|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
As a result, the nanochaperone reduces Aβ burden, attenuates Aβ-induced inflammation, and eventually rescues the cognitive deficits of APP/PS1 transgenic AD mice.
|
31763156 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
To reveal the influence of Kai-Xin-San (KXS) on lipid metabolism in APP/PSI transgenic mice and potential therapeutic targets for treating AD, the brain tissue samples were collected and analyzed by high-throughput lipidomics based on UPLC-Q/TOF-MS tool.
|
31755117 |
2020 |
|
Alzheimer's Disease
|
0.900 |
GeneticVariation
|
disease |
BEFREE |
Here, we applied multilayered N-glycoproteomics to quantify the global protein expres-sion levels, N-glycosylation sites, N-glycans, and site-specific N-glycopeptides in AD (APP/PS1 transgenic) and wild-type mouse brains.
|
31751117 |
2020 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
Behavioral tests further confirmed PTS' potential of overcoming memory deficits in APP/PS1 mice (AD model).
|
31737188 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
Furthermore, Y-CDs were observed to enter cells to inhibit the overexpression of human amyloid precursor protein (APP) and β-amyloid (Aβ) which is a major factor responsible for AD pathology.
|
31730144 |
2019 |
|
Alzheimer's Disease
|
0.900 |
GeneticVariation
|
disease |
BEFREE |
Functional Connectivity (FC) analysis demonstrated early abnormal hypersynchronisation in the TG mice compared to the controls at 8w post DOX treatment, particularly across regions of the default mode-like network, known to be affected in AD.
|
31727182 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
New insight into Alzheimer's disease: Light reverses Aβ-obstructed interstitial fluid flow and ameliorates memory decline in APP/PS1 mice.
|
31720368 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
In this study, using a noninvasive nasal administration, we discovered that a miR-146a agomir (M146AG) rescued cognitive impairment in the APP/PS1 transgenic mouse and alleviated the overall pathological process in the AD mouse model, including neuroinflammation, glia activation, Aβ deposit, and tau phosphorylation in hippocampi.
|
31707205 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
Here we review recent progresses in the field and discuss the physiological importance of APP-Contactin interaction, as well as their roles and contributions in the pathophysiology of AD.
|
31705890 |
2020 |
|
Alzheimer's Disease
|
0.900 |
GeneticVariation
|
disease |
BEFREE |
Among the most commonly used models are transgenic mice overexpressing human amyloid precursor protein (APP) with mutations linked to familial AD, resulting in the formation of amyloid β plaques, one of the pathological hallmarks observed in AD patients.
|
31705038 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
Therefore, the present study used 6‑month‑old APPswe/PS1ΔE9 (APP/PS1) transgenic mice as early AD mouse models and sought to evaluate nicotinamide adenine dinucleotide (NAD+) and FK866 (a NAMPT inhibitor) treatment in APP/PS1 mice to study NAMPT dysmetabolism in the process of AD and elucidate the underlying mechanisms.
|
31702813 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
Here we showed for the first time the neuroprotective effects of Xestospongin C (XeC), a reversible IP3 receptor antagonist, on the cognitive behaviors and pathology of APP/PS1 AD mice.
|
31683484 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
TDP-43 inhibitory peptide alleviates neurodegeneration and memory loss in an APP transgenic mouse model for Alzheimer's disease.
|
31678156 |
2020 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
Therefore, it is likely that amyloid precursor protein and its proteolytic fragments other than amyloid β (Aβ) contribute to the onset of AD.
|
31677937 |
2020 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
This set of genes are implicated in important biological processes and molecular functions commonly affected by genes associated with the etiology of AD such as APP, APOE, and CLU.
|
31664702 |
2020 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
TEN has potential benefit in treating learning and memory deficits in APP/PS1 transgenic AD mice, and its effects may be associated with reversing AD pathology-induced neuronal apoptosis.
|
31664284 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
Here, we report that PBMT reduced Aβ production and plaque formation by shifting amyloid precursor protein (APP) processing toward the nonamyloidogenic pathway, thereby improving memory and cognitive ability in a mouse model of AD.
|
31663252 |
2020 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
We found that AD pathogenic factors appear earlier in APP/PS1 when supplemented with MSG, while wildtype mice were essentially not affected.
|
31658055 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
The amyloid-β (Aβ) peptide is a cleavage product of the amyloid precursor protein and has been implicated as a central player in Alzheimer's disease.
|
31657204 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
Here, we analyze the humoral immune response in AD to survey whether APP<sup>+1</sup> or UBB<sup>+1</sup> frameshift proteins, produced as a consequence of the "molecular misreading" alteration in AD occurring in the APP (amyloid precursor protein) and UBB (ubiquitin-B protein) proteins' mRNA, elicit the production of autoantibodies specific of AD.
|
31654319 |
2020 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
In order to elucidate which APP CTF that are the most common in brain tissue of different species and developmental stages, and whether there are any differences in these fragments between AD and control brain, we investigated the occurrence of these fragments using different APP c-terminal antibodies.
|
31649526 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
Therefore, the purpose of this study was to investigate the effect of progesterone on the glucose metabolism of neurons in amyloid precursor protein (APP)/presenilin 1 (PS1) mice and Aβ-induced AD cell model.
|
31647947 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
Our findings establish SK2 as an important endogenous regulator of both APP processing to Aβ, and oligodendrocyte survival, <i>in vivo</i> These results urge greater consideration of the roles played by oligodendrocyte dysfunction and altered membrane lipid metabolic flux as drivers of neurodegeneration in AD.<b>SIGNIFICANCE STATEMENT</b> Genetic, neuropathological, and functional studies implicate both Aβ and altered lipid metabolism and/or signaling as key pathogenic drivers of Alzheimer's disease.
|
31641049 |
2019 |
|
Alzheimer's Disease
|
0.900 |
Biomarker
|
disease |
BEFREE |
These advances, together with the discovery and characterization of multiple proteins that interact with APP or presenilin, have given rise to an optimistic scenario for future mechanistic understanding of AD.
|
31629221 |
2019 |
|
Alzheimer's Disease
|
0.900 |
GeneticVariation
|
disease |
BEFREE |
Here, we investigated the neuroprotective and restorative involvement of the DA DA-JC1 and liraglutide (Lg), a single GLP-1 receptor analogue, in vitro using human neuroblastoma (SH-SY5Y) against oxidative stress induced by oxygen peroxide (H<sub>2</sub>O<sub>2</sub>), and in vivo, in a mouse model of Alzheimer's disease (AD), APP/PS1.
|
31628935 |
2020 |