Missouri – sequence: 6 givenname: Glen W. surname: Greeson fullname: Greeson, Glen W. organization: Department of Biochemistry, University of Missouri – sequence: 7 givenname: Laurie surname: Erb fullname: Erb, Laurie organization: Department of Biochemistry, University of Missouri, Interdisciplinary Neurosciences Program, University of Missouri – sequence: 8 givenname: Michael J. surname: Petris fullname: Petris, Michael J. organization: Department of Biochemistry, University of Missouri, Interdisciplinary Neurosciences Program, University of Missouri, Department of Nutritional Sciences and Exercise Physiology, University of Missouri – sequence: 9 givenname: Douglas C. surname: Miller fullname: Miller, Douglas C. organization: Department of Pathology and Anatomical Sciences, University of Missouri School of Medicine – sequence: 10 givenname: Grace Y. surname: Sun fullname: Sun, Grace Y. organization: Department of Biochemistry, University of Missouri, Interdisciplinary Neurosciences Program, University of Missouri – sequence: 11 givenname: Gary A. surname: Weisman fullname: Weisman, Gary A. email: weismang@missouri.edu organization: Department of Biochemistry, University of Missouri, Interdisciplinary Neurosciences Program, University of Missouri |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/24193664$$D View this record in MEDLINE/PubMed |
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Snippet | Neuroinflammation is a prominent feature in Alzheimer's disease (AD) and activation of the brain's innate immune system, particularly microglia, has been... Neuroinflammation is a prominent feature in Alzheimer’s disease (AD) and activation of the brain’s innate immune system, particularly microglia, has been... |
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SubjectTerms | Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - pathology Amyloid beta-Peptides - metabolism Animals Biomedical and Life Sciences Biomedicine Brain - metabolism Brain - pathology Cell Biology Disease Models, Animal Disease Progression Female Humans Male Mice Mice, Inbred C3H Mice, Inbred C57BL Mice, Transgenic Neurobiology Neurology Neurosciences Peptide Fragments - metabolism Plaque, Amyloid - metabolism Plaque, Amyloid - pathology Receptors, Purinergic P2Y2 - deficiency Receptors, Purinergic P2Y2 - genetics |
Title | Loss of P2Y2 Nucleotide Receptors Enhances Early Pathology in the TgCRND8 Mouse Model of Alzheimer's Disease |
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