Amyloid-beta peptide A beta p3-42 affects early aggregation of full-length A beta 1-42

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)
Robert Lust (Creator)
Hiromi M. Sanders (Creator)
Jan K. Teller (Creator)
East Carolina University (ECU )
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Abstract: The major amyloid beta (Aβ) peptides found in the brain of familial and late onset Alzheimer’s isease include the full-length Aβ1-42 and N-terminally truncated pyroglutamylated peptides βp3-42 and Aβp11-42. The biophysical properties of Aβ1-42 have been extensively studied yet ittle is known about the other modified peptides. We investigated the aggregation kinetics of brainspecific β peptides to better understand their potential roles in plaque formation. Synthetic peptides ere analyzed individually and in mixtures representing various ratios found in the brain. pectrofluorometric analyses using Thioflavin-T showed that the aggregation of Aβ1-42 was faster ompared to Aβp3-42; however Aβp11-42 displayed similar kinetics. Surprisingly mixtures of fulllength β1-42 and Aβp3-42 showed an initial delay in beta-sheet formation from both equimolar nd non-equimolar samples. Electron microscopy of peptides individually and in mixtures further upported fluorescence data. These results indicate that Aβ-Aβ peptide interactions involving ifferent forms may play a critical role in senile plaque formation and maintenance of the soluble β pool in the brain. Originally published Peptides Vol. 30 No. 5 May 2009

Additional Information

Peptides. 30:5(May 2009) p. 849-854.
Language: English
Date: 2011
Alzheimer's disease, Amyloid-beta peptides, aggregation, pyroglutamate

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