|
Alzheimer's Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Alzheimer's Disease Progression in the 5×FAD Mouse Captured with a Multiplex Gene Expression Array.
|
31683485 |
2019 |
|
Alzheimer's Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
By studying the loss-of-function properties of PS1 mutants, it is possible to successfully screen FAD suppressor mutations and identify γ-secretase modulators (GSMs), which are promising Alzheimer disease therapeutic agents.
|
31602624 |
2019 |
|
Alzheimer's Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Exenatide alleviates mitochondrial dysfunction and cognitive impairment in the 5×FAD mouse model of Alzheimer's disease.
|
31082410 |
2019 |
|
Alzheimer's Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Brains from different transgenic strains and ages developed overt cerebral Aβ deposition, including the β-amyloid precursor protein and presenilin 1 double-transgenic (APP/PS1) mice at ~ 14 months of age, the five familial Alzheimer's disease mutations transgenic (5×FAD) mice at ~ 8 months, the triple-transgenic Alzheimer's disease (3×Tg-AD) mice at ~ 22 months, and aged monkeys (Macaca mulatta and Macaca fascicularis) were examined.
|
29690919 |
2018 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
The fluorescence decay times of native NADH and FAD show a longer relaxation time in AD than in WT tissue, suggesting less non-radiative processes in AD.
|
28464457 |
2018 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Using these features of AD genes, we found that 5×FAD, amyloid β-injected mice, and rats in the initial phases after bilateral common carotid artery occlusion (BCCAO) exhibited patterns that were most similar to those of AD.
|
29656362 |
2018 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this study, we used 5×FAD transgenic mice as an AD model to investigate the effects of curcumin on AD.
|
26910813 |
2017 |
|
Alzheimer's Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
EFAD mice were designed as a temporally useful preclinical FAD-Tg-mouse model expressing the h-<i>APOE</i> genotypes for identifying mechanisms underlying <i>APOE</i>-modulated symptoms of AD pathology.
|
28389477 |
2017 |
|
Alzheimer's Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Taken together, our results demonstrate that nNOS dimers are disrupted in the 5 × FAD cortex, and nNOS-Ser(293), a potential site of CDK5 phosphorylation, may be involved in the decrease in nNOS dimerization and NO production, and the development of AD.
|
27296112 |
2016 |
|
Alzheimer's Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The aim of the present study was to determine whether FAD-linked mutations of APP, known to be associated with early onset of the disease, might impair its synaptotrophic function, potentially contributing to synaptic deficiencies seen in AD.
|
19450683 |
2009 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Decreased FA in of the columns of the fornix is particularly robust in early FAD and may provide a biomarker for early disease in sporadic Alzheimer's disease.
|
17522104 |
2007 |
|
Alzheimer's Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Synthesis of glycosaminoglycans (GAG) and collagen were measured in skin fibroblasts from patients with familial, sporadic AD (FAD and SAD respectively), and from age-matched controls by radiolabeled precursors.
|
17660861 |
2007 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Stimulation of G-proteins in human control and Alzheimer's disease brain by FAD mutants of APP(714-723): implication of oxidative mechanisms.
|
15614786 |
2005 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Two other FAD genes, presenilin-1 and -2, have also been shown to regulate Abeta production; however, studies examining the biological role of these FAD genes suggest an alternative theory for the pathogenesis of AD.
|
10409650 |
1999 |
|
Alzheimer's Disease
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We compared immunohistochemical expression of the transforming growth factor-betas (TGF-beta 1, TGF-beta 2, and TGF-beta 3) using brain tissue from patients with nondominantly inherited Alzheimer's disease (NDAD) (n = 9), autosomal dominantly inherited Alzheimer's disease with linkage to 14q24.3 (FAD-14) (n = 4), and cognitively normal controls (n = 10) to determine whether their pathologic changes are associated with an altered distribution of the TGF-betas.
|
7543987 |
1995 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our results may suggest that late-onset FAD has at least 2 etiologies; AD in some families may be transmitted as a dominant trait, whereas a proportion of cases in these and other late-onset families may be caused by other genetic or shared environmental factors.
|
2314579 |
1990 |