|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The results showed that long-term consumption of alcohol aggravated cognitive decline, increased the permeability of the BBB, led to pathomorphological changes and downregulated some related structural proteins (zonula occludens-1, VE-cadherin, and occludin) and functional proteins (major facilitator superfamily domain-containing protein-2a (Mfsd2a), low-density lipoprotein receptor-related protein-1 (LRP1), receptor for advanced glycation end products (RAGE), and aquaporin-4 (AQP4)) in the BBB but did not increase the concentration of Aβ<sub>1-42</sub>.
|
31746246 |
2019 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Moreover, we show that all RAGE fragments apart from the shortest one (60-62), were able to protect neuronal primary cultures from amyloid toxicity, by preventing the caspase 3 activation induced by Aβ 1-42.
|
30319347 |
2018 |
|
Amyloidosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Lung adenocarcinoma with RAGE expression may be a complication of underlying amyloidosis.
|
28056871 |
2017 |
|
Amyloidosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, the expression of RAGE and proinflammatory mediators, as well as, Aβ accumulation were attenuated.
|
28115220 |
2017 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, TXL improved cognition and decreased Aβ in SHRs in a dose- and time-dependent manner, the underlying mechanism may involved in inhibiting RAGE and β-secretase expression.
|
28274609 |
2017 |
|
Amyloidosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results showed that Acrp30 (a globular form of adiponectin) reduces the expression of proinflammatory cytokines and the expression of RAGE as Aβ transporters into brain.
|
29022894 |
2017 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our results support the involvement of the EC in the development and progression of the synaptic and behavioural deficit during amyloid-dependent neurodegeneration and demonstrate that microglial RAGE activation in presence of Aβ-enriched environment contributes to the EC vulnerability.
|
28205565 |
2017 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our results demonstrate a prominent role for the RAGE-dependent neuroinflammatory pathway in the synaptic failure induced by Aβ and triggered by transient ischemia.
|
24966375 |
2014 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Additionally, following apical exposure to the BBB model, we found that apoE4 bound to Aβ is able to penetrate the BBB more readily than apoE3 bound to Aβ and does so via the RAGE (receptor for advanced glycation end products) transporter.
|
22572854 |
2013 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
RAGE-amyloid-β toxin interaction at the BBB leads to oxidative stress, inflammatory responses and reduced cerebral blood flow.
|
22571615 |
2012 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
LHGDN |
Using immunohistochemistry, AGEs, CML, and RAGE were found within amyloid deposits, more commonly in AA amyloid than in AL amyloid and not in ATTR amyloid.
|
12651613 |
2003 |
|
Amyloidosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
One class of RAGE ligands includes glycoxidation products, termed advanced glycation end products, which occur in diabetes, at sites of oxidant stress in tissues, and in renal failure and amyloidoses.
|
10082470 |
1999 |