|
Alzheimer's Disease
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
The high levels of VDAC1 demonstrated post-mortem in the brains of AD patients and in amyloid precursor protein (APP) transgenic mice prompted the hypothesis that the protein may be associated with neuronal cell destruction since over-expression of VDAC1 triggers cell death.
|
29551631 |
2018 |
|
Alzheimer's Disease
|
0.090 |
Biomarker
|
disease |
BEFREE |
Ceramide-depleted astrocytes contained higher levels of ATP, suggesting that ceramide-induced CAT formation leads to VDAC1 closure, thereby reducing mitochondrial ATP release, and potentially motility and resistance to Aβ<sub>42</sub> Our data also indicate that inhibiting ceramide generation may protect mitochondria in Alzheimer's disease.
|
29321137 |
2018 |
|
Alzheimer's Disease
|
0.090 |
Biomarker
|
disease |
BEFREE |
This computational analysis suggests that metabolically-dependent generation of OMP in the brain mitochondria, controlled by many factors that modulate VDAC1-HKI interaction, VDAC's voltage-gating properties and permeability, might represent one of the physiological mechanisms of regulation of the brain energy metabolism and of neuronal death resistance, and might also be involved in various neurodegenerative disorders, such as Alzheimer's disease.
|
30291922 |
2018 |
|
Alzheimer's Disease
|
0.090 |
Biomarker
|
disease |
BEFREE |
In particular, the principal isoform VDAC1 represents the main mitochondrial docking site of many misfolded proteins, such as amyloid β and Tau in Alzheimer's disease, α-synuclein in Parkinson's disease and several SOD1 mutants in Amyotrophic Lateral Sclerosis.
|
28571556 |
2017 |
|
Alzheimer's Disease
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
VDAC1 is overexpressed in post-mortem brains of Alzheimer disease (AD) patients.
|
26542804 |
2015 |
|
Alzheimer's Disease
|
0.090 |
Biomarker
|
disease |
BEFREE |
The purpose of this article is to review research that has investigated the relationship between VDAC1 and the regulation of MPT pores in AD progression.
|
22995655 |
2013 |
|
Alzheimer's Disease
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Thus, these findings also suggest that the reduction of APP, Tau, and VDAC1 mRNA expressions may have therapeutic value for patients with AD.
|
24063855 |
2013 |
|
Alzheimer's Disease
|
0.090 |
Biomarker
|
disease |
BEFREE |
Based on current study observations, we propose that reduced levels of VDAC1, Aβ and phosphorylated tau may reduce the abnormal interaction between VDAC1 and APP, VDAC1 and Aβ, and VDAC1 and phosphorylated tau; and that reduced levels of VDAC1, Aβ and phosphorylated tau may maintain normal mitochondrial pore opening and pore closure, ultimately leading to normal mitochondrial function, mitochondria supplying ATP to nerve terminals and boosting synaptic and cognitive function in AD.
|
22926141 |
2012 |
|
Alzheimer's Disease
|
0.090 |
AlteredExpression
|
disease |
BEFREE |
Since phospho-VDAC and reduced HXKI levels favors a VDAC1 conformational state more prone to the release proapoptotic factors, regulation of the function of this channel may be a promising therapeutic approach to combat AD.
|
20930307 |
2011 |