Effects of cinnarizine, a calcium antagonist that produces human parkinsonism, in parkin knock out mice

@article{Serrano2005EffectsOC,
  title={Effects of cinnarizine, a calcium antagonist that produces human parkinsonism, in parkin knock out mice},
  author={Alba Serrano and J. Men{\'e}ndez and Mar{\'i}a Jos{\'e} Casarejos and Rosa Mar{\'i}a Solano and Eva Gallego and M. S{\'a}nchez and Mar{\'i}a Angeles Mena and Justo Garc{\'i}a de Y{\'e}benes},
  journal={Neuropharmacology},
  year={2005},
  volume={49},
  pages={208-219}
}
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Susceptibility to rotenone is increased in neurons from parkin null mice and is reduced by minocycline
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TLDR
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Suppression of Parkin enhances nigrostriatal and motor neuron lesion in mice over-expressing human-mutated tau protein.
TLDR
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Differential effects of l‐DOPA on monoamine metabolism, cell survival and glutathione production in midbrain neuronal‐enriched cultures from parkin knockout and wild‐type mice
TLDR
The levels of glutathione were further increased in parkin null mice than in controls both with and without treatment with l‐DOPA, suggesting that a compensatory mechanism may protect DA neurones from neuronal death.
Pregabalin-Induced Parkinsonism: A Case Report
TLDR
This is the first report of full-blown parkinsonism associated with PGB use, and Vigilance of PGB-treated patients is recommended, because of clear link to PGB introduction as well as symmetric limb involvement and symptom intensity.
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It is shown that inactivation of the parkin gene in mice results in motor and cognitive deficits, inhibition of amphetamine-induced dopamine release and inhibition of glutamate neurotransmission, and the levels of dopamine are increased in the limbic brain areas of parkin mutant mice and there is a shift towards increased metabolism of dopamine by MAO.
Flunarizine and cinnarizine inhibit mitochondrial complexes I and II: possible implication for parkinsonism.
TLDR
In intact mitochondria from rat liver, both drugs inhibited respiration rates, with substrates entering at Complex I (glutamate/malate) and Complex II (succinate) and these effects could be explained by potent inhibitions of both complexes.
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TLDR
The finding of dopamine-regulating properties not associated to neurotoxic effects in the dihydropyridines and verapamil provides new putative therapeutics tools for the treatment of neurologic disorders associated with dopamine hyperactivity.
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TLDR
Analysis of proteomic, genetic, and physiological analyses reveal an essential role for parkin in the regulation of mitochondrial function and provide the first direct evidence of mitochondrial dysfunction and oxidative damage in the absence of nigral degeneration in a genetic mouse model of Parkinson's disease.
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TLDR
The production of an experimental model of parkinsonism induced by cinnarizine (CNZ) in three healthy sylvanna monkeys suggests a predominant presynaptic effect on DA and 5-HT neurons; and could account for the longstanding parkinsonistan induced by calcium antagonist in some patients as well as the depression observed in these subjects.
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TLDR
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TLDR
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It is indicated that CCB-induced parkinsonism is not the benign condition previously thought, and an age-related prognosis of this entity is suggested, and this entity's long-term evolution is unknown.
The role of astroglia on the survival of dopamine neurons
TLDR
Several studies suggest that glial cells may be important in the pathogenesis of Parkinson’s disease (PD), a common neurodegenerative disorder characterized by degeneration of the nigrostriatal DA system.
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