INT127122

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Context Info
Confidence 0.69
First Reported 2005
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 11
Total Number 32
Disease Relevance 15.36
Pain Relevance 4.56

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

cytosol (Snca) mitochondrion (Snca) histone binding (Snca)
plasma membrane (Snca) cytoskeleton (Snca) nucleus (Snca)
Anatomy Link Frequency
brain 8
striatum 7
platelet 4
neuronal 4
cortex 3
Snca (Mus musculus)
Pain Link Frequency Relevance Heat
Substantia nigra 444 100.00 Very High Very High Very High
amygdala 6 99.68 Very High Very High Very High
Hippocampus 84 99.62 Very High Very High Very High
withdrawal 4 99.12 Very High Very High Very High
Morphine 8 98.40 Very High Very High Very High
Dopamine 170 98.28 Very High Very High Very High
monoamine 2 97.04 Very High Very High Very High
Ventral tegmentum 2 94.20 High High
Nucleus accumbens 2 93.08 High High
Catecholamine 4 90.48 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 562 100.00 Very High Very High Very High
Disease 971 99.72 Very High Very High Very High
Stress 298 99.20 Very High Very High Very High
Parkinson's Disease 236 99.00 Very High Very High Very High
Dementia 14 98.32 Very High Very High Very High
Toxicity 186 97.64 Very High Very High Very High
Drug Induced Neurotoxicity 4 90.04 High High
Cognitive Disorder 6 86.80 High High
INFLAMMATION 75 82.92 Quite High
Urological Neuroanatomy 72 81.24 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
It is possible that upregulation of DAT expression in the remaining DA terminals of SNCA overexpressing mice might mask the loss of dopaminergic terminals by this measure, though it also is possible that a difference would have been revealed with a larger number of mice in each group.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of SNCA
1) Confidence 0.69 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.31 Pain Relevance 0.03
NAC significantly reduced the amount of overexpressed human SNCA protein in the cortex and striatum of PDGFb-SNCA transgenic mice (Fig. 2E–2H).
Positive_regulation (overexpressed) of Gene_expression (overexpressed) of SNCA protein in striatum associated with targeted disruption
2) Confidence 0.60 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.16 Pain Relevance 0.14
As previously reported, we find that mice overexpressing SNCA display a significant loss of striatal TH+ terminals, and now report the novel finding that chronic oral NAC supplementation protects against this loss (Fig. 1E).
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of SNCA
3) Confidence 0.60 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.39 Pain Relevance 0
Mice overexpressing wild-type human SNCA from the platelet-derived growth factor beta (PDGFb) promoter (line D PDGFb-SNCA) are reported to develop motor impairments in association with progressive loss of dopaminergic terminals [20].
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of SNCA in platelet
4) Confidence 0.60 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 1.31 Pain Relevance 0.24
Taken together, this provides compelling evidence that SNCA overexpression can result in Lewy body parkinsonism and dementia.
Positive_regulation (overexpression) of Gene_expression (overexpression) of SNCA in body associated with parkinson's disease and dementia
5) Confidence 0.50 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2612658 Disease Relevance 1.32 Pain Relevance 0.08
Control mice showed alpha-synuclein mainly in the periphery of the neuronal soma (Figure 1A) while in treated mice, the amount of alpha-synuclein was increased and it was present both inside and outside the neural soma (Figure 1B), with larger alpha-synuclein accumulations (>6 µm) in 20% of the analyzed ganglia after 3 months treatment (Figure 1C).
Spec (analyzed) Positive_regulation (accumulations) of Gene_expression (present) of alpha-synuclein in neuronal
6) Confidence 0.50 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2808242 Disease Relevance 0.23 Pain Relevance 0.04
Control mice showed alpha-synuclein mainly in the periphery of the neuronal soma (Figure 1A) while in treated mice, the amount of alpha-synuclein was increased and it was present both inside and outside the neural soma (Figure 1B), with larger alpha-synuclein accumulations (>6 µm) in 20% of the analyzed ganglia after 3 months treatment (Figure 1C).
Positive_regulation (increased) of Gene_expression (present) of alpha-synuclein in neuronal
7) Confidence 0.50 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2808242 Disease Relevance 0.23 Pain Relevance 0.04
We did not detect significant differences in the dopaminergic innervation of the striatum (Figure 4E–F), brain tau protein, lipofucsin granules or alpha-synuclein accumulation in other brain areas (e.g. cerebellum, cortex or striatum) (data not shown) between treated and control animals at any time-point, confirming that observed changes in alpha-synuclein accumulation and aggregation are confined within selected pathways of the intestine-cerebral axis.


