INT234160

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Context Info
Confidence 0.16
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 4
Disease Relevance 3.80
Pain Relevance 0.74

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

extracellular region (Igfals) cell adhesion (Igfals) nucleus (Igfals)
Anatomy Link Frequency
lateral 1
neurons 1
motor neurons 1
Igfals (Mus musculus)
Pain Link Frequency Relevance Heat
Multiple sclerosis 27 100.00 Very High Very High Very High
Central nervous system 51 97.96 Very High Very High Very High
Neuropeptide 13 89.92 High High
Inflammation 59 75.00 Quite High
Peripheral nerve injury 3 71.80 Quite High
withdrawal 10 69.68 Quite High
long-term potentiation 1 65.84 Quite High
chemokine 6 65.52 Quite High
Inflammatory mediators 20 60.56 Quite High
imagery 3 55.68 Quite High
Disease Link Frequency Relevance Heat
Disease 149 100.00 Very High Very High Very High
Motor Neuron Diseases 47 100.00 Very High Very High Very High
Multiple Sclerosis 29 100.00 Very High Very High Very High
Autoimmune Disease 15 99.86 Very High Very High Very High
Chronic Fatigue Syndrome 11 99.60 Very High Very High Very High
Creutzfeldt Jakob Disease 12 99.16 Very High Very High Very High
Neurodegenerative Disease 41 96.44 Very High Very High Very High
Lifespan 3 85.08 High High
Targeted Disruption 14 81.52 Quite High
INFLAMMATION 105 75.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
There are important diseases of the CNS that are associated with the accumulation of misfolded proteins either extracellularly, such as Alzheimer's disease and prion diseases, or intracellularly, such as Parkinson's disease and ALS (amyotrophic lateral sclerosis) (Soto, 2003).
Localization (disease) of ALS in lateral associated with creutzfeldt jakob disease, disease and motor neuron diseases
1) Confidence 0.16 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2954441 Disease Relevance 0.71 Pain Relevance 0.16
Nevertheless, several studies have suggested that SOD1 mutations in neurons alone are insufficient to cause ALS and that dysfunction in support glia may contribute to disease development and progression [129-132].
Localization (cause) of ALS in neurons associated with disease and motor neuron diseases
2) Confidence 0.11 Published 2009 Journal Mol Neurodegener Section Body Doc Link PMC2784760 Disease Relevance 1.03 Pain Relevance 0.18
Research investigating interactions between cytoplasmic dynein and mutant SOD1 includes reports of co-localization of dynein components and mutant SOD1 in ALS mouse models [17], the interaction of mutant SOD1 proteins with cytoplasmic dynein [18] and perturbation of transport of mitochondria in motor neurons from SOD1G93A mice [19].
Localization (localization) of ALS in motor neurons associated with motor neuron diseases
3) Confidence 0.09 Published 2008 Journal Genome Biol Section Body Doc Link PMC2397497 Disease Relevance 0.46 Pain Relevance 0
Autoimmunity as an etiology in MS, ALS, PD, and CFS remains controversial.
Localization (etiology) of ALS associated with chronic fatigue syndrome, multiple sclerosis, autoimmune disease, disease and motor neuron diseases
4) Confidence 0.08 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2695238 Disease Relevance 1.60 Pain Relevance 0.39

General Comments

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