INT36893

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Context Info
Confidence 0.55
First Reported 1987
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 36
Total Number 40
Disease Relevance 22.24
Pain Relevance 5.47

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

molecular_function (Coq10a) cellular_component (Coq10a) biological_process (Coq10a)
Anatomy Link Frequency
liver 3
striatum 2
heart 2
brains 1
MMA 1
Coq10a (Mus musculus)
Pain Link Frequency Relevance Heat
Morphine 7 99.46 Very High Very High Very High
fortral 18 99.36 Very High Very High Very High
Fibrositis 4 99.28 Very High Very High Very High
cerebral cortex 46 98.76 Very High Very High Very High
depression 40 98.72 Very High Very High Very High
withdrawal 12 98.12 Very High Very High Very High
Paracetamol 9 97.88 Very High Very High Very High
Central nervous system 26 96.96 Very High Very High Very High
analgesia 4 94.72 High High
tolerance 4 93.76 High High
Disease Link Frequency Relevance Heat
Congenital Anomalies 31 99.98 Very High Very High Very High
Disease 720 99.96 Very High Very High Very High
Hyperalgesia 5 99.76 Very High Very High Very High
Ataxia 228 99.36 Very High Very High Very High
Motor Neuron Diseases 156 99.28 Very High Very High Very High
Sleep Disorders 4 99.28 Very High Very High Very High
Parkinson's Disease 186 99.16 Very High Very High Very High
Increased Venous Pressure Under Development 18 99.08 Very High Very High Very High
Chronic Fatigue Syndrome 600 99.00 Very High Very High Very High
Mitochondrial Encephalomyopathies 12 98.98 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These results provide the first evidence indicating that treatment with a neuraminidase inhibitor, oseltamivir, blocks morphine's hyperalgesic effects by decreasing neuronal levels of GM1.
Negative_regulation (decreasing) of GM1 in neuronal associated with hyperalgesia and morphine
1) Confidence 0.55 Published 2004 Journal Brain Res. Section Abstract Doc Link 14672816 Disease Relevance 0.49 Pain Relevance 1.81
This benefit was observed only after a year of treatment, thus a symptomatic effect of CoQ10 is unlikely to explain it.
Negative_regulation (effect) of CoQ10
2) Confidence 0.49 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785862 Disease Relevance 0.47 Pain Relevance 0.06
We have reported previously [20–22] that a novel cytosolic NADPH-CoQ reductase is responsible for the reduction of CoQ10 to H2CoQ10 in biomembranes.
Negative_regulation (reduction) of CoQ10
3) Confidence 0.41 Published 2007 Journal Journal of Clinical Biochemistry and Nutrition Section Body Doc Link PMC2275764 Disease Relevance 0.70 Pain Relevance 0
CoQ10 deficiency is a rare disorder with variable phenotypic presentations including pure myopathy, myopathy with encephalopathy, cerebellar atrophy with ataxia, and infantile multisystem disease including encephalopathy and nephropathy.20,21 The most common is the ataxic variant.22 Huntsman and colleagues recently reported a case of hypotonia and infantile spasms which they hypothesized to be a new phenotype of CoQ10 deficiency.23 Response to CoQ10 supplementation in this disorder is variable, though it is the best response of any mitochondrial encephalomyopathy to CoQ10 supplementation.22 The causes of primary CoQ10 deficiency are yet to be completely elucidated.
Negative_regulation (deficiency) of CoQ10 associated with infantile spasms, muscle hypotonia, ataxia, encephalopathy, renal disease, frailty, muscle disease, mitochondrial encephalomyopathies and disease
4) Confidence 0.36 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785862 Disease Relevance 1.09 Pain Relevance 0.07
CoQ10 deficiency is a rare disorder with variable phenotypic presentations including pure myopathy, myopathy with encephalopathy, cerebellar atrophy with ataxia, and infantile multisystem disease including encephalopathy and nephropathy.20,21 The most common is the ataxic variant.22 Huntsman and colleagues recently reported a case of hypotonia and infantile spasms which they hypothesized to be a new phenotype of CoQ10 deficiency.23 Response to CoQ10 supplementation in this disorder is variable, though it is the best response of any mitochondrial encephalomyopathy to CoQ10 supplementation.22 The causes of primary CoQ10 deficiency are yet to be completely elucidated.
Negative_regulation (deficiency) of CoQ10 associated with infantile spasms, muscle hypotonia, ataxia, encephalopathy, renal disease, frailty, muscle disease, mitochondrial encephalomyopathies and disease
5) Confidence 0.36 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785862 Disease Relevance 1.10 Pain Relevance 0.09
Induced CoQ10 deficiency in cells genetically altered to lack autophagy resulted in apoptosis, indicating that the autophagy was likely protective.25

Mitochondrial dysfunction and neurodegenerative disease: A rationale for testing CoQ10

