ArticleJournal of molecular neuroscience : MN2015
Insufficient resolution response in the hippocampus of a senescence-accelerated mouse model--SAMP8.
Article in Journal of molecular neuroscience : MN, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Effects of n-3 FA supplementation on the release of proresolving lipid mediators by blood mononuclear cells: the OmegAD study.Journal of lipid research · 2015Trial
- Senescence accelerated mouse-prone 8: a model of neuroinflammation and aging with features of sporadic Alzheimer's disease.Stem cells (Dayton, Ohio) · 2025Review
- Ketogenic Diet: An Effective Treatment Approach for Neurodegenerative Diseases.Current neuropharmacology · 2022Review
- Molecular Pathogenesis and Interventional Strategies for Alzheimer's Disease: Promises and Pitfalls.ACS pharmacology & translational science · 2020Review
- n-3 Polyunsaturated Fatty Acids and Their Derivates Reduce Neuroinflammation during Aging.Nutrients · 2020Review
- The Contribution of Formyl Peptide Receptor Dysfunction to the Course of Neuroinflammation: A Potential Role in the Brain Pathology.Current neuropharmacology · 2020Review
- Microglial Hyperreactivity Evolved to Immunosuppression in the Hippocampus of a Mouse Model of Accelerated Aging and Alzheimer's Disease Traits.Frontiers in aging neuroscience · 2020Article
- The Effects of Doxorubicin-based Chemotherapy and Omega-3 Supplementation on Mouse Brain Lipids.Metabolites · 2019Article
- Can inflammation be resolved in Alzheimer's disease?Therapeutic advances in neurological disorders · 2018Review
- Understanding Epigenetics in the Neurodegeneration of Alzheimer's Disease: SAMP8 Mouse Model.Journal of Alzheimer's disease : JAD · 2018Review
- Impact of Dietary Fats on Brain Functions.Current neuropharmacology · 2018Review
- Impaired Resolution of Inflammation in Alzheimer's Disease: A Review.Frontiers in immunology · 2017Review
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Authors and funding
5 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is the primary risk factor for Alzheimer's disease (AD), and it is known that inflammation is associated with both aging and AD. To resolve inflammation, biosynthesis of the specialized pro-resolving mediators (SPMs) is enhanced in a programmed and active manner. We investigated the effect of age on resolution by analyzing hippocampal tissue from 2- and 9-month-old senescence-accelerated mouse prone 8 (SAMP8), as well as age-matched senescence-accelerated mouse resistant 1 (SAMR1). Pro-inflammatory markers increased upon age in SAMP8 mice and were also higher than those in age-matched SAMR1 mice. However, neither SPMs nor their receptors were enhanced upon age in SAMP8 mice compared to age-matched SAMR1 mice. Analysis of SPM biosynthetic enzymes revealed elevated levels of leukocyte type 12-lipoxygenase (L12-LOX) and decreased 5-LOX levels upon age in SAMR1 mice, whereas they remained unchanged in SAMP8 mice. Moreover, we found partial co-localization of L12-LOX and amyloid beta (Aβ) staining, as well as correlation between L12-LOX and phosphorylated tau levels in SAMP8, but not SAMR1 mice. Thus, we conclude that the resolution response in SAMP8 mice is insufficient to counteract the increased inflammation with age, and this may have a role in the development of AD-like pathologies.
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