The neuroprotective effects of CGP 3466B in the best in vivo model of Parkinson’s disease, the bilaterally MPTP-treated rhesus monkey

Andringa, Gerda; Cools, A.R.

doi:10.1007/978-3-7091-6301-6_14

Cited by 17 publications

(12 citation statements)

References 18 publications

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“…CGP3466B and related drugs exert neuroprotective actions in animal models of motor neuron disease (50), muscular dystrophy (51,52), amyotrophic lateral sclerosis (46) and Parkinson’s Disease (53,54), though limited clinical trials in Parkinson’s Disease have not been promising (55). It is worth noting that CGP3466B post-treatment had neurorescuing effects in multiple neurotoxicity models (46).…”

Section: Discussionmentioning

confidence: 99%

Nitric Oxide-GAPDH Transcriptional Signaling Mediates Behavioral Actions of Cocaine

Harraz¹,

Snyder

2015

CNSNDDT

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Psychotropic actions of cocaine are generally thought to involve its blockade of monoamine transporters leading to increased synaptic levels of monoamines, especially dopamine. Subsequent intracellular events have been less well characterized. We describe a signaling system wherein lower behavioral stimulant doses of cocaine, as well as higher neurotoxic doses, activate a cascade wherein nitric oxide nitrosylates glyceraldehyde-3-phosphate dehydrogenase (GAPDH) to generate a complex with the ubiquitin-E3-ligase Siah1 which translocates to the nucleus. With lower cocaine doses, nuclear GAPDH augments CREB signaling, while at higher doses p53 signaling is enhanced. The drug CGP3466B very potently blocks GAPDH nitrosylation, hindering both signaling cascades and inhibits both behavioral activating and neurotoxic effects of cocaine. This system affords potentially novel approaches to the therapy of cocaine abuse.

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Section: Discussionmentioning

confidence: 99%

Nitric Oxide-GAPDH Transcriptional Signaling Mediates Behavioral Actions of Cocaine

Harraz¹,

Snyder

2015

CNSNDDT

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“…26 We therefore decided to test its efficacy in the most frequently used animal model for ALS, the G93A mSOD1 transgenic mouse. Here, we show that CGP 3466B does not, at any of the concentrations tested, delay disease onset or progression, and does not extend survival.…”

Section: Discussionmentioning

confidence: 99%

CGP 3466B has no effect on disease course of (G93A) mSOD1 transgenic mice

Groeneveld

Muiswinkel

Weenen³

et al. 2004

Amyotrophic Lateral Sclerosis and Other Motor Neuron Disorders

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“…Andringa and Cools, 2000;Kupsch et al, 2001), very little is known regarding the effects of these compounds on cognitive function in non-human primates. It is known, however, that noradrenergic neurons are necessary for certain frontal lobe-mediated cognitive processes.…”

Section: Discussionmentioning

confidence: 99%

Potential cognitive actions of (n-propargly-(3r)-aminoindan-5-yl)-ethyl, methyl carbamate (tv3326), a novel neuroprotective agent, as assessed in old rhesus monkeys in their performance of versions of a delayed matching task

et al. 2003

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The neuroprotective effects of CGP 3466B in the best in vivo model of Parkinson’s disease, the bilaterally MPTP-treated rhesus monkey

Cited by 17 publications

References 18 publications

Nitric Oxide-GAPDH Transcriptional Signaling Mediates Behavioral Actions of Cocaine

Nitric Oxide-GAPDH Transcriptional Signaling Mediates Behavioral Actions of Cocaine

CGP 3466B has no effect on disease course of (G93A) mSOD1 transgenic mice

Potential cognitive actions of (n-propargly-(3r)-aminoindan-5-yl)-ethyl, methyl carbamate (tv3326), a novel neuroprotective agent, as assessed in old rhesus monkeys in their performance of versions of a delayed matching task

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