Resumen de Microglia and prion disease: a review
Prion diseases are characterized by the accumulation of PrP se, an altered isoform of a normal cellular protein, Prpc. The prion hypothesis holds that the process of conformational change from Prpc to Prpsc under theinfluence of PrPSc constitutes the basic infectious mechanism in prion diseases. It is these diseases, which include spongiform degeneration, nerve cell loss and gliosis, are the result of neurotoxicity of PrPSc, loss of function of PrPC or some other mechanism. Recent in vitro findings using a synthetic peptide of human PrPc implicate microglia as a mediator of pathological changes. The mechanism of the toxicity of this peptide involves activation o f microglia, oxidative stress, and direct interactions with PrPc-synthesizing neurones that reduce their ability to cope with oxidatvie stres. Microglia thus see to emerge as a mediator of neuronal degeneration and cell deathi prion diseases
