|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
To address this concern, we investigated sAβ effects on functional resting-state networks in transgenic mature-onset amyloidosis Tet-Off APP (TG) mice.
|
31727182 |
2019 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
Familial Alzheimer's disease (FAD)-associated presenilin 1 (PS1) serves as a catalytic subunit of γ-secretase complex, which mediates the proteolytic liberation of β-amyloid (Aβ) from β-amyloid precursor protein (APP).
|
30682043 |
2019 |
|
Amyloidosis
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Finally, we also describe purification strategies for Aβ40 and Aβ55 using FPLC and/or reverse phase HPLC.
|
31022450 |
2019 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
Graphical abstract The production of misfolded Aβ<sub>42</sub> peptide from amyloid precursor protein initiates amyloidosis pathway which ends with the deposition of fibrils via the oligomerization and aggregation of Aβ<sub>42</sub> monomers.
|
30868446 |
2019 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
BACE1 can hydrolyze amyloid precursor protein (APP), the precursor of Aβ.
|
31379559 |
2019 |
|
Amyloidosis
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The mRNA and protein levels of amyloid precursor protein, amyloid-β40 and amyloid-β42 were evaluated by quantitative real-time polymerase chain reaction, western blot assays and enzyme-linked immunosorbent assays. swAPP695-HEK293 cells were transfected with miR-15b-5p mimic, or treated with 1 μM curcumin 24 hours before miR-15b-5p inhibitor transfection.
|
31089060 |
2019 |
|
Amyloidosis
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The study suggests that both HIIT and MICT alleviate cognitive decline and down-regulat Aβ level in the hippocampus in APP/PS1 transgenic mice, which may be mediated by improvements in mitochondrial morphology and dynamics.
|
31445975 |
2019 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
Alternative processing of the amyloid precursor protein by β-secretase also generates the Aβ<sub>11- x</sub> species.
|
30582328 |
2019 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
In conclusion the present paper describes a novel pathway for Aβ clearance by astrocytes involving sAPPα as an enhancer of SR-A-dependent Aβ phagocytosis.
|
31536785 |
2019 |
|
Amyloidosis
|
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 |
|
Amyloidosis
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Mutations in APP and presenilins play major roles in Aβ pathology in rare autosomal-dominant forms of AD, whereas pathomechanisms of sporadic AD, accounting for the majority of cases, remain unknown.
|
30747419 |
2019 |
|
Amyloidosis
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Therefore, we investigated in the present study the App<sup>NL-G-F</sup>model, an App knock-in (App-KI) mouse model that develops amyloidosis in the absence of APP-overexpression.
|
31705038 |
2019 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
In this study, we highlighted that TREM2 triggers synaptic loss during AD pathology development.-Sheng, L., Chen, M., Cai, K., Song, Y., Yu, D., Zhang, H., Xu, G. Microglial Trem2 induces synaptic impairment at early stage and prevents amyloidosis at late stage in APP/PS1 mice.
|
31219699 |
2019 |
|
Amyloidosis
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
The γ-secretase-mediated cleavage of the APP C-terminal membrane stub leads to the production of various amyloid β (Aβ) species.
|
28332150 |
2018 |
|
Amyloidosis
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Recently, we reported that presenilin 1 considerably increased the expression level of U1 small nuclear RNA (snRNA) accompanied with the adverse change of amyloid precursor protein (APP) expression, β-amyloid (Aβ) production and cell apoptosis.
|
29395359 |
2018 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
Ex vivo intrinsic clotting of plasma from AD mice expressing human amyloid precursor protein (APP) was also delayed in an age-dependent manner, suggesting that this phenotype is related to APP, the parent protein of Aβ.
|
29700007 |
2018 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
Chronic cSNK peptide immunization of APP/PS1 mice engendered an anti-AβO<sup>cSNK</sup> IgG1 response without epitope spreading to Aβ monomers or fibrils and was accompanied by preservation of global PSD95 expression and improved cued fear memory.
|
29614860 |
2018 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
To enhance the process of protein secretion and accumulation, we adopted a chemical strategy of induction to modulate post-translational pathways of APP using an Amyloid-β Forty-Two Inducer named Aftin-5.
|
30557391 |
2018 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
Beta-amyloid is generated by the sequential cleavage of beta (<i>β</i>) and gamma (<i>γ</i>) sites in the amyloid precursor protein (APP) by <i>β</i>- and <i>γ</i>-secretase enzymes and its accumulation can result from either a decreased A<i>β</i> clearance or increased metabolism of APP.
|
30498753 |
2018 |
|
Amyloidosis
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Microglial activity decreases relative to ongoing amyloidosis with aging in APP-SL70 mice.
|
30400912 |
2018 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
RGFP-966, a brain-penetrant and selective HDAC3 inhibitor, or HDAC3 silencing, increases BDNF expression, increases histone H3 and H4 acetylation, decreases tau phosphorylation and tau acetylation at disease-associated sites, reduces β-secretase cleavage of the amyloid precursor protein (APP), and decreases Aβ<sub>1-42</sub> accumulation in HEK-293 cells overexpressing APP with the double Swedish mutation (HEK/APP<sub>sw</sub>).
|
30397132 |
2018 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
The objective of this study was to evaluate amyloid β (Aβ) deposition patterns in different groups of cerebral β amyloidosis: (1) nondemented with amyloid precursor protein overproduction (Down syndrome); (2) nondemented with abnormal processing of amyloid precursor protein (preclinical autosomal dominant Alzheimer disease); (3) presumed alteration in Aβ clearance with clinical symptoms (late-onset AD); and (4) presumed alterations in Aβ clearance (preclinical AD).
|
29477284 |
2018 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
These results indicate that during this brief and early phase of amyloid deposition, beneficial mitochondrial alterations in the newly recruited third of microglial cells were not sufficient to affect the amyloidosis in APP-transgenic mice.
|
30040730 |
2018 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
The results of immunohistochemistry, Western blotting and quantitative real-time PCR showed that APP and its downstream products (i.e. amyloid-β42) were more highly expressed in SK than in paired adjacent normal skin tissues.
|
29487944 |
2018 |
|
Amyloidosis
|
0.400 |
Biomarker
|
disease |
BEFREE |
Amyloid precursor protein (APP), a key molecule of Alzheimer disease, is metabolized in 2 antagonist pathways generating the soluble APP alpha (sAPPα) having neuroprotective properties and the beta amyloid (Aβ) peptide at the origin of neurotoxic oligomers, particularly Aβ1-42.
|
29032190 |
2018 |