|
Alzheimer's Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Importantly, inhibition of PKCδ by rottlerin markedly reduces BACE1 expression, Aβ levels, and neuritic plaque formation and rescues cognitive deficits in an APP Swedish mutations K594N/M595L/presenilin-1 with an exon 9 deletion-transgenic AD mouse model.
|
29739836 |
2018 |
|
Alzheimer's Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
In this study, we used the amyloid precursor protein Swedish mutations K594N/M595L (APPswe)/presenilin 1 with the exon-9 deletion (PS1dE9) transgenic mouse model of AD, which was successfully established by the expression of amyloid β precursor protein and presenilin 1 (PS1).
|
30303857 |
2018 |
|
Alzheimer's Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
To probe for a function of ABCA7 in vivo, we crossed Abca7(-/-) mice with J20 mice, an amyloidogenic transgenic AD mouse model [B6.Cg-Tg(PDGFB-APPSwInd)20Lms/J] expressing a mutant form of human APP bearing both the Swedish (K670N/M671L) and Indiana (V717F) familial AD mutations.
|
26517904 |
2015 |
|
Alzheimer's Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
We investigated the effect of the familial AD APP (Amyloid precursor protein) K670N/M671L double mutation, APP Swedish mutation (APPswe), on the expression of 5-HT1B, SERT, MAOA, p11 and 5-HT and its metabolite 5-HIAA in SH-SY5Y human neuroblastoma cell line stably transfected with APPswe mutation.
|
25841787 |
2015 |
|
Alzheimer's Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Therefore, in the current study using proteomics, we tested the hypothesis that several brain proteins involved in pathways such as energy and metabolism, antioxidant activity, proteasome degradation, and pH regulation are altered in J20Tg versus M631L Tg AD mice.
|
22500616 |
2012 |
|
Alzheimer's Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
In this study, we examined the effect of obovatol on cognitive deficits in two separate AD models: (i) mice that received intracerebroventricular (i.c.v.) infusion of Aβ(1-42) (2.0 μg/mouse) and (ii) Tg2576 mice-expressing mutant human amyloid precursor protein (K670N, M671L).
|
22212065 |
2012 |
|
Alzheimer's Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
An early-onset AD transgenic mouse model expressing the double-mutant form of human amyloid precursor protein (APP); Swedish (K670N/M671L) and Indiana (V717F), corroborated in vitro findings by showing lower levels of Aβ and amyloid plaques in the brain, when they were fed a low fat diet enriched in DHA.
|
20971855 |
2011 |
|
Alzheimer's Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
Moreover, blockade of gap junction hemichannel also significantly improved memory impairments without altering amyloid β deposition in double transgenic mice expressing human amyloid precursor protein with K595N and M596L mutations and presenilin 1 with A264E mutation as an Alzheimer's disease mouse model.
|
21712989 |
2011 |
|
Alzheimer's Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
We have studied synaptic function in a transgenic mouse strain relevant to Alzheimer's disease (AD), overexpressing the 695 amino acid isoform of human amyloid precursor protein with K670N and M671L mutations (APP(695)SWE mice), which is associated with early-onset familial AD.
|
11425896 |
2001 |
|
Alzheimer's Disease
|
|
0.100 |
GeneticVariation
|
BEFREE |
The mutant APP(K670N,M671L) transgenic line, Tg2576, shows markedly elevated amyloid beta-protein (A beta) levels at an early age and, by 9-12 months, develops extracellular AD-type A beta deposits in the cortex and hippocampus.
|
9427614 |
1998 |