Protein Adsorption at Polymer Surfaces: A Study Using Total Internal Reflection Fluorescence

Anderson, Aron B.; Darst, Seth A.; Robertson, Channing R.

doi:10.1021/bk-1987-0343.ch020

Cited by 4 publications

(1 citation statement)

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“…In the NN diet group, the amount of 14 C activity recovered as intact ARA (subfraction V) was similar in the Cb, Cx, and Hc of WT animals (~55%), suggesting that extent of ARA degradation does not differ greatly across brain regions in WT animals on an ω3-replete diet (figure 5, lower panels, figure S1, and table S4). However, subfraction V activity was significantly lower in the Cx of TG animals in the NN diet group, consistent with previously published results showing that the oxidative degradation of ARA is increased in TG animals (Anderson et al, 1987). Subfraction V activity also trended lower in the Cb and Hc of TG animals, but results did not meet criteria for statistical significance.…”

Section: Resultssupporting

confidence: 85%

The effects of omega-3 fatty acid deficiency during development on oxidative fatty acid degradation during maturity in a mouse model of Alzheimer's disease

Furman

Axelsen

2019

Neurobiology of Aging

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Metabolic conditions during brain development may have long-term consequences on brain metabolism, thereby influencing the risk of neurodegenerative disease in later life. To ascertain the long-term consequences of ω3 fatty acid deficiency during brain development on oxidative fatty acid degradation in the brain and the development of Alzheimer-like pathology, wild-type (WT) female mice were fed diets that were either replete or deficient in ω3 fatty acids for five weeks. These females were then mated with hemizygous 5xFAD male transgenic (TG) mouse models of Alzheimer's disease (AD), and the progeny were continued on diets that were either ω3-replete or ω3-deficient. When the progeny were six months of age, they received radiolabeled arachidonic acid (ARA) by intracerebroventricular injection. Five days after these injections, the brains were harvested and oxidative degradation of the radiolabeled ARA was characterized. Among the progeny of female mice on an ω3-replete diet, TG progeny had lower PSD-95 expression, and higher oxidative ARA degradation, than WT progeny. Progeny on an ω3-deficient diet, however, had no significant differences in PSD-95 expression between TG and WT mice, or in the extent of ARA degradation. In TG mice, an ω3-deficient diet reduced oxidative ARA degradation to a greater extent than in WT mice. The reductions in oxidative ARA degradation occurred even if the progeny of female mice on an ω3-deficient diet resumed an ω3-replete diet immediately upon weaning. These results demonstrate that dietary ω3 fatty acid deficiency during development can cause long-term changes in the expression of a synaptic marker, and long-term reductions in the rate of ARA degradation in the WT brain, that are not completely alleviated by an ω3-replete diet after weaning. The elimination of differences between TG and WT mice by an ω3-deficient diet suggest that mechanisms regulating PSD-95 expression and the oxidative degradation of ARA are related, and that the timing of dietary ω3 intake during development may influence AD-related pathological changes later in life.

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Section: Resultssupporting

confidence: 85%