Positive_regulation (innervation) of Gene_expression (accumulation) of alpha-synuclein in striatum
8) Confidence 0.50 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2808242 Disease Relevance 0.13 Pain Relevance 0.06
It is possible that upregulation of DAT expression in the remaining DA terminals of SNCA overexpressing mice might mask the loss of dopaminergic terminals by this measure, though it also is possible that a difference would have been revealed with a larger number of mice in each group.
Positive_regulation (upregulation) of Gene_expression (overexpressing) of SNCA
9) Confidence 0.49 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.33 Pain Relevance 0.03
Despite the transient nature of the impact of NAC on brain glutathione, the loss of dopaminergic terminals at 1 year associated with SNCA overexpression was significantly attenuated by NAC supplementation, as measured by immunoreactivity for tyrosine hydroxylase in the striatum (p?
Positive_regulation (overexpression) of Gene_expression (overexpression) of SNCA in brain
10) Confidence 0.49 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2925900 Disease Relevance 0.60 Pain Relevance 0.15
In contrast, levels of alpha-synuclein protein, as assessed by Western blotting, were significantly increased in the amygdala and striatum/accumbens (but not in the mesencephalon) of morphine-withdrawn mice.
Positive_regulation (increased) of Gene_expression (levels) of alpha-synuclein protein in mesencephalon associated with amygdala and morphine
11) Confidence 0.47 Published 2005 Journal J. Neurosci. Section Abstract Doc Link 15901780 Disease Relevance 0 Pain Relevance 0.88
In both brain regions, levels of alpha-synuclein were elevated for as long as 2 weeks after treatment cessation.
Positive_regulation (elevated) of Gene_expression (levels) of alpha-synuclein in brain
12) Confidence 0.47 Published 2005 Journal J. Neurosci. Section Abstract Doc Link 15901780 Disease Relevance 0 Pain Relevance 0.88
Multiple transgenic mouse models have been developed based on overexpression of SNCA, each with advantages and limitations [45], [46].
Positive_regulation (overexpression) of Gene_expression (overexpression) of SNCA associated with targeted disruption
13) Confidence 0.46 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.62 Pain Relevance 0
Functionally, SNCA multiplications result in a copy-number related increase in both ?
Positive_regulation (result) of Gene_expression (multiplications) of SNCA
14) Confidence 0.44 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2612658 Disease Relevance 1.45 Pain Relevance 0.09
In order to test the ability of naked siRNA to reduce SNCA expression in vivo, we identified the hippocampus and the cortex as having the highest expression of SNCA in the murine brain (data not shown).
Positive_regulation (having) of Gene_expression (expression) of SNCA in brain associated with hippocampus
15) Confidence 0.44 Published 2008 Journal Mol Neurodegener Section Body Doc Link PMC2612658 Disease Relevance 0 Pain Relevance 0.10
We selected this model (line D PDGFb-SNCA) which overexpresses wild-type human SNCA from the PDGFb promoter, in part, based on the fact that increased expression of wild-type SNCA in humans can cause PD, as demonstrated in families with autosomal dominant PD due to duplication or triplication of the normal (wild-type) SNCA gene [21], [22], [47], [48].
Positive_regulation (increased) of Gene_expression (expression) of SNCA associated with disease
16) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.52 Pain Relevance 0
0.0133) in transgenic mice overexpressing SNCA (Fig. 3).
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of SNCA associated with targeted disruption
17) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.49 Pain Relevance 0.14
The high levels of oxidative stress in the SN may be compounded by the presence of increased SNCA in the PDGFb-SNCA transgenics, and this increased oxidative stress may “prime” the cells of the SN in the SNCA overexpressing mice to upregulate glutathione synthesis when provided with additional cysteine precursor, whereas this may be less necessary in cortical cells.
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of SNCA associated with stress and substantia nigra
18) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.57 Pain Relevance 0.27
We selected this model (line D PDGFb-SNCA) which overexpresses wild-type human SNCA from the PDGFb promoter, in part, based on the fact that increased expression of wild-type SNCA in humans can cause PD, as demonstrated in families with autosomal dominant PD due to duplication or triplication of the normal (wild-type) SNCA gene [21], [22], [47], [48].
Positive_regulation (overexpresses) of Gene_expression (overexpresses) of SNCA associated with disease
19) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.58 Pain Relevance 0
Transgenic mice overexpressing SNCA showed a mean decrease of 45.2% (95% CI 31.5–59.0%; p<0.001) in the percentage of striatal area covered by tyrosine hydroxylase positive (TH+) terminals compared to wild-type littermate controls at 1 year of age (Fig. 1A, 1C,1E).
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of SNCA associated with targeted disruption
20) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2925900 Disease Relevance 0.39 Pain Relevance 0.03

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