Accelerated Amyloid Deposition in the Brains of Transgenic Mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins
Open Access
- 1 October 1997
- Vol. 19 (4) , 939-945
- https://doi.org/10.1016/s0896-6273(00)80974-5
Abstract
No abstract availableKeywords
This publication has 45 references indexed in Scilit:
- A vector for expressing foreign genes in the brains and hearts of transgenic miceGenetic Analysis: Biomolecular Engineering, 1996
- Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In VivoNeuron, 1996
- A novel presenilin 1 mutation resulting in familial Alzheimerʼs disease with an onset age of 29 yearsNeuroReport, 1996
- The structure of the presenilin 1 (S182) gene and identification of six novel mutations in early onset AD familiesNature Genetics, 1995
- Visualization of Aβ42(43) and Aβ40 in senile plaques with end-specific Aβ monoclonals: Evidence that an initially deposited species is Aβ42(43)Neuron, 1994
- The carboxy terminus of the .beta. amyloid protein is critical for the seeding of amyloid formation: Implications for the pathogenesis of Alzheimer's diseaseBiochemistry, 1993
- Release of Excess Amyloid β Protein from a Mutant Amyloid β Protein PrecursorScience, 1993
- Peptides homologous to the amyloid protein of Alzheimer's disease containing a glutamine for glutamic acid substitution have accelerated amyloid fibril formationBiochemical and Biophysical Research Communications, 1991
- Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's diseaseNature, 1991
- Clinical diagnosis of Alzheimer's diseaseNeurology, 1984