Negative_regulation (deficiency) of CoQ10 associated with parkinson's disease, neurodegenerative disease and apoptosis
6) Confidence 0.36 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785862 Disease Relevance 0.76 Pain Relevance 0
Serum CoQ10 levels were decreased at baseline in FA patients, and were significantly increased in both groups (3.4-fold in the low-dose group, 12.2-fold in the high-dose group).
Negative_regulation (decreased) of CoQ10 associated with ataxia
7) Confidence 0.36 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785862 Disease Relevance 0.49 Pain Relevance 0
Nine genes are presumed to be involved in CoQ10 biosynthesis, and as of now, mutations in three genes have been shown to result in primary CoQ10 deficiency: PDSS1, PDSS2, and COQ2.21 Duncan and colleagues found an autosomal recessive form of neonatal-onset primary coenzyme Q10 deficiency resulting from a nonsense mutation in COQ9.24
Negative_regulation (deficiency) of coenzyme Q10
8) Confidence 0.36 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785862 Disease Relevance 0.91 Pain Relevance 0.03
Consequences of CoQ10 deficiency
Negative_regulation (deficiency) of CoQ10
9) Confidence 0.36 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785862 Disease Relevance 1.00 Pain Relevance 0.09
Coincident with aberrant mitochondrial function in PD, CoQ10 levels are significantly decreased in mitochondria from SN neurons and platelets in PD patients, and levels of CoQ10 have been shown to correlate with activity of complexes I and II/III.37 Decreased levels of CoQ10 in brain cortex relative to age-matched controls have also been demonstrated, though no reduction was found in the SN, cerebellum, or striatum.51 In serum, there is a reduction in the ratio of reduced to oxidized CoQ10 in PD37,52,53 and ALS.38,40 However, serum total levels are no different from controls in PD,54 HD,55 and ALS.40,56

Evidence of neuroprotective effects of coenzyme Q10 in vitro

Negative_regulation (decreased) of CoQ10 in striatum associated with disease and motor neuron diseases
10) Confidence 0.36 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785862 Disease Relevance 1.09 Pain Relevance 0.03
Coincident with aberrant mitochondrial function in PD, CoQ10 levels are significantly decreased in mitochondria from SN neurons and platelets in PD patients, and levels of CoQ10 have been shown to correlate with activity of complexes I and II/III.37 Decreased levels of CoQ10 in brain cortex relative to age-matched controls have also been demonstrated, though no reduction was found in the SN, cerebellum, or striatum.51 In serum, there is a reduction in the ratio of reduced to oxidized CoQ10 in PD37,52,53 and ALS.38,40 However, serum total levels are no different from controls in PD,54 HD,55 and ALS.40,56

Evidence of neuroprotective effects of coenzyme Q10 in vitro

Negative_regulation (effects) of coenzyme Q10 in striatum associated with disease and motor neuron diseases
11) Confidence 0.36 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785862 Disease Relevance 1.12 Pain Relevance 0
Increased lactate concentrations in the cerebral cortex and basal ganglia, as measured by 1H-MRS, have been shown to decrease with CoQ10 administration, and subsequently elevate upon withdrawal of treatment.84 This finding supports the predicted metabolic effect of oral CoQ10 in cerebral tissue, and is suggestive of an effect upon mitochondrial metabolism.
Negative_regulation (decrease) of CoQ10 in cerebral cortex associated with withdrawal and cerebral cortex
12) Confidence 0.36 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785862 Disease Relevance 0.62 Pain Relevance 0.10
These abnormalities reversed partially with coenzyme Q10 supplementation.25 Increased levels of lysosomal markers, enhanced expression of genes involved in autophagy, and findings on electron microscopy all provided evidence for massive degradation of dysfunctional mitochondria, which was eradicated with administration of antioxidants.
Negative_regulation (reversed) of coenzyme Q10 associated with congenital anomalies
13) Confidence 0.36 Published 2009 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2785862 Disease Relevance 0.74 Pain Relevance 0
Therefore it was confirmed that the co-operative effect of GM1 and A?
Negative_regulation (effect) of GM1
14) Confidence 0.35 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2838405 Disease Relevance 0 Pain Relevance 0
To confirm the cytotoxic effect of GM1 and A?
Negative_regulation (effect) of GM1
15) Confidence 0.35 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2838405 Disease Relevance 0.09 Pain Relevance 0
However, it is unclear whether exogenously added GM1 and A?
Spec (whether) Negative_regulation (added) of GM1
16) Confidence 0.35 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2838405 Disease Relevance 0.07 Pain Relevance 0
The exogenously added GM1 and A?
Negative_regulation (added) of GM1
17) Confidence 0.35 Published 2010 Journal ASN NEURO Section Abstract Doc Link PMC2838405 Disease Relevance 0.50 Pain Relevance 0
On the contrary, a decreased number of NECs were cultured in the presence of a combination of GM1 and A?
Negative_regulation (combination) of GM1
18) Confidence 0.35 Published 2010 Journal ASN NEURO Section Abstract Doc Link PMC2838405 Disease Relevance 0.50 Pain Relevance 0
These results indicate that the NECs treated with GM1 and/or A?
Negative_regulation (treated) of GM1
19) Confidence 0.35 Published 2010 Journal ASN NEURO Section Body Doc Link PMC2838405 Disease Relevance 0.47 Pain Relevance 0.04
Decreased CoQ10 might be thus a serious problem, as most hypercholesterolemia patients who take statins are elderly.
Negative_regulation (Decreased) of CoQ10 associated with hyperlipidemia
20) Confidence 0.35 Published 2007 Journal Journal of Clinical Biochemistry and Nutrition Section Body Doc Link PMC2275764 Disease Relevance 0.10 Pain Relevance 0

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