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Ther hand, recent studies showed that HFD feeding causes obesity, T2DM, and cognitive impairment, but is not sufficient to cause AD [45,46]. Therefore, it's likely that chronic HFD feeding which results in peripheral insulin resistance may provide a second-hit, and that combined with low-dose nitrosamine or other environmental exposures, it may increase the severity of neurodegeneration. In the pr
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Res of AD cerebellar atrophy include, reductions in Purkinje cell population, atrophy of the molecular and granule cell layers [68], increased amyloid deposition and gliosis in the cortex [69]; increased ubiquitin-immunoreactivity in senile plaques and degenerating neurites [70]; extensive abnormalities in dendritic spine density and synaptic structure in vestibulocerebellar, visual, and auditory
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S such as diabetes mellitus [74], chronicTong et al. BMC Endocrine Disorders 2010, 10:4 http://www.biomedcentral.com/1472-6823/10/Page 3 ofalcoholism [75], or obesity with metabolic syndrome [45,46]. These systemic diseases share in common with primary central nervous system (CNS) degenerative diseases, impairments in cognition, and deficits in insulin and IGF signaling mechanisms, insulin/IGF res
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Anied with a higher tendency towards aggressive behaviour as a consequence to gasoline inhalation.11. 12.13. 14.AbbreviationsNa+, K+-ATPase: total adenosine triphosphatase; SOD: superoxide dismutase; AChE: acetylcholinesterase; GSH: reduced glutathione; TBARS: lipid peroxidation; DA: dopamine; NE: norepinephrine; 5-HT: serotonin; CNS: central nervous system; ROS: reactive oxygen species; MMT: meth
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Al microenvironment. Cell Cycle. 2010;9(17):3515?3. 56. Martinez-Outschoorn UE, Balliet RM, Rivadeneira DB, Chiavarina B, Pavlides S, Wang C, et al. Oxidative stress in cancer associated fibroblasts drives tumorstroma co-evolution: A new paradigm for understanding tumor metabolism, the field effect and genomic instability in cancer cells. Cell Cycle. 2010;9(16):3256?6. 57. Chiavarina B, Whitaker-M
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Sulin receptor substrate gene expression, and reduced expression of tau and choline acetyltransferase (ChAT), which are regulated by insulin and IGF-1. In addition, increased levels of 4-hydroxynonenal and nitrotyrosine were measured in cerebella of HFD ?NDEA treated rats, and overall, NDEA+HFD treatment reduced brain levels of Tau, phospho-GSK-3b (reflecting increased GSK-3b activity), glial fibr
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Software (GraphPad Software, Inc., San Diego, CA). Software generated significant P-values are shown in the graphs or included in the tables.ResultsEffects of NDEA and HFD on Serum Biomarkers of T2DM (Table 2)Tissue homogenates were prepared in radioimmunoprecipitation assay buffer containing protease and phosphatase inhibitors, as previously described [46]. Direct ELISAs were performed in 96-well
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N.edu 1 Department of Pathology (Neuropathology), Rhode Island Hospital, 593 Eddy Street, Providence, RI 02903, USAnoted that the striking increases in AD and PD mortality rates followed sharply increased consumption of processed foods, use of preservatives, and demand for nitrogen-containing fertilizers [4]. A common theme resonating from these unnecessary lifestyle trends is that we have inadver