Quantifying an amyloid β model for Alzheimer's disease.

摘要

The gist of the amyloid cascade hypothesis is that amyloid-beta (Abeta) deposition in brain drives tau phosphorylation, tangle formation, synapse loss, neuron death, and clinical impairment. Qualitative models for the expression of a clinical phenotype of Alzheimer's disease (AD) propose initial changes in Abeta concentrations in the CSF, followed in sequence by Abeta accumulation in brain (measured, for example by carbon-11-labelled Pittsburgh compound [~(11)C-PiB]-PET), increases in CSF tau, hippocampus and grey matter volume losses (measured by MRI), decreased glucose metabolism (assessed by ~(18)F-fluorodeoxyglucose ~(18)FDG PET), memory impairment, and dementia.