Acceleration of Alzheimer's fibril formation by apolipoprotein E in vitro.
Acceleration of Alzheimer's fibril formation by apolipoprotein E in vitro.
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发表时间:
1994-11
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通讯作者:
Thomas;Wisniewski;E. M. Castaño;A. Golabek;T. Vogel;B. Frangione
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作者:
Thomas;Wisniewski;E. M. Castaño;A. Golabek;T. Vogel;B. Frangione
Numerous studies have established a linkage between the apolipoprotein (apo) E4 allele and late-onset Alzheimer's disease. It remains unclear if apo E plays a direct role in the pathogenesis of Alzheimer's disease and what, if any, are its significant interactions with amyloid beta (A beta) and tau. Apo E has been found immunohistochemically in all types of amyloid deposits and apo E fragments have been isolated from amyloid. Furthermore, apo E has been shown to bind soluble A beta. It has been proposed that apo E acts to promote and/or modulate A beta fibril formation. It is well established that peptides homologous to A beta will form amyloid-like fibrils in solution. With the use of electron microscopy and a thioflavin T assay for fibril formation we found that apo E and apo E4 in particular enhance this spontaneous fibrillogenesis of A beta peptides under the in vitro conditions used. These in vitro data suggest that the apo E4 isoform is a risk factor for Alzheimer's disease that acts to accelerate a process that can occur in its absence.