ArticleFrontiers in cellular neuroscience2022
Prostacyclin Promotes Degenerative Pathology in a Model of Alzheimer's Disease.
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Potassium-Hydroxide-Based Extraction of Nicotinamide Adenine Dinucleotides from Biological Samples Offers Accurate Assessment of Intracellular Redox Status.International journal of molecular sciences · 2025Article
- Integrated Microbiome and Metabolomics Analysis Reveals Altered Aggressive Behaviors in Broiler Chickens Showing Different Tonic Immobility.Animals : an open access journal from MDPI · 2025Article
- Prostaglandins in the Inflamed Central Nervous System: Potential Therapeutic Targets.Current drug targets · 2024Review
- Modifiable Innate Biology within the Gut-Brain Axis for Alzheimer's Disease.Biomedicines · 2022Review
- Prostacyclin Promotes Degenerative Pathology in a Model of Alzheimer's Disease.Frontiers in cellular neuroscience · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the most common form of dementia in aged populations. A substantial amount of data demonstrates that chronic neuroinflammation can accelerate neurodegenerative pathologies. In AD, chronic neuroinflammation results in the upregulation of cyclooxygenase and increased production of prostaglandin H2, a precursor for many vasoactive prostanoids. While it is well-established that many prostaglandins can modulate the progression of neurodegenerative disorders, the role of prostacyclin (PGI2) in the brain is poorly understood. We have conducted studies to assess the effect of elevated prostacyclin biosynthesis in a mouse model of AD. Upregulated prostacyclin expression significantly worsened multiple measures associated with amyloid-β (Aβ) disease pathologies. Mice overexpressing both Aβ and PGI2 exhibited impaired learning and memory and increased anxiety-like behavior compared with non-transgenic and PGI2 control mice. PGI2 overexpression accelerated the development of Aβ accumulation in the brain and selectively increased the production of soluble Aβ
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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.