INT193452

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.06
First Reported 2006
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 11
Total Number 12
Disease Relevance 10.32
Pain Relevance 1.23

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

mitochondrion (Ndufaf1) molecular_function (Ndufaf1) biological_process (Ndufaf1)
cytoplasm (Ndufaf1)
Anatomy Link Frequency
blood platelets 3
Neurons 2
substantia nigra 1
brain 1
Ndufaf1 (Mus musculus)
Pain Link Frequency Relevance Heat
Central nervous system 45 99.44 Very High Very High Very High
Dopamine 43 99.12 Very High Very High Very High
Substantia nigra 47 98.64 Very High Very High Very High
Spinal cord 126 97.16 Very High Very High Very High
cerebral cortex 7 96.30 Very High Very High Very High
monoamine 17 90.64 High High
medulla 20 89.44 High High
midbrain 80 49.20 Quite Low
Inflammation 39 40.36 Quite Low
Glutamate 30 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Disease 673 99.84 Very High Very High Very High
Parkinson's Disease 336 99.64 Very High Very High Very High
Apoptosis 32 99.36 Very High Very High Very High
Death 153 99.28 Very High Very High Very High
Motor Neuron Diseases 57 96.56 Very High Very High Very High
Stress 57 95.80 Very High Very High Very High
Drug Induced Neurotoxicity 21 95.76 Very High Very High Very High
Aging 53 94.16 High High
Neurodegenerative Disease 44 92.28 High High
Syndrome 4 87.28 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This controversy is based on the difficulty to separate the effect of dopamine loss in the CNS and the effect of systemic inhibition of mitochondrial Complex I activity on the motor functions and the spontaneous motor activity of the mice [33].
Negative_regulation (inhibition) of mitochondrial Complex I associated with dopamine and central nervous system
1) Confidence 0.06 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2808242 Disease Relevance 0.16 Pain Relevance 0.17
The results showed no mitochondrial Complex I activity reduction in muscle or brain of 1.5 months treated mice when compared to the controls (Figure S1).


Neg (no) Negative_regulation (reduction) of mitochondrial Complex I in brain
2) Confidence 0.04 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2808242 Disease Relevance 0.05 Pain Relevance 0.14
Rotenone is an extremely potent mitochondrial Complex I inhibitor.
Negative_regulation (inhibitor) of mitochondrial Complex I
3) Confidence 0.04 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2808242 Disease Relevance 0.12 Pain Relevance 0.16
DBH prevented rotenone mediated inhibition of mitochondrial complex I but not malonate inhibition of complex II.
Negative_regulation (inhibition) of mitochondrial complex I
4) Confidence 0.03 Published 2006 Journal BMC Neurosci Section Abstract Doc Link PMC1488864 Disease Relevance 1.20 Pain Relevance 0.05
Decreased mitochondrial complex I activity has been measured in platelets [10], biopsied muscle and the spinal cord of ALS patients [4,11,12].
Negative_regulation (Decreased) of mitochondrial complex I in platelets associated with motor neuron diseases and spinal cord
5) Confidence 0.03 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1488864 Disease Relevance 1.51 Pain Relevance 0.05
DA metabolism and auto-oxidation combined with increased iron, decreased total glutathione levels, and mitochondrial complex I inhibition can lead to cell death by exceeding the oxidative capacity of DA-containing cells in the region [25].

2.3.5.

Negative_regulation (inhibition) of mitochondrial complex I associated with death
6) Confidence 0.02 Published 2010 Journal Neurology Research International Section Body Doc Link PMC2989867 Disease Relevance 0.88 Pain Relevance 0.09
RotenoneDue to its ability of inhibiting mitochondrial complex I (NADH dehydrogenase), rotenone has become one of the toxic models used to study PD in animals [33, 53].Chronic systemic exposure to rotenone reproduced many features of PD, including nigrostriatal dopaminergic degeneration and the formation of cytoplasmic inclusions in these neurons.
Negative_regulation (inhibiting) of mitochondrial complex I in neurons associated with parkinson's disease and disease
7) Confidence 0.02 Published 2010 Journal Neurology Research International Section Body Doc Link PMC2989867 Disease Relevance 1.15 Pain Relevance 0.09
in Mitochondrial Dysfunction and Neuronal Cell Death of MPTP/MPP+-Treated Neurons

Aberrant mitochondrial function appears to play a central role in dopaminergic neuronal loss in Parkinson's disease (PD). 1-methyl-4-phenylpyridinium iodide (MPP+), the active metabolite of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), is a selective inhibitor of mitochondrial complex I and is widely used in rodent and cell models to elicit neurochemical alterations associated with PD.

Negative_regulation (inhibitor) of mitochondrial complex I in Neurons associated with parkinson's disease, disease and death
8) Confidence 0.02 Published 2009 Journal PLoS ONE Section Title Doc Link PMC2675062 Disease Relevance 1.24 Pain Relevance 0
A defect in mitochondrial complex I activity in PD was identified in substantia nigra [2] as well as in platelet mitochondria of PD patients [4].
Negative_regulation (defect) of mitochondrial complex I in platelet associated with substantia nigra and disease
9) Confidence 0.02 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2675062 Disease Relevance 1.35 Pain Relevance 0.09
The relationship between mitochondrial dysfunction and DA-cell degeneration was reported for the first time by Schapira et al. (1990) who found reduced activity of mitochondrial complex I (NADH-quinone oxidoereductase) in the substantia nigra of parkinsonian patients.
Negative_regulation (reduced) of mitochondrial complex I in substantia nigra associated with parkinson's disease and substantia nigra
10) Confidence 0.01 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2978035 Disease Relevance 0.89 Pain Relevance 0.09
Once inside the cell, MPP+ can exert its neurotoxic effect by means of different mechanisms, including the inhibition of the mitochondrial complex I (Nicklas et al., 1985; Di Monte et al., 1986a; Mizuno et al., 1988).
Negative_regulation (inhibition) of mitochondrial complex I
11) Confidence 0.01 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2978035 Disease Relevance 0.85 Pain Relevance 0.15
The enzymatic deficiency was later confirmed in the cerebral cortex (Keeney et al., 2006; Parker et al., 2008), and in blood platelets (Krige et al., 1992; Haas et al., 1995; Schapira, 2008), suggesting that a number of patients can undergo a systemic decrease in mitochondrial complex I activity.
Negative_regulation (decrease) of mitochondrial complex I in blood platelets associated with cerebral cortex
12) Confidence 0.01 Published 2010 Journal Frontiers in Neuroanatomy Section Body Doc Link PMC2978035 Disease Relevance 0.91 Pain Relevance 0.15

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox