APOE 4 polymorphism results in early cognitive deficits in an EAE model

Tu, Jiyuan; Zhao, Chongbo; Vollmer, Timothy; Coons, Stephen W.; Lin, Hao-jie; Marsh, Stephen J.; Treiman, David M.; Shi, Jiong

doi:10.1016/j.bbrc.2009.04.153

Cited by 35 publications

(22 citation statements)

References 22 publications

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“…Regional decreases in choline acetyltransferase in the hippocampus might explain these deficits [126]. This is in accordance with MS studies on human [114, 127].…”

Section: The Role Of Apoe In Eaesupporting

confidence: 83%

The Immune‐Modulatory Role of Apolipoprotein E with Emphasis on Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis

Zhang

Zhu

2010

Journal of Immunology Research

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Apolipoprotein E (apoE) is a 34.2 kDa glycoprotein characterized by its wide tissue distribution and multiple functions. The nonlipid-related properties of apoE include modulating inflammation and oxidation, suppressing T cell proliferation, regulating macrophage functions, and facilitating lipid antigen presentation by CD1 molecules to natural killer T (NKT) cells, and so forth. Increasing studies have revealed that APOE ε allele might be associated with multiple sclerosis (MS), although evidence is still not sufficient enough. In this review, we summarized the current progress of the immunomodulatory functions of apoE, with special focus on the association of APOE ε allele with the clinical features of MS and of its animal model experimental autoimmune encephalomyelitis (EAE).

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“…Regional decreases in choline acetyltransferase in the hippocampus might explain these deficits [126]. This is in accordance with MS studies on human [114, 127].…”

Section: The Role Of Apoe In Eaesupporting

confidence: 83%

The Immune‐Modulatory Role of Apolipoprotein E with Emphasis on Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis

Zhang

Zhu

2010

Journal of Immunology Research

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“…Cognitive deficits are considered an early manifestation of the disease in MS patients. Similar memory impairment in EAEinduced mice is shown in many other studies [6][7][8][9]. EAE causes deficits in hippocampal-dependent learning and memory sight that is associated with early microglial activation, synaptic loss and neurodegeneration [7].…”

Section: Introductionsupporting

confidence: 72%

Influenza vaccine and learning in C57BL mice with an acute experimental autoimmune encephalomyelitis

et al. 2013

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Literature data suggest possible link between influenza vaccination and development of autoimmune processes. Therefore, the aim of the study was to investigate the effect of influenza vaccination on spatial learning in mice with experimental autoimmune encephalomyelitis (EAE). EAE was induced in eight-week-old C57BL/6J female mice by subcutaneous immunization (MOG35–55 in complete Freund’s adjuvant) and Pertussis vaccine injected intraperitoneally. Mice were vaccinated with influenza vaccine three days before MOG immunization. The hippocampal-dependent spatial learning test, Morris Water Maze test (MWM), was performed before and after EAE induction. Significant difference (P < 0.05) in the time for completing the Morris Water Maze task was found between mice with mild clinical signs of EAE when compared to other mice. However no significant difference was observed between mice with EAE and mice with EAE that were vaccinated with influenza vaccine. Hippocampal tissue lesions in EAE mice are in correlation with memory impairment. Study shows no influence of influenza vaccine on progression of clinical signs of EAE, spatial learning and memory impairment.

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“…In mouse models, APOE4 brains have increased susceptibility to diseases associated with inflammation (Farrer et al, 1997; Tu et al, 2009), or inflammation caused by LPS (Zhu et al, 2012) or Aβ (Rodriguez et al, 2014). Treatment of a mouse model of amyloid with ibuprofen for 6 months led to decreased brain amyloid levels and glial activation (Lim et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Identification and modification of amyloid-independent phenotypes of APOE4 mice

DiBattista

Dumanis

Newman

et al. 2016

Experimental Neurology

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Background Over 70 million Americans inherit the strongest genetic risk factor for Alzheimer’s disease (AD), apolipoprotein E4 (APOE4), but have no course for reducing their risk. The association of non-steroidal anti-inflammatory drug (NSAID) use with reduced risk of AD for APOE4-carriers suggests that NSAIDs may be useful in AD prevention. Methods We identified phenotypes associated with APOE4 in APOE knock-in mice in order to define modifiable measures that correlate with risk of AD. Results APOE4 mouse brains showed altered post-translational modifications and biochemical distribution of APOE compared to APOE3 mice; these differences were also observed in brains of human APOE4 carriers. Two-month treatment with ibuprofen significantly altered the expression pattern of APOE in APOE4 mice to that of APOE3 mice; PPAR-γ agonist pioglitazone also had a significant effect. APOE4 mice also show deficits in dendritic spine density, and ibuprofen and pioglitazone significantly increased dendritic spine density. Conclusions We report new phenotypes associated with APOE4 in control human and APOE knock-in mice and their mitigation with NSAID treatment, through COX-2 inhibition and PPAR-γ activation.

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APOE 4 polymorphism results in early cognitive deficits in an EAE model

Cited by 35 publications

References 22 publications

The Immune‐Modulatory Role of Apolipoprotein E with Emphasis on Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis

The Immune‐Modulatory Role of Apolipoprotein E with Emphasis on Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis

Influenza vaccine and learning in C57BL mice with an acute experimental autoimmune encephalomyelitis

Identification and modification of amyloid-independent phenotypes of APOE4 mice

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