ABSTRACT
Glycosaminoglycans (GAGs) have been shown to contribute to the development of amyloid diseases. In Alzheimer’s disease (AD), senile plaques, which are mostly composed of the ß-amyloid peptide (Aß), colocalize with GAGs. Activated microglial cells are also associated with amyloid plaques and contribute to the neuronal damage seen in AD patients. Aggregated and soluble Aß have been shown to differentially activate microglia in vitro leading to the production of inflammatory mediators such as nitric oxide and cytokines. Cortices from newborn Sprague Dawley-CD rats were mechanically dissociated in cold Dulbecco’s Modified Eagle Medium (DMEM)-gentamycin. Synthetic Aß1-42 peptide was treated with 1,1,1,3,3,3-hexafluoro-2-propanol (HFIP), sonicated, and stored at -80°C. In the presence of a priming concentration of IFN-γ, Aß1-42 induced the activation of the microglial culture as measured by the amount of nitrite in the supernatant.
