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S B Vyas

Publications and source records attributed to S B Vyas.

3 recordsLinked to original sources

Stabilization of secondary structure of Alzheimer beta-protein by aluminum(III) ions and D-Asp substitutions.

The CD spectra of the D-Asp substituted analogs of amyloid peptides, beta 6-25 and beta 1-40, showed a distinct blue-shift on Al3+ complexation. The influence of Al3+ coordination was most significant on the triply substituted beta 1-40 (D-Asp 1,7,23). This analog showed a reduction of the minima near 210nm and a simultaneous increase in the maxima near 200nm as compared to the native L-Asp beta 1-40. These observations suggest that Al3+ interaction with D-Asp induces the peptide backbone to increase its antiparallel beta-sheet character. D-Asp substitution and chelation by Al3+ lead to increased stability of higher molecular weight species of beta 1-40, and thereby could increase the toxicity of the Alzheimer amyloid protein.

Amyloid beta-Peptides↗

Interaction of synthetic Alzheimer beta-protein-derived analogs with aqueous aluminum: a low-field 27Al NMR investigation.

Synthetic peptides corresponding to the soluble Alzheimer beta-protein, i.e., beta 1-40 and beta 6-25, were utilized to investigate the association of aluminum using low-field 27Al nuclear magnetic resonance (NMR) spectroscopy and reversed-phase high-performance liquid chromatography (RP-HPLC). Addition of beta 1-40 or beta 6-25 to aqueous Al3+ gives rise to a 27Al NMR signal corresponding to the association of Al3+ with the peptides; this effect is not easily reversed by EDTA. Based on the relative intensity of the Al(3+)-peptide signal between pH 4 and 6, there are at least 4 Al3+ ions associated with each peptide molecule. Microheterogeneity is observed with RP-HPLC on incubating solutions of Al3+ with beta 1-40 and beta 6-25. The 27Al NMR spectra of chromatographically pure fractions of beta 1-40 and beta 6-25 indicate that the peptide-associated Al3+ is released below pH 3.5. We propose that soluble beta 1-40 provides an anchor for Al3+ to bind, eventually leading to an increased deposition of amyloid in the Alzheimer brain.

Aluminum↗