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Brains of Aged Apolipoprotein E‐Deficient Mice Have Increased Levels of F 2 ‐Isoprostanes, In Vivo Markers of Lipid Peroxidation
Author(s) -
Praticò Domenico,
Rokach Joshua,
Tangirala Rajendra K.
Publication year - 1999
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1999.0730736.x
Subject(s) - apolipoprotein e , endocrinology , lipid peroxidation , medicine , isoprostane , neurodegeneration , apolipoprotein b , in vivo , neuroprotection , isoprostanes , biology , chemistry , cholesterol , oxidative stress , disease , microbiology and biotechnology
: Apolipoprotein E (apoE) is the major apolipoprotein of the CNS. Differential expression of apoE isoforms has been linked to longevity and to the pathogenesis of Alzheimer's disease. Several studies have demonstrated that this glycoprotein is important in mature as well as in aging CNS, where it may serve neurotrophic and/or neuroprotective functions. Some reports have shown that apoE‐deficient mice have age‐dependent neurodegeneration and cognitive impairment ; others have not confirmed these observations. ApoE‐deficient mice also develop hypercholesterolemia on a chow diet and have in vivo increased plasma lipid peroxidation products. F 2 ‐isoprostanes are prostaglandin F 2α isomers and chemically stable peroxidation products of arachidonic acid. Both isoprostane F 2α ‐III and isoprostane F 2α ‐VI were markedly elevated in the brains of aged apoE‐deficient mice compared with either wild‐type C57 B1/6 mice or a distinct mouse model of hypercholesterolemia, the low‐density lipoprotein receptor‐deficient mouse. By contrast, no difference in isoprostane levels was observed in young apoE‐deficient mice compared with age‐matched wild‐type control mice. Our findings indicate that disorder of lipid metabolism in the absence of apoE can induce an age‐dependent increase in brain lipid peroxidation products.