[HTML][HTML] Accelerated plaque accumulation, associative learning deficits, and up-regulation of α7 nicotinic receptor protein in transgenic mice co-expressing mutant …
KT Dineley, X Xia, D Bui, JD Sweatt, H Zheng - Journal of Biological …, 2002 - ASBMB
Familial Alzheimer's disease-associated mutations in presenilin 1 or 2 or amyloid precursor
protein result in elevated β-amyloid, β-amyloid accumulation, and plaque formation in the
brains of affected individuals. By crossing presenilin 1 transgenic mice carrying the A246E
mutation with plaque-producing amyloid precursor protein K670N/M671L transgenic mice
(Tg2576), we show that co-expression of both mutant transgenes results in acceleration of
amyloid accumulation and associative learning deficits. At 5 months of age with no …
protein result in elevated β-amyloid, β-amyloid accumulation, and plaque formation in the
brains of affected individuals. By crossing presenilin 1 transgenic mice carrying the A246E
mutation with plaque-producing amyloid precursor protein K670N/M671L transgenic mice
(Tg2576), we show that co-expression of both mutant transgenes results in acceleration of
amyloid accumulation and associative learning deficits. At 5 months of age with no …