INT174133

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Context Info
Confidence 0.19
First Reported 2003
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 3
Disease Relevance 3.00
Pain Relevance 0.08

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

nucleus (Igfals, Sod1) mitochondrion (Sod1) aging (Sod1)
peroxisome (Sod1) intracellular (Sod1) protein complex (Sod1)
Igfals (Mus musculus)
Sod1 (Mus musculus)
Sod1 - G93A (1)
Pain Link Frequency Relevance Heat
Spinal cord 24 79.60 Quite High
medulla 5 78.96 Quite High
Glutamate 21 5.00 Very Low Very Low Very Low
Inflammation 8 5.00 Very Low Very Low Very Low
Gabapentin 8 5.00 Very Low Very Low Very Low
intrathecal 5 5.00 Very Low Very Low Very Low
COX-2 inhibitor 4 5.00 Very Low Very Low Very Low
Lamotrigine 4 5.00 Very Low Very Low Very Low
agonist 3 5.00 Very Low Very Low Very Low
Central nervous system 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Motor Neuron Diseases 270 100.00 Very High Very High Very High
Targeted Disruption 45 100.00 Very High Very High Very High
Toxicity 9 97.56 Very High Very High Very High
Spinal Muscular Atrophy 7 89.52 High High
Frontotemporal Dementia 2 83.76 Quite High
Dementia 15 81.76 Quite High
Death 22 75.36 Quite High
Injury 5 74.96 Quite High
Neurodegenerative Disease 18 73.84 Quite High
Disease 58 43.88 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Animal drug-screening studies in ALS almost exclusively utilized the mutant SOD1 (G93A) mouse, but it remains to be firmly demonstrated that the SOD1 transgenic mouse models are an accurate and useful model for sporadic ALS.103,159 The role of biochemically altered SOD1 in sporadic ALS remains speculative and some pathogenetic mechanisms are different between familial and sporadic ALS.3 Alternative models that better represent pathological features observed in sporadic ALS should be therefore obtained.23 However, until a model of sporadic ALS will be developed, a possible strategy will be to require multiple preclinical information both from in vitro and in vivo studies before the start of clinical trials on ALS patients.


ALS Binding (utilized) of SOD1 (G93A) associated with targeted disruption and motor neuron diseases
1) Confidence 0.19 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785861 Disease Relevance 1.22 Pain Relevance 0
SOD1 aggregates have been widely observed in mutant SOD1 transgenic mice and in human ALS caused by SOD1 mutations [11,14,35,36].
ALS Binding (aggregates) of SOD1 associated with targeted disruption and motor neuron diseases
2) Confidence 0.05 Published 2003 Journal BMC Neurosci Section Body Doc Link PMC169170 Disease Relevance 0.52 Pain Relevance 0
Fifteen loci are known to be associated with ALS, and eight causative genes have been identified, the most common of which is SOD1 (Cu/Zn superoxide dismutase 1) [2].
ALS Binding (associated) of SOD1 associated with motor neuron diseases
3) Confidence 0.04 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844426 Disease Relevance 1.26 Pain Relevance 0.08

General Comments

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