ArticleNeuroscience letters2022
Probing changes in brain esterified oxylipin concentrations during the early stages of pathogenesis in Alzheimer's Disease transgenic rats.
Article in Neuroscience letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Decoding the Oxylipin Chemical Space Using Ion Identity Molecular Networking.Analytical chemistry · 2026Article
- Oxylipin composition of high-density lipoprotein is altered in men and Hispanic adults with mild cognitive impairment.Journal of lipid research · 2026Article
- Article
- Plasma and feces multiomics unveil cognition-associated perturbations of chronic inflammatory pathways of the gut-microbiota-brain axis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Air pollution and Alzheimer disease phenotype deplete esterified proresolving lipid mediator reserves in the brain.JCI insight · 2025Article
- Insights From TgF344-AD, a Double Transgenic Rat Model in Alzheimer's Disease Research.Physiological research · 2025Review
- A Soluble Epoxide Hydrolase Inhibitor Improves Cerebrovascular Dysfunction, Neuroinflammation, Amyloid Burden, and Cognitive Impairments in the hAPP/PS1 TgF344-AD Rat Model of Alzheimer's Disease.International journal of molecular sciences · 2025Article
- The Octadecanoids: Synthesis and Bioactivity of 18-Carbon Oxygenated Fatty Acids in Mammals, Bacteria, and Fungi.Chemical reviews · 2025Review
- 12-Hydroxyeicosatetraenoic acid is the only enzymatically produced HETE increased under brain ischemia.Prostaglandins, leukotrienes, and essential fatty acids · 2024Article
- Cytochrome P450 and Epoxide Hydrolase Metabolites in Aβ and tau-induced Neurodegeneration: Insights frombioRxiv : the preprint server for biology · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Despite known pathological hallmarks of Alzheimer's Disease (AD) including neuronal loss, gliosis (inflammation), beta-amyloid plaque deposition and neurofibrillary tangle accumulation in the brain, little is known about inflammation resolution in early AD pathogenesis. In the brain, inflammation and resolution pathways are mediated by free oxylipins which are mostly bound (i.e. esterified), and therefore must be released (i.e. become free) to exert bioactivity. Recently, we showed reductions in brain esterified pro-resolving oxylipins in a transgenic rat model of AD (TgF344-AD rat) at 15 months of age, suggesting deficits in the source and availability of free pro-resolving oxylipins. In the present study, we tested whether these changes are discernable earlier in the disease process, i.e., at age of 10 months. We observed significant reductions in esterified pro-resolving 8(9)-epoxyeicosatrienoic acid (8(9)-EpETrE), 13-hydroxyoctadecatrienoic acid (13-HOTrE) and 15-hydroxyeicosapentaenoic acid (15-HEPE) oxylipins, and in pro-inflammatory 13-hydroxy-octadecadienoic acid (13-HODE), 20-hydroxy-eicosatetraenoic acid (20-HETE), 15-deoxy-prostaglandin J2 (15-deoxy-PGJ2) and prostaglandin E2 (PGE2) oxylipins in male and/or female transgenic AD rats compared to wildtype controls. These findings point to a deficit in esterified pro-resolving lipid mediators in the early stages of AD, concident with. changes in esterified lipid mediators involved in promoting inflammation.
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