ArticleNeurobiology of aging2014
Modulation of lipopolysaccharide-induced memory insult, γ-secretase, and neuroinflammation in triple transgenic mice by 5-lipoxygenase.
Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 30 citations in OpenAlex.
- The 3xTg-AD Mouse Model: A Comprehensive Tool for Understanding Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- Prenatal immune activation and adult Poly(I:C) re-challenge promote neuroimmune priming and AD-related behavioural, cellular and molecular alterations in wild-type mice.Frontiers in immunology · 2026Article
- Anti-Inflammatory Peptide Prevents AβCells · 2025Article
- TLR4-mediated chronic neuroinflammation has no effect on tangle pathology in a tauopathy mouse model.Frontiers in aging neuroscience · 2024Article
- Potential Use ofPlants (Basel, Switzerland) · 2022Review
- Lipopolysaccharide-induced neuroinflammation disrupts functional connectivity and community structure in primary cortical microtissues.Scientific reports · 2021Article
- Emodin Prevented Depression in Chronic Unpredicted Mild Stress-Exposed Rats by Targeting miR-139-5p/5-Lipoxygenase.Frontiers in cell and developmental biology · 2021Article
- The Impact of Systemic Inflammation on Alzheimer's Disease Pathology.Frontiers in immunology · 2021Review
- Phosphorylation of 5-LOX: The Potential Set-point of Inflammation.Neurochemical research · 2020Review
- Peripheral inflammation promotes brain tau transmission via disrupting blood-brain barrier.Bioscience reports · 2020Article
- Plasmon-Activated Water Reduces Amyloid Burden and Improves Memory in Animals with Alzheimer's Disease.Scientific reports · 2019Article
- Systemic inflammation impairs microglial Aβ clearance through NLRP3 inflammasome.The EMBO journal · 2019Article
- The 5-Lipoxygenase as modulator of Alzheimer's γ-secretase and therapeutic target.Brain research bulletin · 2016Review
- Article
- Suppression of LPS-induced tau hyperphosphorylation by serum amyloid A.Journal of neuroinflammation · 2016Article
- The Lipoxygenases: Their Regulation and Implication in Alzheimer's Disease.Neurochemical research · 2016Article
- Fundamental role of pan-inflammation and oxidative-nitrosative pathways in neuropathogenesis of Alzheimer's disease.American journal of neurodegenerative disease · 2016Review
- Fundamental role of pan-inflammation and oxidative-nitrosative pathways in neuropathogenesis of Alzheimer's disease in focal cerebral ischemic rats.American journal of neurodegenerative disease · 2016Review
- Absence of ALOX5 gene prevents stress-induced memory deficits, synaptic dysfunction and tauopathy in a mouse model of Alzheimer's disease.Human molecular genetics · 2014Article
- Lipolysaccharide-Induced Neuroinflammation Is Associated with Alzheimer-Like Amyloidogenic Axonal Pathology and Dendritic Degeneration in Rats.Advances in Alzheimer's disease · 2014Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Besides amyloid and tau pathology, a constant feature of Alzheimer's disease (AD) is an intense inflammatory response, which is considered an active player in its pathogenesis. The 5-Lipoxygenase (5LO) is a proinflammatory enzyme and an endogenous modulator of AD-like phenotype in mouse models of the disease. To further understand the role of 5LO in AD pathogenesis, we exposed the triple transgenic (3×Tg) and 3×Tg/5LO knockout mice to lipopolysaccharide (LPS), a known inducer of neuroinflammation, and evaluated its effect on their AD-like phenotype. 3×Tg mice treated with LPS manifested a worsening of behavior, γ-secretase up-regulation, and increased neuroinflammatory responses. These effects were completely prevented in 3×Tg mice genetically deficient for 5LO. By contrast, the absence of 5LO did not protect against increase in tau phosphorylation at specific epitopes that were mediated by the activation of the cyclin-dependent kinase 5. Our data demonstrate that the 5LO pathway affects key neuropathological features of the AD-like phenotype (behavior, abeta, microgliosis, astrocytosis) but not others (tau pathology) in the LPS-dependent neuroinflammation model. The opposite ways whereby 5LO influences the LPS-dependent effects in vivo supports the complex nature of the neuroinflammatory response in AD and its differential role in modulating amyloid and tau neuropathology.
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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.