Cognition Disorders
|
0.400 |
GeneticVariation
|
group |
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 |
Cognition Disorders
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Here, we confirmed that the increase of miR-34a expression in APP/PS1 mice was earlier than the relevant AD pathological characteristics, such as amyloid-β production, amyloid plaque deposition, and cognitive deficits.
|
29378298 |
2018 |
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
Here, we determined whether dietary D-PUFA would ameliorate Aβ pathology and/or cognitive deficits in a mouse model of AD (amyloid precursor protein/presenilin 1 double mutant transgenic mice).
|
29579687 |
2018 |
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
Our data demonstrates that psen1 splicing interference induces phenotypes that resemble early-stage AD, including cognitive deficit, Aβ<sub>1-42</sub> accumulation and synaptic reduction, reinforcing the potential contribution of zebrafish larvae to studies of human brain diseases.
|
28623607 |
2017 |
Cognition Disorders
|
0.400 |
Biomarker
|
group |
CTD_human |
Long-term exposure to ELF-MF ameliorates cognitive deficits and attenuates tau hyperphosphorylation in 3xTg AD mice.
|
26945731 |
2016 |
Cognition Disorders
|
0.400 |
GeneticVariation
|
group |
BEFREE |
In contrast, deltaE9 mice with mutant APP and mutant presenilin-1 develop amyloid plaques early but show typical cognitive deficits in old age.
|
25862638 |
2015 |
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
Chronic LTG treatment rescues the suppressed long-term potentiation, loss of spines and cognitive deficits in AβPP/PS1 mice, known to overexpress a chimeric mouse/human mutant amyloid-β protein precursor (AβPP) and a mutant human presenilin 1 (PS1).
|
25854934 |
2015 |
Cognition Disorders
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Indeed, the most popular genetic AD mouse lines bearing mutations of the amyloid precursor protein (APP) and presenilin 1 genes (PS1), often fail to present robust cognitive deficits or show them only at very advanced ages.
|
22014620 |
2012 |
Cognition Disorders
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Neuropsychologic evaluation revealed global cognitive deficits; he was found to be a carrier of a PS-1 point mutation at position G206A.
|
18797263 |
2008 |
Cognition Disorders
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Both synaptic and cognitive deficits are reproduced in mice double transgenic for amyloid precursor protein (AA substitution K670N,M671L) and presenilin-1 (AA substitution M146V).
|
15578094 |
2004 |
Cognition Disorders
|
0.400 |
GeneticVariation
|
group |
BEFREE |
These data suggest that PS1 mutation could lead to cognitive deficits through subtoxic physiological effects.
|
10467268 |
1999 |