Peptides homologous to the amyloid protein ofAlzheimer's disease containing a glutamine for glutamic acid substitution have accelerated amyloid fibril formation.
T. Wisniewski, J. Ghiso, B. Frangione
Bok 1991 T Wisniewski
Flere språk: Engelsk
| Utgitt | 1991
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| Opplysninger | - beta-Amyloid (A beta) deposition in fibril form is thecentral event in a number of diseases, including Alzheimer'sdisease (AD) and hereditary cerebral hemorrhage with amyloidosis - Dutchtype (HCHWA-D). A beta is produced by degradation of a largeramyloid precursor protein (APP). Recently a mutation in the APPgene has been found in HCHWA-D causing a glutamine for glutamic acid substitution at residue 22 of A beta. The influence of this mutation on fibrillogenesis is not known, although it isclear that affected patients have accelerated cerebrovascularamyloid deposition, with disease symptoms early in life. We reportthe in vitro demonstration of accelerated fibril formation in a 28 residue synthetic peptide homologous to the Dutch variant Abeta. Furthermore, in eight residue peptides homologous to A betathe presence of the mutation is necessary for fibril formation.These findings provide a mechanism for accelerated amyloidformation in the Dutch variant of APP.
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