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S. Nutr Rev 2007, 65(12 Pt 2):S152-156. 2. Launer LJ: Next steps in Alzheimer's disease research: interaction between epidemiology and basic science. Curr Alzheimer Res 2007, 4(2):141-143. 3. Wang XP, Ding HL: Alzheimer's disease: epidemiology, genetics, and beyond. Neurosci Bull 2008, 24(2):105-109. 4. de la Monte SM, Neusner A, Chu J, Lawton M: Epidemilogical Trends Strongly Suggest Exposures as
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R-group comparisons were made using ANOVA with the post-hoc Bonferroni multiple comparisons test of significance. Significant P-values are indicated within the panels.suggesting that early life exposures may contribute to the pathogenesis of AD, perhaps through gene imprinting. Although chronic HFD feeding and limited NDEA exposure increased body weight and caused T2DM/peripheral insulin resistanc
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Erations in the sphingolipid metabolism pathways during progression of dementia and Alzheimer's disease: a shift toward ceramide accumulation at the earliest recognizable stages of Alzheimer's disease? Neurochem Res 2007, 32(4-5):845-856. 91. Nakane M, Kubota M, Nakagomi T, Tamura A, Hisaki H, Shimasaki H, Ueta N: Lethal forebrain ischemia stimulates sphingomyelin hydrolysis and ceramide generatio
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Www.biomedcentral.com/1472-6823/10/Page 6 ofthe context of peripheral insulin resistance or T2DM. Similar results have been reported previously, in which the investigators generated models with much higher doses of NDEA [84]. One potential explanation for this paradox is that homeostatic mechanisms may have shifted toward increased storage of lipids/triglycerides in adipose tissue, skeletal muscle
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Ative stress with lipid peroxidation, as occur in AD. The finding that chronic HFD feeding did not significantly alter tau or AbPP expression also supports our previous conclusion that HFD feeding contributes to, but is not sufficient to cause AD-type neurodegeneration [45,46]. The combined effect of early, limited NDEA exposure plus chronic HFD feeding significantly reduced insulin and ChAT mRNA
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Could serve as biomarkers of insulin-resistance mediated neurodegeneration. Finally, the findings suggest that our insulin resistance disease epidemics are linked to sub-mutagenicTong et al. BMC Endocrine Disorders 2010, 10:4 http://www.biomedcentral.com/1472-6823/10/Page 13 ofexposures to nitrosamines and related compounds, combined with chronic consumption of high fat content foods, indicating t
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E formation of DNA and protein adducts [105-107] that can serve as persistent sources of oxidative stress, and cause further DNA damage and protein dysfunction. Recently, we demonstrated a role for ceramidemediated neurodegeneration in a model of diet-induced obesity with T2DM [45], and showed that in vitro ceramide exposure causes neurodegeneration with impairments in neuronal viability, energy m
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N Alzheimer's disease. Neurobiol Aging 2006, 27(1):38-41. 42. Reger MA, Craft S: Intranasal insulin administration: a method for dissociating central and peripheral effects of insulin. Drugs Today (Barc) 2006, 42(11):729-739. 43. Reger MA, Watson GS, Frey WH, Baker LD, Cholerton B, Keeling ML, Belongia DA, Fishel MA, Plymate SR, Schellenberg GD, Cherrier MM, Craft S: Effects of intranasal insulin