Transthyretin sequesters amyloid beta protein and prevents amyloid formation

Addition of amyloid beta protein (Abeta) to cerebrospinal fluid (CSF) of patients with Alzheimer's disease and normals reveals that transthyretin (TTR), a CSF protein, sequesters Abeta protein into stable complexes. Sequestration prevents aggregation of Abeta proteins leading to amyloid fibrils, which are associated with Alzheimer disease. In vitro studies show that apolipoprotein E does not complex with Abeta in CSF.