Amyloid beta: Difference between revisions

'''Alzheimer's disease''' is characterized by extracellular proteic plaques and intracellular neurofibril tangles.<ref name="structure">PMID: 12423364</ref> These plaques are collections of beta-amyloid <scene name='Amyloid_beta/Fibrils/1'>fibrils</scene> of beta-sheets. The fibrils form when normally soluble amyloid beta proteins reach a critical concentration and become insoluble, misfold, and aggregate.<ref name="stuff">PMID:22108203</ref> When amyloid beta comes into contact with metal ions and oxygen the result is the production of reactive oxygen species (especially hydrogen peroxide) without oxygen and metal ions amyloid beta ca induce pore formation in neuronal and endothelial cells, triggering cell death.<ref name="structure" /><ref name="alz" /> Yet another source of amyloid beta toxicity stems from its ability to induce endothelial cell damage through the production of superoxide, though the mechanism of such induction is unclear.<ref name="alz" /> While the presence of the fibril plaques remains a marker for Alzheimer's disease recent studies have suggested that alymoild beta oligomers most devestating effect is the impairment of long-term potentiation which decreases dendritic spine density in the hippocampal brain and impairs memory.<ref name="recent">PMID:22114742</ref>