|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
We previously showed that the amyloid scavenger, insulin-degrading enzyme (IDE), generates T40-derived amyloidogenic species that, as a peptide mixture, seed Aβ fibrillization.
|
30787102 |
2019 |
|
Amyloidosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The present study confirmed this hypothesis by showing that PPARγ agonist pioglitazone attenuated the neuronal apoptosis of primary rat hippocampal neurons induced by Aβ<sub>1-42</sub>, downregulated CDK5 expression, weakened the binding of CDK5 to PPARγ, reduced PPARγ phosphorylation, increased the expression of PPARγ and IDE, decreased the expression of BACE1, reduced APP production, and downregulated intraneuronal Aβ<sub>1-42</sub> levels.
|
31379559 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Membrane metalloendopeptidase (MME) and insulin-degrading enzyme (IDE) are two types of proteases that could cleave beta-amyloid (Aβ) peptides generated by neuron cells of AD patients.
|
31151136 |
2019 |
|
Amyloidosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Overall, our results suggest sustained reduction of NEP and IDE expression in response to Pb sensitizes recovery SH-SY5Y cells to Aβ accumulation; however, administration of VPA is demonstrated to be beneficial in modulating Aβ clearance.
|
30593950 |
2019 |
|
Amyloidosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The increased levels of β-amyloid were due to a decrease in the release of insulin-degrading enzyme by the model senescent microglia.
|
30052418 |
2018 |
|
Amyloidosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Molecular analysis revealed that GAS exerted the protective effect via reducing the levels of Aβ1-40/42, APP, and β-site APP-cleaving enzyme 1 expression, and increasing Aβ-related protein, a disintegrin and metalloprotease 10, and insulin degrading enzyme expression.
|
29755351 |
2018 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Further relevant studies are still needed to verify whether IDE is one of the factors affecting Aβ abnormal accumulation and throw new insights for AD detection or therapy.
|
29357797 |
2018 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, further studies on IDE unraveled its ability to degrade several other polypeptides, such as β-amyloid, amylin, and glucagon, envisaging the possible implication of IDE dys-regulation in the "aggregopathies" and, in particular, in neurodegenerative diseases.
|
28635330 |
2017 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the present study, we measured plasma levels of amyloid-β1-42(0.142±0.029μg/L)and furin(2.292±1.54μg/L), together with those of the metalloproteinases, insulin-degrading enzyme(1.459±1.14μg/L) and neprilysin(0.073±0.015μg/L), in order to develop biomarkers for AD.
|
28719622 |
2017 |
|
Amyloidosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Protein levels of insulin-degrading enzyme (IDE), which is linked to insulin signaling and degrades Aβ, significantly increased in the 3xTg-AD mice brain compared with non-transgenic mice, and were further increased by APO.
|
28550243 |
2017 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the Tg2576 mouse model of Alzheimer's disease, UE2316 treatment of mice aged 14 months for 4 weeks also decreased the number of β-amyloid (Aβ) plaques in the cerebral cortex, associated with a selective increase in local insulin-degrading enzyme (involved in Aβ breakdown and known to be glucocorticoid regulated).
|
26305888 |
2015 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although evidence suggests that NEP is down-regulated in Alzheimer's disease (AD), the role of IDE and ECE in the Aβ accumulation in aging and dementia remains less certain.
|
20663017 |
2010 |
|
Amyloidosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Effects of 4-hydroxy-nonenal and Amyloid-beta on expression and activity of endothelin converting enzyme and insulin degrading enzyme in SH-SY5Y cells.
|
19363254 |
2009 |
|
Amyloidosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Moreover they raise the possibility that IDE inhibition or inactivation is a pathogenic mechanism that may open novel strategies for the treatment of cerebrovascular Abeta amyloidoses.
|
15489232 |
2004 |