Article
Molecular dissection of domains in mutant presenilin 2 that mediate overproduction of amyloidogenic forms of amyloid beta peptides. Inability of truncated forms of PS2 with familial Alzheimer's disease mutation to increase secretion of Abeta42.
The Journal of biological chemistry - 14 Aug 1998
Tomita T, Tokuhiro S, Hashimoto T, Aiba K, Saido T C, Maruyama K, Iwatsubo T
Abstract excerpt
Mutations in presenilin (PS) 1 or PS2 genes account for the majority of early-onset familial Alzheimer's disease, and these mutations have been shown to increase production of species of amyloid beta peptide (Abeta) ending at residue 42, i.e. the most amyloidogenic form of Abeta. To gain insight...
Topics
- Alzheimer Disease
- Amyloid
- Amyloid beta-Peptides
- Animals
- Base Sequence
- COS Cells
- Cell Line
- DNA Primers
- Membrane Proteins
- Mice
- Mutation
- Peptide Fragments
- Presenilin-2
- Subcellular Fractions