|
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 |
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 |
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 |
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 |
GeneticVariation
|
disease |
BEFREE |
The main constituent of senile plaques is amyloid beta-peptide (A beta) and in recent years, pathogenic mutations in the amyloid precursor protein (APP) gene have been discovered in some AD families.
|
8577398 |
1995 |
|
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 |
GeneticVariation
|
disease |
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 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
In addition, for animals older than 12 months, we confirmed our previous report that only the two genotypes that form amyloid plaques (APP and PS/APP) have significantly reduced T(2) values compared with NTg controls.
|
17451178 |
2007 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The PDAPP transgenic mouse overexpresses human amyloid precursor protein V717F (PDAPP minigene) and develops age-related cerebral amyloid-beta protein (Abeta) deposits similar to senile plaques in Alzheimer's disease.
|
9278541 |
1997 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Exploratory activity and spatial learning in 12-month-old APP(695)SWE/co+PS1/DeltaE9 mice with amyloid plaques.
|
16169151 |
2005 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Because expression of sorLA is reduced in the brain of patients with Alzheimer's disease (AD), we tested involvement of this receptor in intracellular transport and processing of the amyloid precursor protein (APP) to the amyloid beta-peptide (Abeta), the principal component of senile plaques.
|
16174740 |
2005 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Expression of apoE3 and apoE4 in APP(V717F) TG, apoE(-/-) mice resulted in fibrillar Abeta deposits and neuritic plaques by 15 months of age and substantially (>10-fold) more fibrillar deposits were observed in apoE4-expressing APP(V717F) TG mice.
|
10694577 |
2000 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Additionally, all beta-amyloid-containing neuritic plaques in the hippocampal and cortical regions of APP and APP+PS1 transgenic mice were immunopositive for both lysosomal enzymes, whereas only a subset of the plaques displayed IGF-II/M6P receptor immunoreactivity.
|
17561313 |
2009 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
APP cleavage leads to the production of the beta-amyloid peptide (Abeta), which is the major constituent of the amyloid core of senile plaques found in the brains of patients with Alzheimer disease (AD).
|
20400860 |
2010 |
|
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 |
GeneticVariation
|
disease |
BEFREE |
Characteristic senile plaques in AD consist of amyloid-β peptide (Aβ) generated from the amyloid precursor protein.
|
29678763 |
2018 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Collectively, our results suggest that different pathological mechanisms, namely an intracellular accumulation of APP or extracellular amyloid plaques, may lead to spine abnormalities in young adult APP23 and deltaE9 mice, respectively.
|
25862638 |
2015 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
High selective expression of alpha7 nicotinic receptors on astrocytes in the brains of patients with sporadic Alzheimer's disease and patients carrying Swedish APP 670/671 mutation: a possible association with neuritic plaques.
|
15698636 |
2005 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Hypoxia treatment markedly increased Abeta deposition and neuritic plaque formation and potentiated the memory deficit in Swedish mutant APP transgenic mice.
|
17121991 |
2006 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The transmembrane domain and a portion of the C-terminus (A beta) of the amyloid precursor protein, are known to form the nucleus of the amyloid plaque.
|
10192224 |
1999 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
In the present study we demonstrated that repeated hypoxia increased beta-amyloid (Abeta) generation and neuritic plaques formation by elevating beta-cleavage of APP in APP(swe)+PS1(A246E) transgenic mice.
|
18063223 |
2009 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Clinical course of patients with familial early-onset Alzheimer's disease potentially lacking senile plaques bearing the E693Δ mutation in amyloid precursor protein.
|
21846988 |
2011 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Presenile Alzheimer dementia characterized by amyloid angiopathy and large amyloid core type senile plaques in the APP 692Ala-->Gly mutation.
|
9754958 |
1998 |
|
Senile Plaques
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The amyloid beta-peptide (Abeta), a proteolytic fragment of amyloid beta precursor protein (APP), aggregates to form neuritic plaques and has a causative role in AD.
|
17003227 |
2007 |