|
Cognition Disorders
|
0.400 |
GeneticVariation
|
group |
BEFREE |
We tested the efficacy of losartan (10 mg/kg/day for three months), a selective angiotensin II type 1 receptor antagonist, in alleviating cerebrovascular and cognitive deficits in double-transgenic mice (six months at endpoint) that overexpress a mutated form of the human amyloid precursor protein (APP<sub>Swe,Ind</sub>) and a constitutively active form of the transforming growth factor-β1, thereafter named A/T mice.
|
27389178 |
2017 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
We found that the lack of Nrf2 significantly exacerbates cognitive deficits in APP/PS1, without altering gross motor function.
|
29036636 |
2017 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
We conclude that increased susceptibility to excitotoxicity rather than a specific effect on LTP is the primary cause of cognitive deficits in APP(695)SWE mice.
|
11425896 |
2001 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
We compared learning and spatial memory in the APPswe, PSEN1dE985Dbo (APP/PS1) mouse model of AD and studied the ability of acute intraperitoneal and oral Bryostatin-1 to reverse cognitive deficits in this model.
|
25523423 |
2015 |
|
Cognition Disorders
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Using a gene therapy approach, here we show that increasing brain p62 expression rescues cognitive deficits in APP/PS1 mice, a widely used animal model of AD.
|
27573878 |
2017 |
|
Cognition Disorders
|
0.400 |
AlteredExpression
|
group |
BEFREE |
To understand the mechanism underlying cognitive deficits in AIDS patients, we examined the influence of gp41 peptides on the expression and the secretion of Alzheimer's amyloid precursor protein (APP) in human astroglial cell line T98G.
|
10527458 |
1999 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
To elucidate these issues, we investigated the McGill-R-Thy1-APP transgenic rat, which exhibits progressive intracellular and extracellular amyloid-beta (Aβ) pathology and ensuing cognitive deficits.
|
28865749 |
2017 |
|
Cognition Disorders
|
0.400 |
GeneticVariation
|
group |
BEFREE |
This interpretation of one aspect of the cognitive deficit in human mutant APP mice has parallels to deficits observed in patients with Alzheimer's disease, further supporting the validity of transgenic models of the disease.
|
18772249 |
2008 |
|
Cognition Disorders
|
0.400 |
AlteredExpression
|
group |
BEFREE |
This "accelerated aging" with regard to hippocampal PEP expression in young APP transgenic mice might be one factor contributing to the observed cognitive deficits in these mice in the pre-plaque phase and could also explain in part the cognition-enhancing effects of PEP inhibitors in several experimental paradigms.
|
16187206 |
2006 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
These results suggest that sildenafil could restore cognitive deficits in Tg APP/PS1 mice by the regulation of PKG/pCREB signaling, anti-inflammatory response and reduction of Aβ levels.
|
23685322 |
2013 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
These results indicated that L-NBP might stimulate the proliferation, migration, and differentiation of hippocampal neural stem cells and reversed cognitive deficits in APP/PS1 mice.
|
29728920 |
2018 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
These results indicate that DISC1 attenuates Aβ generation and cognitive deficits of APP/PS1 transgenic mice through promoting lysosomal degradation of BACE1.
|
26062786 |
2016 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
These findings provided evidence that neuroinflammation might be involved in the development and progression of cognitive deficits in APP/PS1 mice, suggesting novel intervention and prevention strategies for AD.
|
28191738 |
2017 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
These findings implicate complex relationships between accumulating Aβ and activities of APP, soluble APP ectodomains, and/or APP C-terminal fragments in mediating cognitive deficits in this model of amyloidosis.
|
23447589 |
2013 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
Therefore, the dual-regulation on NGF signaling was attributed to the improvements of cognitive deficits and Aβ depositions in APP/PS1 mice.
|
24846616 |
2014 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
The SUMO1-APP transgenics displayed normal APP processing but, at later ages, exhibited increased insoluble Aβ and plaque density accompanied by increased dendritic spine loss, more pronounced synaptic and cognitive deficits.
|
29217476 |
2018 |
|
Cognition Disorders
|
0.400 |
AlteredExpression
|
group |
BEFREE |
The protection against disturbance of spontaneous motor activity and cognitive deficits in AD was strongly correlated with increased n-3: n-6 PUFAs ratio and endogenous n-3 PUFAs, reduced APP generation, inhibited amyloid β peptide aggregation, suppressed nuclear factor-kappa B and astroglia activation, and reduced death of neurons in the cortex of APP/fat-1 mice compared with APP mice controls.
|
27474225 |
2016 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
The present study is to investigate the effects of LIG on cognitive deficits and metabolism of both APP and Klotho and its underlying mechanism in AD double-transgenic (APP/PS1) mice and cultured human cells.
|
29163135 |
2017 |
|
Cognition Disorders
|
0.400 |
AlteredExpression
|
group |
BEFREE |
The effects of rapamycin on the reduction of Aβ, up-regulation of chaperones, and amelioration of AD-like cognitive deficits were recapitulated by transgenic over-expression of heat-shock factor 1 in PDAPP mice.
|
23121022 |
2013 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
The data showed that miR-574 was increased significantly in the hippocampus of 5-month-old APP/PS1 mice, which were concomitant with that APP/PS1 mice at the same age displayed a significant synaptic loss and cognitive deficits.
|
26423933 |
2015 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
Taurine treatment rescued cognitive deficits in APP/PS1 mice up to the age-matching wild-type mice in Y-maze and passive avoidance tests without modifying the behaviours of cognitively normal mice.
|
25502280 |
2014 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
Taken together, our findings show that the TIPE2 expression level was negatively correlated with the pathogenesis of Alzheimer's disease, and overexpression of TIPE2 attenuates cognitive deficits in APP/PS1 mice, suggesting TIPE2 is a potential target for pharmacological intervention and improvement of cognitive deficits.Graphical Abstract .
|
31286344 |
2019 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
Taken together, our data demonstrated that the reversal effect of FFPM on cognitive deficits in APP/PS1 transgenic mice might be related to stimulation of the cAMP/PKA/CREB/BDNF pathway and anti-inflammatory effects.
|
28065587 |
2017 |
|
Cognition Disorders
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Surprisingly, humanized APP knock-in mouse models carrying a single APP Swedish mutation (AppNL), failed to develop amyloid plaque aggregation or cognitive deficits.
|
30320577 |
2018 |
|
Cognition Disorders
|
0.400 |
Biomarker
|
group |
BEFREE |
Rescue of cognitive deficits in APP/PS1 mice by accelerating the aggregation of β-amyloid peptide.
|
31847879 |
2019 |