INT147429

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Context Info
Confidence 0.40
First Reported 2008
Last Reported 2011
Negated 1
Speculated 0
Reported most in Body
Documents 8
Total Number 8
Disease Relevance 8.73
Pain Relevance 2.78

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

cell adhesion (App) Golgi apparatus (App) plasma membrane (App)
extracellular matrix organization (App) DNA binding (App) cytoplasm (App)
Anatomy Link Frequency
cortex 3
plaque 2
forebrain 2
head 2
hippocampus 1
App (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 95 100.00 Very High Very High Very High
Abeta 38 100.00 Very High Very High Very High
agonist 11 99.98 Very High Very High Very High
Hippocampus 19 99.28 Very High Very High Very High
Intracerebroventricular 4 99.14 Very High Very High Very High
Nerve growth factor 1 99.00 Very High Very High Very High
Eae 2 98.08 Very High Very High Very High
Inflammatory response 6 88.60 High High
cINOD 51 61.44 Quite High
cytokine 23 54.80 Quite High
Disease Link Frequency Relevance Heat
INFLAMMATION 115 100.00 Very High Very High Very High
Alzheimer's Dementia 56 100.00 Very High Very High Very High
Brain Injury 8 99.90 Very High Very High Very High
Targeted Disruption 93 99.56 Very High Very High Very High
Disease 285 99.28 Very High Very High Very High
Cognitive Disorder 36 95.52 Very High Very High Very High
Herpes Simplex Virus 1 95.28 Very High Very High Very High
Syndrome 5 94.64 High High
Drug Induced Neurotoxicity 18 92.16 High High
Injury 19 90.04 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In transgenic mice expressing high levels of wt APP, there is no plaque formation even when large amounts of A?
Neg (no) Negative_regulation (is) of Positive_regulation (levels) of APP in plaque associated with targeted disruption
1) Confidence 0.40 Published 2010 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2938309 Disease Relevance 1.27 Pain Relevance 0.03
Another study showed that increased doses of APP markedly decreased retrograde transport of nerve growth factor and resulted in degeneration of forebrain cholinergic neurons in a mouse model of Down's Syndrome [32].
Negative_regulation (decreased) of Positive_regulation (increased) of APP in forebrain associated with nerve growth factor and syndrome
2) Confidence 0.37 Published 2011 Journal Mol Brain Section Body Doc Link PMC3022812 Disease Relevance 0.32 Pain Relevance 0.05
For mutants that predominantly produce Abeta(42), the ability of fenofibrate to further increase Abeta(42) levels became diminished, whereas Abeta(38) levels were altered to varying extents for all mutants analyzed.
Negative_regulation (diminished) of Positive_regulation (increase) of Abeta associated with abeta
3) Confidence 0.35 Published 2008 Journal J. Biol. Chem. Section Abstract Doc Link 17962197 Disease Relevance 0.70 Pain Relevance 0.81
Strikingly, even the mutations that showed no effect on Abeta(42) levels allowed a robust increase of Abeta(38) upon treatment with sulindac sulfide.
Negative_regulation (allowed) of Positive_regulation (increase) of Abeta associated with abeta
4) Confidence 0.35 Published 2008 Journal J. Biol. Chem. Section Abstract Doc Link 17962197 Disease Relevance 0.69 Pain Relevance 0.80
Work in a porcine model of head injury has shown accumulation of APP and BACE in injured axons and it is suggested that the abnormal accumulation of these proteins may favour A?
Negative_regulation (shown) of Positive_regulation (accumulation) of APP in head associated with brain injury
5) Confidence 0.34 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2442055 Disease Relevance 1.22 Pain Relevance 0.23
In relation to AD, it is well known that M1 agonists increase the non-amyloidogenic processing of the amyloid precursor protein (APP), reducing A?
Negative_regulation (reducing) of Positive_regulation (increase) of APP associated with alzheimer's dementia, agonist and disease
6) Confidence 0.30 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2515306 Disease Relevance 0.86 Pain Relevance 0.23
Inhibition of solTNF signaling in triple transgenic mice (APPSwe, tauP301L, and PS1M146V) by either hippocampal infusion of DN-TNF inhibitors or intracerebroventricular injection of a lentivirus encoding DN-TNF reduced inflammation-induced accumulation of C-terminal APP fragments in the hippocampus, cortex, and amygdale.
Negative_regulation (reduced) of Positive_regulation (accumulation) of APP in cortex associated with targeted disruption, inflammation, hippocampus and intracerebroventricular
7) Confidence 0.16 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2577641 Disease Relevance 1.84 Pain Relevance 0.31
Inhibition of solTNF signaling in triple transgenic mice (APPSwe, tauP301L, and PS1M146V) by either hippocampal infusion of DN-TNF inhibitors or intracerebroventricular injection of a lentivirus encoding DN-TNF reduced inflammation-induced accumulation of C-terminal APP fragments in the hippocampus, cortex, and amygdale.
Negative_regulation (reduced) of in hippocampus Positive_regulation (accumulation) of APP in cortex associated with targeted disruption, inflammation, hippocampus and intracerebroventricular
8) Confidence 0.06 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2577641 Disease Relevance 1.84 Pain Relevance 0.31

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