The focus of research on Alzheimer's disease begins to shift away from amyloid plaques: "Cell death in the brain causes one to grow forgetful, confused and, eventually, catatonic. Recently approved drugs provide mild relief for symptoms but there is no consensus on the underlying mechanism of the disease. ... We don't know what the problem is in terms of toxicity. This makes the disease difficult to cure. ... Accumulations of amyloid plaques have long been associated with the disease and were presumed to be its cause. These long knotty fibrils, formed from misfolded protein fragments, are almost always found in the brains of diseased patients. Because of their ubiquity, amyloid fibrils were considered a potential source of the toxicity that causes cell death in the brain. However, the quantity of fibrils does not correspond with the degree of dementia and other symptoms. New findings support a hypothesis that fibrils are a by-product of the disease rather than the toxic agent itself. This paradigm shift changes the focus of inquiry to smaller, intermediate molecules that form and dissipate quickly. These molecules are difficult to perceive in brain tissue. ... For decades, it was believed that fibrils were a toxic species, but increasingly researchers are looking at small, soluble precursor forms of the fibrils, known as oligomers. ... These oligomers may be toxic by inserting themselves into membranes and causing a damage to the membrane. The membrane is critical for the cell viability."