|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Phosphorylated tau in neuritic plaques of APP(sw)/Tau (vlw) transgenic mice and Alzheimer disease.
|
18679696 |
2008 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Compared to the control group, consisting of animals carrying only mutant APP, bigenic mice showed a higher number of senile plaques in the cerebral cortex, while APP transcription and Abeta40/Abeta42 levels were unchanged.
|
15917101 |
2005 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The APP(E693Q) mice did not develop amyloid plaques at any age studied, up to 30 months.
|
20641005 |
2010 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
The main component of SP is amyloid-beta peptide (Aβ), a 39 to 43 amino acid peptide, generated by the proteolytic cleavage of amyloid precursor protein (APP) by the action of beta- and gamma-secretases.
|
21726674 |
2011 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
The administration of NAD+ alleviated the spatial learning and memory of APP/PS1 mice and reduced senile plaques.
|
31702813 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Furthermore, administration of THA effectively improved the learning ability of APP/PS1 transgenic mice, and markedly reduced the number of senile plaques in their hippocampus and cortex.
|
27694908 |
2017 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Trafficking and proteolytic processing of amyloid precursor protein (APP) have been the focus of numerous investigations in the past two decades, since the identification of Abeta as the principal component of brain senile plaques and the cloning of APP cDNA.
|
16432149 |
2006 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our results demonstrated that social housing improved the behavioral performance of APP/PS1 mice in Morris Water Maze testing, without significantly altering the rates of amyloid plaque deposition or amyloidogenic APP processes.
|
31034995 |
2019 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
A constituent of senile plaques in AD is beta-amyloid, a hydrophobic peptide of 39-43 amino acids and a fragment of the amyloid precursor protein (APP).
|
7585189 |
1995 |
|
Senile Plaques
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
We found that: (1) DA5-CH administration effectively improved working-memory and long-term spatial memory of 9-month-old AD mice in Y-maze and Morris water maze tests; (2) DA5-CH also reduced hippocampal amyloid senile plaques and phosphorylated tau protein levels; (3) DA5-CH basically reversed the deficits in hippocampal late-phase long-term potentiation; (4) DA5-CH up-regulated the levels of p-PI3K and p-AKT growth factor kinases and prevented excessive activation of p-GSK3β in the hippocampus of APP/PS1 mice.
|
29551659 |
2018 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Molecular characterization of Netrin-1 and APP receptor binding: New leads to block the progression of senile plaques in Alzheimer's disease.
|
28501620 |
2017 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
One important pathologic feature of AD is the formation of extracellular senile plaques in the brain, whose major components are small peptides called beta-amyloid (Abeta) that are derived from beta-amyloid precursor protein (APP) through sequential cleavages by beta-secretase and gamma-secretase.
|
18045146 |
2007 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
CTD_human |
Virgin coconut oil (VCO) by normalizing NLRP3 inflammasome showed potential neuroprotective effects in Amyloid-β induced toxicity and high-fat diet fed rat.
|
29729307 |
2018 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The generation of Aβ, the main component of senile plaques in Alzheimer's disease (AD), is precluded by α-secretase cleavage within the Aβ domain of the amyloid precursor protein (APP).
|
24055016 |
2013 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
To identify epigenetically regulated genes involved in the pathogenesis of Alzheimer's disease (AD) we analyzed global mRNA expression and methylation profiles in amyloid precursor protein (APP)-Swedish mutant-expressing AD model cells, H4-sw and selected heme oxygenase-1 (HMOX1), which is associated with pathological features of AD such as neurofibrillary tangles and senile plaques.
|
27058954 |
2016 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
CTD_human |
Up-regulated expression of amyloid precursor protein (APP) occurs early in the cascade of events that leads to amyloid plaque formation in the human brain.
|
19818510 |
2009 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
In addition, administration of TBTC (30mg/kg/day) in the transgenic APP-PS1 mice could also reduce the formation of senile plaques and improve the daily living activity of the mice.
|
26026644 |
2015 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Alzheimer's disease (AD) is a degenerative disorder typified by progressive deterioration of memory and the appearance of β-amyloid peptide (Aβ)-rich senile plaques.
|
28740171 |
2017 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Amyloid-beta (Abeta) the primary component of the senile plaques found in Alzheimer's disease (AD) is generated by the rate-limiting cleavage of amyloid precursor protein (APP) by beta-secretase followed by gamma-secretase cleavage.
|
15452128 |
2004 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Histopathological hallmarks are represented by aggregates of beta-amyloid peptide (Aβ) in senile plaques and deposition of hyperphosphorylated tau protein in neurofibrillary tangles in the brain.
|
25927677 |
2015 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The characteristic hallmarks of the disease are extracellular senile plaques (SPs) and intracellular neurofibrillary tangles (NFTs) with neuropil threads, which are a direct result of amyloid precursor protein (APP) processing to Aβ, and τ hyperphosphorylation.
|
30260518 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Transgenic (Tg) mouse models overexpressing amyloid precursor protein (APP) develop senile plaques similar to those found in Alzheimer's disease in an age-dependent manner.
|
12223540 |
2002 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Tph2 Genetic Ablation Contributes to Senile Plaque Load and Astrogliosis in APP/PS1 Mice.
|
30827242 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Stress increases cognitive dysfunction, generates amyloid precursor protein (APP), hyperphosphorylated tau, neurofibrillary tangles (NFTs), and amyloid plaques (APs) in the brain.
|
30837843 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
beta-amyloid peptide (A beta) and complement-derived membrane attack complex (MAC) are co-localized in senile plaques of brains from Alzheimer's disease (AD) patients.
|
9689469 |
1998 |