作者: B. Frangione , E. M. Castaño , F. Prelli , C. Soto , J. Ghiso
DOI: 10.1007/978-3-642-80109-9_13
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摘要: Alzheimer’s amyloid beta (Aβ) has long been known to be a highly insoluble and “sticky” protein. More recently it become evident that several apolipoproteins (apo) can interact with Aβ. Apo J is major carrier protein of normal soluble β (sAβ), which may well the precursor On other hand, apoE4 linked late-onset disease modulate Aβ fibril formation in vitro. Furthermore, carboxyl terminus apoE constituent plaque amyloid. It our working hypothesis apoE, possibly chaperone proteins, play role conformational transition from fibrils.