Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized pathologically by amyloid beta (Aβ) deposition, microgliosis, and iron dyshomeostasis. Increased labile iron due to homeostatic dysregulation is believed to facilitate amyloidogenesis. Free iron is incorporated into aggregating amyloid peptides during Aβ plaque formation and increases potential for oxidative stress surrounding plaques.
View Article and Find Full Text PDFImpaired brain iron homeostatic mechanisms, independent of pathological hallmarks, are harmful to the brain because excess free iron can cause DNA, protein, and lipid damage via oxidative stress. The goal of this study was to evaluate the longitudinal effect of chronic iron overload and deficiency in the vertebrate brain. Ten-week-old C57BL6 male mice were randomly assigned to one of four unique dietary regiments for 1 year: iron-deficient, normal iron, and two different concentrations of lipophilic iron diet containing 3,5,5-trimethylhexanoyl ferrocene (TMHF).
View Article and Find Full Text PDFThe preparation of hierarchically structured organosilicon microcapsules from commercially available starting materials is described. Using a microfluidic device, an emulsion of dichlorodiphenylsilane is formed in a continuous phase of aqueous glycerol. The silane droplets undergo hydrolysis, condensation, and crystallization within minutes to form self-assembled, core-shell microcapsules.
View Article and Find Full Text PDFAngew Chem Int Ed Engl
February 2006
Inflammatory processes play a key role in the pathogenesis of a number of common neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Abnormal iron accumulation is frequently noted in these diseases and compelling evidence exists that iron is involved in inflammatory reactions. Histochemical stains for iron repeatedly demonstrate that oligodendrocytes, under normal conditions, stain more prominently than any other cell type in the brain.
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