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> In the presence of oxygen and metal ions amyloid beta produces reactive oxygen species (especially hydrogen peroxide) in the absence of such molecules it can induce pore formation in neuronal and endothelial cells, and trigger cell death.<ref name="structure" /><ref name="alz">PMID:18305836</ref> 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 devastating 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>