|
Alzheimer's Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The levels of the p75 neurotrophin receptor (p75NTR), an Aβ1-42 receptor, were down-regulated in the ADH1B overexpressing AD model cell and up-regulated in cells transfected with the shRNA vector of ADH1B.
|
31231206 |
2019 |
|
Alzheimer's Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Neurotrophin Receptor p75 mRNA Level in Peripheral Blood Cells of Patients with Alzheimer's Disease.
|
30977102 |
2019 |
|
Alzheimer's Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The degeneration of cholinergic basal forebrain (cBF) neurons in Alzheimer's disease (AD) leads to the cognitive impairment associated with this condition. cBF neurons express the p75 neurotrophin receptor (p75<sup>NTR</sup>), which mediates cell death, and the extracellular domain of p75<sup>NTR</sup> can bind to amyloid beta (Aβ) and promote its degradation.
|
30374941 |
2019 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Neurotrophin receptor p75 (p75<sup>NTR</sup>) is a receptor for Aβ and mediates Aβ neurotoxicity, implying that p75<sup>NTR</sup> may mediate Aβ-induced tau phosphorylation in AD.
|
31394202 |
2019 |
|
Alzheimer's Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The expression of p75 neurotrophin receptor is elevated in the brain of AD patients, suggesting its involvement in this disease.
|
28869759 |
2018 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
The p75 neurotrophin receptor (p75NTR) is an amyloid-β (Aβ) receptor that both mediates Aβ neurotoxicity and regulates Aβ production and deposition, thus playing an important role in the pathogenesis of Alzheimer's disease (AD).
|
29578485 |
2018 |
|
Alzheimer's Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Induction of apoptosis and p75 ICD internalization by AD patients-derived proBDNF is further enhanced in neuron cultures from the AD model expressing the APP/PS1∆E9 transgene.Our results indicate the importance of proBDNF neurotoxic signaling in AD pathology essentially by three mechanisms: i) by an increase of proBDNF stability due to ROS-induced post-traductional modifications; ii) by the increase of expression of the p75 co-receptor, Sortilin and iii) by the increase of the basal levels of p75 processing found in AD.
|
30428894 |
2018 |
|
Alzheimer's Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, this study demonstrates that sulforaphane can ameliorate neurobehavioral deficits and reduce the Aβ burden in Alzheimer's disease model mice, and the mechanism underlying these effects may be associated with up-regulation of p75 neurotrophin receptor mediated, apparently at least in part, via reducing the expression of histone deacetylase1 and 3.
|
28507518 |
2017 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
The p75 neurotrophin receptor (p75NTR) is involved in degenerative mechanisms related to Alzheimer's disease (AD).
|
24898660 |
2014 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Degeneration of basal forebrain cholinergic neurons contributes significantly to the cognitive deficits associated with Alzheimer's disease (AD) and has been attributed to aberrant signaling through the neurotrophin receptor p75 (p75NTR).
|
25153701 |
2014 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
This review discusses recent findings that strongly link the p75 neurotrophin receptor (p75(NTR)) to both cholinergic neuron degeneration and the production of toxic forms of amyloid-beta (Abeta), which is found deposited as amyloid plaques in the brains of Alzheimer's disease patients.
|
19458382 |
2009 |
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
Oligomeric forms of amyloid-beta (Abeta) are thought to play a causal role in Alzheimer's disease (AD), and the p75 neurotrophin receptor (p75(NTR)) has been implicated in Abeta-induced neurodegeneration.
|
19710315 |
2009 |
|
Alzheimer's Disease
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
NGF, BDNF, NT-3, NT-4/5, as well as trkB, trkC and p75 mRNA levels were unchanged in AD parietal cortex and cerebellum as compared to controls.
|
9507943 |
1998 |