ArticleThe American journal of pathology2010
Suppressed accumulation of cerebral amyloid {beta} peptides in aged transgenic Alzheimer's disease mice by transplantation with wild-type or prostaglandin E2 receptor subtype 2-null bone marrow.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 51 citations in OpenAlex.
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- Microglial pro-inflammatory mechanisms induced by monomeric C-reactive protein are counteracted by soluble epoxide hydrolase inhibitors.International immunopharmacology · 2025Article
- Prostacyclin Promotes Degenerative Pathology in a Model of Alzheimer's Disease.Frontiers in cellular neuroscience · 2022Article
- EP2 Antagonists (2011-2021): A Decade's Journey from Discovery to Therapeutics.Journal of medicinal chemistry · 2021Review
- Effects of IL-34 on Macrophage Immunological Profile in Response to Alzheimer's-Related AβFrontiers in immunology · 2020Article
- Prostaglandins as the Agents That Modulate the Course of Brain Disorders.Degenerative neurological and neuromuscular disease · 2020Review
- PGEProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Associations between Use of Specific Analgesics and Concentrations of Amyloid-β 42 or Phospho-Tau in Regions of Human Cerebral Cortex.Journal of Alzheimer's disease : JAD · 2018Article
- Friend or Foe? Resident Microglia vs Bone Marrow-Derived Microglia and Their Roles in the Retinal Degeneration.Molecular neurobiology · 2017Review
- Clearance of cerebral Aβ in Alzheimer's disease: reassessing the role of microglia and monocytes.Cellular and molecular life sciences : CMLS · 2017Review
- Optical Coherence Tomography in Alzheimer's Disease and Other Neurodegenerative Diseases.Frontiers in neurology · 2017Review
- Inhibition of STAT3- and MAPK-dependent PGEJournal of neuroinflammation · 2016Article
- Targeting innate immunity for neurodegenerative disorders of the central nervous system.Journal of neurochemistry · 2016Review
- Cyclooxygenase inhibition targets neurons to prevent early behavioural decline in Alzheimer's disease model mice.Brain : a journal of neurology · 2016Article
- Untangling the Web: Toxic and Protective Effects of Neuroinflammation and PGE2 Signaling in Alzheimer's Disease.ACS chemical neuroscience · 2016Review
- Article
- Inflammatory Cyclooxygenase Activity and PGECurrent immunology reviews · 2015Article
- Therapeutic window for cyclooxygenase-2 related anti-inflammatory therapy after status epilepticus.Neurobiology of disease · 2015Article
- Prostaglandin signaling suppresses beneficial microglial function in Alzheimer's disease models.The Journal of clinical investigation · 2015Article
- Prostaglandin E2 receptor subtype 2 regulation of scavenger receptor CD36 modulates microglial Aβ42 phagocytosis.The American journal of pathology · 2015Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
A complex therapeutic challenge for Alzheimer's disease (AD) is minimizing deleterious aspects of microglial activation while maximizing beneficial actions, including phagocytosis/clearance of amyloid beta (Abeta) peptides. One potential target is selective suppression of microglial prostaglandin E(2) receptor subtype 2 (EP2) function, which influences microglial phagocytosis and elaboration of neurotoxic cytokines. To test this hypothesis, we transplanted bone marrow cells derived from wild-type mice or mice homozygous deficient for EP2 (EP2(-/-)) into lethally irradiated 5-month-old wild-type or APPswe-PS1DeltaE9 double transgenic AD mouse model recipients. We found that cerebral engraftment by bone marrow transplant (BMT)-derived wild-type or EP2(-/-) microglia was more efficient in APPswe-PS1DeltaE9 than in wild-type mice, and APPswe-PS1DeltaE9 mice that received EP2(-/-) BMT had increased cortical microglia compared with APPswe-PS1DeltaE9 mice that received wild-type BMT. We found that myeloablative irradiation followed by bone marrow transplant-derived microglia engraftment, rather than cranial irradiation or BMT alone, was responsible for the approximate one-third reduction in both Abeta plaques and potentially more neurotoxic soluble Abeta species. An additional 25% reduction in cerebral cortical Abeta burden was achieved in mice that received EP2(-/-) BMT compared with mice that received wild-type BMT. Our results provide a foundation for an adult stem cell-based therapy to suppress soluble Abeta peptide and plaque accumulation in the cerebrum of patients with AD.
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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.