INT119777

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Context Info
Confidence 0.40
First Reported 2004
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 9
Total Number 16
Disease Relevance 5.93
Pain Relevance 10.11

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

peptidase activity (Naalad2) cellular_component (Naalad2)
Anatomy Link Frequency
brain 3
PAGM 1
Naalad2 (Mus musculus)
Pain Link Frequency Relevance Heat
Glutamate 36 100.00 Very High Very High Very High
Analgesic 106 99.84 Very High Very High Very High
Eae 112 99.32 Very High Very High Very High
analgesia 136 99.24 Very High Very High Very High
Pain 168 99.12 Very High Very High Very High
Spinal cord 26 99.10 Very High Very High Very High
Intracerebroventricular 120 99.08 Very High Very High Very High
neuralgia 8 98.98 Very High Very High Very High
Central nervous system 34 98.16 Very High Very High Very High
Inflammation 46 97.84 Very High Very High Very High
Disease Link Frequency Relevance Heat
Inflammatory Pain 100 99.32 Very High Very High Very High
Pain 165 99.12 Very High Very High Very High
INFLAMMATION 46 97.84 Very High Very High Very High
Neuropathic Pain 44 97.44 Very High Very High Very High
Disease 1 92.80 High High
Toxicity 8 90.52 High High
Injury 3 89.32 High High
Cancer 1 88.64 High High
Schizophrenia 1 81.52 Quite High
Nervous System Injury 2 81.12 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This concentration is about 100,000 fold more than is needed for inhibition of NAAG peptidase, and indicates very good penetration to the brain.
Negative_regulation (inhibition) of NAAG in brain
1) Confidence 0.40 Published 2006 Journal Neuropharmacology Section Abstract Doc Link 16926034 Disease Relevance 0.15 Pain Relevance 0.18
Systemic administration of inhibitors of the enzymes that inactivate NAAG results in decreased pain responses in rat models of inflammatory and neuropathic pain.
Negative_regulation (inactivate) of NAAG associated with pain, inflammation and neuropathic pain
2) Confidence 0.34 Published 2007 Journal Eur. J. Neurosci. Section Abstract Doc Link 17241276 Disease Relevance 0.51 Pain Relevance 0.82
Local administration of N-acetylaspartylglutamate (NAAG) peptidase inhibitors is analgesic in peripheral pain in rats.
Negative_regulation (inhibitors) of NAAG associated with pain, neuralgia and analgesic
3) Confidence 0.34 Published 2007 Journal Eur. J. Neurosci. Section Title Doc Link 17241276 Disease Relevance 0.57 Pain Relevance 1.30
GCP II is believed to mediate the hydrolysis of N-acetyl-aspartyl-glutamate (NAAG) to glutamate and N-acetyl-aspartate, and inhibition of NAAG peptidase activity (by GCP II and other peptidases) is neuroprotective.
Negative_regulation (inhibition) of NAAG associated with glutamate
4) Confidence 0.18 Published 2005 Journal J. Neurochem. Section Abstract Doc Link 16190866 Disease Relevance 0.44 Pain Relevance 0.49
The data presented here support the conclusion that while the spinal cord and sensory neurons represent loci at which NAAG peptidase inhibition may contribute to analgesia, there also is at least one locus in the brain where NAAG directly mediates analgesia and that this brain region is accessible via the lateral ventricles.
Negative_regulation (inhibition) of NAAG peptidase in brain associated with analgesia and spinal cord
5) Confidence 0.11 Published 2008 Journal Mol Pain Section Body Doc Link PMC2517065 Disease Relevance 0.70 Pain Relevance 1.04
NAAG peptidase inhibitors and their potential for diagnosis and therapy.
Negative_regulation (inhibitors) of NAAG peptidase
6) Confidence 0.09 Published 2005 Journal Nat Rev Drug Discov Section Title Doc Link 16341066 Disease Relevance 0.58 Pain Relevance 0.13
These data contribute to proof of the concept that NAAG peptidase inhibition is a novel therapeutic approach to inflammatory pain and that these inhibitors achieve analgesia by elevating synaptic levels of NAAG within pain processing circuits in brain.



