[HTML][HTML] Early-onset amyloid deposition and cognitive deficits in transgenic mice expressing a double mutant form of amyloid precursor protein 695
MA Chishti, DS Yang, C Janus, AL Phinney… - Journal of Biological …, 2001 - ASBMB
We have created early-onset transgenic (Tg) models by exploiting the synergistic effects of
familial Alzheimer's disease mutations on amyloid β-peptide (Aβ) biogenesis. TgCRND8
mice encode a double mutant form of amyloid precursor protein 695 (KM670/671NL+
V717F) under the control of the PrP gene promoter. Thioflavine S-positive Aβ amyloid
deposits are present at 3 months, with dense-cored plaques and neuritic pathology evident
from 5 months of age. TgCRND8 mice exhibit 3,200–4,600 pmol of Aβ42 per g brain at age …
familial Alzheimer's disease mutations on amyloid β-peptide (Aβ) biogenesis. TgCRND8
mice encode a double mutant form of amyloid precursor protein 695 (KM670/671NL+
V717F) under the control of the PrP gene promoter. Thioflavine S-positive Aβ amyloid
deposits are present at 3 months, with dense-cored plaques and neuritic pathology evident
from 5 months of age. TgCRND8 mice exhibit 3,200–4,600 pmol of Aβ42 per g brain at age …