|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Based on the amyloid cascade hypothesis, the main component of senile plaques, the amyloid-beta (Aβ) peptide, and its derivative called amyloid precursor protein (APP) both have been found to place their central roles in AD development for years.
|
31811496 |
2020 |
|
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 |
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 |
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 |
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 |
In addition, the level of soluble Aβ1-42 has been shown to correlate with cognitive impairment in animal models before the presence of senile plaques or other histological features of AD.
|
31273712 |
2019 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Mutations in the genes encoding amyloid precursor protein (APP) or presenilin (PS) cause early onset familial Alzheimer's disease (AD), and sequential cleavages of the APP by β-secretase and γ-secretase/presenilin generate amyloid β protein (Aβ), the major component of pathological hallmark, neuritic plaques, in brains of AD patients.
|
30763650 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
We investigated the proteomic profiles of amyloid plaques (APs) from Alzheimer's disease (AD) and age-matched non-AD brains and APP/PS1 transgenic model mice.
|
30502339 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
The anomalous processing of APP by β-secretases and γ-secretases leads to production of Aβ<sub>40</sub> and Aβ<sub>42</sub> monomers, which further oligomerize and aggregate into senile plaques.
|
31410002 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Exposure of APP mice to fluoride elevated the number of senile plaques and level of Aβ42, Iba-1, and BACE1, while reducing the level of ADAM10 in their brains.
|
31010414 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Brain slices from APP/PS1 (amyloid precursor protein/presenilin 1) transgenic mice were mounted on slides, rinsed, coverslipped and observed for details of the imaging and spectral characteristics of the auto-F of SPs.
|
31127445 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
The cleavage by the α-secretase A Disintegrin And Metalloprotease 10 (ADAM10) releases the soluble portion (sAβPPα) and prevents senile plaques.
|
30836275 |
2019 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The identification of amyloid-β precursor protein (APP) pathogenic mutations in familial early onset Alzheimer's disease (AD), along with knowledge that amyloid-β (Aβ) was the principle protein component of senile plaques, led to the establishment of the amyloid cascade hypothesis.
|
30760863 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
β-Amyloid peptide (Aβ), the major element of senile plaques in Alzheimer's disease (AD), has been found to accumulate in brain regions critical for memory and cognition.
|
30474774 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Age Moderates the Effects of Traumatic Brain Injury on Beta-Amyloid Plaque Load in APP/PS1 Mice.
|
30623730 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Amyloid precursor protein (APP), a transmembrane glycoprotein, is the parent of Abeta, the major component of senile plaques in AD.
|
31448273 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
This disorder is characterized by the accumulation of beta amyloid plaques (Aβ) resulting from impaired amyloid precursor protein (APP) metabolism, together with the formation of neurofibrillary tangles and tau protein hyperphosphorylation.
|
31816853 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
The major components of β-amyloid plaques are Aβ<sub>1-42</sub> and Aβ<sub>1-40</sub> peptides derived from the APP.
|
30526133 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Amyloid-β (Aβ) peptides, major components of amyloid plaques and crucial pathogenic molecules in terms of the amyloid hypothesis, are derived from successive proteolytic processing of amyloid-β precursor protein (APP).
|
31606373 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Amyloid precursor protein and its derivative amyloid-β play an important role in the formation of senile plaques and the time course of immunoreactive expression may be related to the pathogenic process of Alzheimer-type dementia.
|
30086988 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Complex formation with GBRs stabilizes APP at the cell surface and reduces proteolysis of APP to Aβ, a component of senile plaques in Alzheimer's disease patients.
|
30902970 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
Amyloid-β (Aβ) is derived from the proteolytic processing of amyloid precursor protein (APP), and the deposition of extracellular Aβ to form amyloid plaques is a pathologic hallmark of Alzheimer's disease (AD).
|
31373844 |
2019 |
|
Senile Plaques
|
0.400 |
Biomarker
|
disease |
BEFREE |
In human amyloid precursor protein transgenic Tg2576 mice with amyloid plaque pathology, similar neuronal HTT expression patterns and a distinct association of HTT with Abeta plaques were revealed by immunohistochemical double labelling.
|
31109380 |
2019 |
|
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 |