Negative_regulation (inhibition) of NAAG peptidase in brain associated with pain, eae and analgesia
7) Confidence 0.08 Published 2008 Journal Mol Pain Section Abstract Doc Link PMC2517065 Disease Relevance 0.47 Pain Relevance 1.01
If NAAG peptidase inhibition continues to show promise as an analgesic pharmacotherapy, this prodrug development strategy is likely to be important in reducing the amount of drug required to achieve analgesia, thus reducing the probability of secondary effects and toxicity in other tissues.


Negative_regulation (inhibition) of NAAG peptidase associated with toxicity, analgesic and analgesia
8) Confidence 0.08 Published 2008 Journal Mol Pain Section Body Doc Link PMC2517065 Disease Relevance 0.63 Pain Relevance 0.90
ZJ45 and 2-PMPA are NAAG peptidase inhibitors [16-18].
Negative_regulation (inhibitors) of NAAG peptidase
9) Confidence 0.08 Published 2008 Journal Mol Pain Section Body Doc Link PMC2517065 Disease Relevance 0 Pain Relevance 0.36
In contrast, strategies that enhance the actions of endogenously released transmitters, such as NAAG peptidase inhibition, enhance the effects of the normal action of the circuit.
Negative_regulation (inhibition) of NAAG peptidase
10) Confidence 0.08 Published 2008 Journal Mol Pain Section Body Doc Link PMC2517065 Disease Relevance 0.20 Pain Relevance 0.54
AK and JZ intellectual contribution was the designed ZJ43 within a series of related NAAG peptidase inhibitors.
Negative_regulation (inhibitors) of NAAG peptidase
11) Confidence 0.08 Published 2008 Journal Mol Pain Section Body Doc Link PMC2517065 Disease Relevance 0 Pain Relevance 0.19
Two enzymes that inactivate synaptically released NAAG, glutamate carboxypeptidase II and III, have been cloned and characterized [11-15].
Negative_regulation (inactivate) of NAAG associated with glutamate
12) Confidence 0.07 Published 2008 Journal Mol Pain Section Body Doc Link PMC2517065 Disease Relevance 0.32 Pain Relevance 0.74
Intracerebroventricular administration of N-acetylaspartylglutamate (NAAG) peptidase inhibitors is analgesic in inflammatory pain

Background

Negative_regulation (inhibitors) of NAAG associated with eae, analgesic and intracerebroventricular
13) Confidence 0.07 Published 2008 Journal Mol Pain Section Title Doc Link PMC2517065 Disease Relevance 0.32 Pain Relevance 0.84
Thus, elevation of extracellular NAAG, induced by the inhibition of NAAG peptidase, activates group II mGluRs and produces an analgesic effect in neuropathic and inflammatory and pain models.
Negative_regulation (inhibition) of NAAG peptidase associated with pain, inflammation, analgesic and neuropathic pain
14) Confidence 0.03 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15233757 Disease Relevance 0.73 Pain Relevance 0.99
We recently developed a series of potent NAAG peptidase inhibitors, including ZJ-11, ZJ-17 and ZJ-43.
Negative_regulation (inhibitors) of NAAG peptidase
15) Confidence 0.02 Published 2004 Journal Eur. J. Neurosci. Section Abstract Doc Link 15233757 Disease Relevance 0.24 Pain Relevance 0.57
CONCLUSIONS: The reduction of NAAG in the PAGM suggests altered neuromodulation of the antinociceptive systems in subjects with CDH.
Negative_regulation (reduction) of NAAG in PAGM
16) Confidence 0.00 Published 2006 Journal Rev Neurol Section Body Doc Link 16941423 Disease Relevance 0.08 Pain Relevance 0

General Comments

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