|
Forgetful
|
0.200 |
AlteredExpression
|
phenotype |
BEFREE |
More severe learning and memory impairment and higher Aβ1-40 expression in brain and plasma were detected in the APP/PS1 mice of 27-OHC treatment group.
|
30582229 |
2019 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Spatial learning and memory impairment and increased locomotion in a transgenic amyloid precursor protein mouse model of Alzheimer's disease.
|
21443906 |
2011 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
The results demonstrated that EA treatment ameliorated spatial learning and memory impairment in APP/PS1 mice and significantly reduced neuronal apoptosis and Aβ deposition in the hippocampus (P<0.05 and P<0.01).
|
30542451 |
2018 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
HPO |
|
|
|
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Although the primary causes of these disturbances are still under investigation, a growing body of evidence suggests that the amyloid precursor protein (APP) intracellular C-terminal fragment β (C99), generated by cleavage of APP by β-site APP cleaving enzyme 1 (BACE-1), is the primary cause of the endosome enlargement in AD and the earliest initiator of synaptic plasticity and long-term memory impairment.
|
28254759 |
2017 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
These results suggest that the sensorimotor gating is impaired with the progressing of AD phenotype, and its deficit may be correlated to cerebral Aβ neuropathology and memory impairment in the APP/PS1 transgenic mouse model of AD.
|
22595040 |
2012 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
The results suggest that plaque formation is not a necessary condition for the neuronal beta-APP(751) transgene-induced memory impairment, which may be caused by beta-APP overexpression, isoform misexpression, or elevated soluble Abeta.
|
11724968 |
2001 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Metformin treatment prevents amyloid plaque deposition and memory impairment in APP/PS1 mice.
|
29253574 |
2018 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Here, we show that amyloid-beta-induced hyperexcitability of hippocampal inhibitory parvalbumin (PV) interneurons importantly contributes to neuronal network dysfunction and memory impairment in APP/PS1 mice, a mouse model of increased amyloidosis.
|
31431685 |
2019 |
|
Forgetful
|
0.200 |
AlteredExpression
|
phenotype |
BEFREE |
Accumulations increased with age, and this was paralleled by decreased brain sizes on volumetric MRI, compared to age-matched and similar transgene-expressing APP wild-type mice, although, with these levels of transgenic expression we did not detect neuronal loss or significant memory impairment.
|
17112635 |
2008 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
In contrast, C57 APP/PS1 and SAMP8 wild type mice were inconspicuous in all of these tasks and properties except C57 APP/PS1 mice which showed motor memory impairment in the shuttle box task at 9 months old.
|
24095271 |
2013 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Here, we investigated the roles of NDRG2 in the development of memory impairment in AD using mouse models established by amyloid β injection or crossing of APP/PS1 mice.
|
31778735 |
2020 |
|
Forgetful
|
0.200 |
GeneticVariation
|
phenotype |
BEFREE |
Tg19959 mice carry human APP with two mutations and develop amyloid plaques and memory impairment starting at 3-4 months of age.
|
19914323 |
2010 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Tooth loss induces memory impairment and neuronal cell loss in APP transgenic mice.
|
23773908 |
2013 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Restraint/isolation stress induced significant depressive-like behaviors in APP/PS1 mice at 4 months of age and memory impairment at 10 months of age, while 6 months of icariin administration relieved the memory damage.
|
31001073 |
2019 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Therefore, we also investigated the dynamic of other protein markers involved in cognition and memory impairment such as metabotropic glutamate receptor 5 (mGluR5), ionotropic NMDA receptor (NMDAR2B), prion protein (PrPc) and amyloid precursor protein (APP), whose activity depends on membrane lipid organization.
|
31068782 |
2019 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Qingxin kaiqiao fang ameliorates memory impairment and inhibits apoptosis in APP/PS1 double transgenic mice through the MAPK pathway.
|
30774310 |
2019 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
The memory impairment associated to APP/PS1 transgene was accelerated in these mice.
|
30096288 |
2018 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Second, we used an APPswe/PS1E9 (APP/PS1) double transgenic mice to evaluate the amelioration ability of simvastatin against the memory impairment in vivo.
|
28528185 |
2017 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Flavonoids extracted from leaves of Diospyros kaki regulates RhoA activity to rescue synapse loss and reverse memory impairment in APP/PS1 mice.
|
29481523 |
2018 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Here, we show that xanthoceraside at doses of 0.08 and 0.32 mg/kg/d for 6 months significantly improved learning and memory impairment in APP transgenic mice assessed by the Y maze and novel object recognition tests.
|
24810883 |
2014 |
|
Forgetful
|
0.200 |
AlteredExpression
|
phenotype |
BEFREE |
We show that prolonged treatment with selegiline fails to reduce aberrant astrocytic GABA levels and rescue memory impairment in APP/PS1 mice, an animal model of AD, because of increased activity in compensatory genes for a GABA-synthesizing enzyme, diamine oxidase (DAO).
|
30906861 |
2019 |
|
Forgetful
|
0.200 |
GeneticVariation
|
phenotype |
BEFREE |
Transgenic mice carrying AD-causing mutations in APP develop spontaneous age-related beta-amyloid (A beta) deposition and memory impairment.
|
9052714 |
1997 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Here, we demonstrated that HFD markedly deteriorated memory impairment and increased β-amyloid (Aβ) oligomers as well as Aβ deposition in amyloid precursor protein (APP) transgenic mice, which was reversed by exposure to an enriched environment for 10 weeks, despite the continuation of HFD.
|
22197104 |
2012 |
|
Forgetful
|
0.200 |
Biomarker
|
phenotype |
BEFREE |
Moreover, while promoting apoE interaction with APP by ApoEp exacerbated Aβ and tau brain pathologies in 3XTg-AD mice, disrupting this interaction by 6KApoEp ameliorated cerebral Aβ and tau pathologies, neuronal apoptosis, synaptic loss, and hippocampal-dependent learning and memory impairment in 5XFAD mice without altering cholesterol, low-density lipoprotein receptor, and apoE expression levels.
|
31208706 |
2019 |