Description

(Glu20)-Amyloid β-Protein (1-42) is a slower fibrillizing variant of amyloid β-protein (Aβ). The Glu20 mutation reduces the aggregation propensity of Aβ42 and prevents accumulation of the slowly fibrillizing peptide. Amyloid β-protein is the primary component of both vascular and parenchymal amyloid deposits in Alzheimer’s disease[1][2].—–C199H309N55O62S—-[1]Poduslo JF, et al. Receptor-mediated transport of human amyloid beta-protein 1-40 and 1-42 at the blood-brain barrier. Neurobiol Dis. 1999 Jun;6(3):190-9. |[2]Williams TL, et al. The effect of Alzheimer’s Aβ aggregation state on the permeation of biomimetic lipid vesicles. Langmuir. 2010 Nov 16;26(22):17260-8. –1802086-22-1–4495.98—-O=C(N[C@@H](C)C(N[C@@H](CCC(O)=O)C(N[C@@H](CC1=CC=CC=C1)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC2=CNC=N2)C(N[C@@H](CC(O)=O)C(N[C@@H](CO)C(NCC(N[C@@H](CC3=CC=C(C=C3)O)C(N[C@@H](CCC(O)=O)C(N[C@@H](C(C)C)C(N[C@@H](CC4=CNC=N4)C(N[C@@H](CC5=CNC=N5)C(N[C@@H](CCC(N)=O)C(N[C@@H](CCCCN)C(N[C@@H](CC(C)C)C(N[C@@H](C(C)C)C(N[C@@H](CC6=CC=CC=C6)C(N[C@@H](CCC(O)=O)C(N[C@@H](C)C(N[C@@H](CCC(O)=O)C(N[C@@H](CC(O)=O)C(N[C@@H](C(C)C)C(NCC(N[C@@H](CO)C(N[C@@H](CC(N)=O)C(N[C@@H](CCCCN)C(NCC(N[C@@H](C)C(N[C@@H]([C@@H](C)CC)C(N[C@@H]([C@@H](C)CC)C(NCC(N[C@@H](CC(C)C)C(N[C@@H](CCSC)C(N[C@@H](C(C)C)C(NCC(NCC(N[C@@H](C(C)C)C(N[C@@H](C(C)C)C(N[C@@H]([C@@H](C)CC)C(N[C@@H](C)C(O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H](CC(O)=O)N–Neurological Disease–10 mM in DMSO–Amyloid-β—-Neuronal Signaling–Peptides