Toward a Comprehensive Theory for Alzheimer's Disease. Hypothesis: Alzheimer's Disease Is Caused by the Cerebral Accumulation and Cytotoxicity of Amyloid β‐Protein

By D. Selkoe. Annals of the New York Academy of Sciences, 2000

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Alzheimer’s disease prevention: from risk factors to early intervention (2017, background): “It has been suggested that diabetes could increase the risk by directly affecting Aβ accumulation in the brain since hyperinsulinemia disrupts brain Aβ clearance by competing for the insulin-degrading enzyme [12, 13].”
A "mitochondrial cascade hypothesis" for sporadic Alzheimer's disease. (2004, background): “At the same time, our hypothesis predicts mitochondria should occupy a relatively upstream position in the amyloid cascade hierarchy, rather than the peripheral, downstream location most reviews typically ascribe them [17,18].”
An Overview of APP Processing Enzymes and Products (2010, neutral): “The currently predominant hypothesis states that Aβ forms soluble oligomers in the extracellular space and that these oligomers inhibit NMDA-mediated synaptic transmission and ultimately cause spine and synapse loss through mechanisms not yet fully understood (Selkoe 2000).”
APP processing and synaptic function. (2003, neutral): “It is now widely believed that the accumula-1Cold Spring Harbor Laboratory tion of A , a small peptide with a high propensity to formCold Spring Harbor, New York 11724 aggregates, is central to the pathogenesis of disease2 Graduate Program in Genetics (Selkoe, 2000).”