Lack of β-Amyloidosis in transgenic mice expressing low levels of familial Alzheimer's disease missense mutations
- 2 March 1996
- journal article
- Published by Elsevier in Neurobiology of Aging
- Vol. 17 (2) , 205-214
- https://doi.org/10.1016/0197-4580(95)02070-5
Abstract
No abstract availableKeywords
This publication has 19 references indexed in Scilit:
- Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor proteinNature, 1995
- Making models for Alzheimer's diseaseNature Genetics, 1995
- The Alzheimer's Aβ peptide induces neurodegeneration and apoptotic cell death in transgenic miceNature Genetics, 1995
- Transgenic mouse brain histopathology resembles early Alzheimer's diseaseAnnals of Neurology, 1994
- Comparative molecular neuroanatomy of cloned GABAAreceptor subunits in the rat CNSJournal of Comparative Neurology, 1992
- Mutation of the β-amyloid precursor protein in familial Alzheimer's disease increases β-protein productionNature, 1992
- A pathogenic mutation for probable Alzheimer's disease in the APP gene at the N–terminus of β–amyloidNature Genetics, 1992
- A mutation in the Amyloid Precursor Protein Associated with Hereditary Alzheimer's DiseaseScience, 1991
- Early-onset Alzheimer's disease caused by mutations at codon 717 of the β-amyloid precursor protein geneNature, 1991
- Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's diseaseNature, 1991