Myelin, copper, and the cuprizone model of schizophrenia.

@article{Herring2011MyelinCA,
  title={Myelin, copper, and the cuprizone model of schizophrenia.},
  author={Nicole R. Herring and Christine Konradi},
  journal={Frontiers in bioscience},
  year={2011},
  volume={3},
  pages={
          23-40
        }
}
In recent years increasing evidence is pointing toward white matter abnormalities in schizophrenia and other psychiatric disorders. The present paper will provide an overview over the role of myelin in cognition and brain function, and its potential involvement in brain disorders. Furthermore, we will examine one particular experimental model for the study of dysmyelination, created by the administration of the toxin cuprizone. Cuprizone, a copper chelator, causes white matter abnormalities in… 

Figures from this paper

Myelin, myelin-related disorders, and psychosis
White Matter Abnormalities and Animal Models Examining a Putative Role of Altered White Matter in Schizophrenia
TLDR
Some of recent human studies showing white matter abnormalities in schizophrenic brains and altered oligodendrocyte-(OL-) and myelin-related genes in patients with schizophrenia are reviewed and the emphasis will be put on the cuprizone (CPZ) model, which suggests that it is a novel animal model of schizophrenia.
Cuprizone-induced demyelination in mice: age-related vulnerability and exploratory behavior deficit
TLDR
An age-related vulnerability to demyelination with a concurrent behavioral deficit is demonstrated, providing supporting evidence for better understanding the susceptibility of the young to the onset of schizophrenia.
Iron and copper in progressive demyelination--New lessons from Skogholt's disease.
Impaired copper transport in schizophrenia results in a copper-deficient brain state: A new side to the dysbindin story
TLDR
These results provide the first evidence of disrupted copper transport in schizophrenia SN that appears to result in a copper-deficient state, and suggest copper homeostasis may be modulated by specific dysbindin isoforms and antipsychotic treatment.
Procyanidin B2 mitigates behavioral impairment and protects myelin integrity in cuprizone-induced schizophrenia in mice
TLDR
Data indicated that procyanidin B2 could mitigate behavioral impairment and protect myelin integrity in the cuprizone-induced model via regulating oxidative stress by activating Nrf2 signaling.
Lithium and brain plasticity - studies on glial cell changes and electroconvulsive treatment-induced amnesia in rats
TLDR
Chronic lithium treatment unlike its stimulating effect on hippocampal neurogenesis, decreased NG2 cell proliferation in the rat dentate hilus of hippocampus, amygdala and corpus callosum is shown, which could reflect decreased oligodendrogenesis or possibly cell cycle arrest in favour of differentiation into oligodendedrocytes.
...
...

References

SHOWING 1-10 OF 240 REFERENCES
The reduced neuropil hypothesis: a circuit based model of schizophrenia
Quetiapine facilitates oligodendrocyte development and prevents mice from myelin breakdown and behavioral changes
TLDR
Findings suggest a new neural mechanism of antipsychotic action of QUE, and help to establish a role for oligodendrocytes in the etiopathology and treatment of schizophrenia.
White matter changes in schizophrenia: evidence for myelin-related dysfunction.
TLDR
Support for the hypothesis that oligodendroglial dysfunction and even death, with subsequent abnormalities in myelin maintenance and repair, contribute to the schizophrenic syndrome is supported.
Copper and zinc dismetabolism in the mouse brain upon chronic cuprizone treatment
TLDR
Upon cuprizone treatment, mice developed a pronounced astrocytosis, with brain oedema and spongiosis characterised by vacuolisations of the neuropil predominantly in the white matter, with increasing metal ion concentrations particularly in the CNS.
The Neurotoxicant, Cuprizone, as a Model to Study Demyelination and Remyelination in the Central Nervous System
TLDR
The reproducibility of the model indicates that it may allow for testing of manipulations which may accelerate or repress the process of demyelination and or remyelinated areas, and which can be tested more rigorously with the cuprizone model.
White matter and cognitive function in schizophrenia.
TLDR
This paper explores what is known about white-matter deficits in relation to schizophrenia, cognitive deficits, or both together in order to generate a theoretical model for the role that compromise of white matter might play in producing cognitive impairment in schizophrenia.
Convergence and Divergence in the Etiology of Myelin Impairment in Psychiatric Disorders and Drug Addiction
  • Yue Feng
  • Psychology, Biology
    Neurochemical Research
  • 2008
TLDR
The current findings support the hypothesis that aberrant dopamine action on OLs is a common pathologic mechanism for myelin impairment in the aforementioned mental morbidities, whereas inherited genetic variations that specifically affect OL development and myelinogenesis may further increase myelin vulnerability in psychiatric disorders.
White matter in learning, cognition and psychiatric disorders
  • R. Fields
  • Psychology, Biology
    Trends in Neurosciences
  • 2008
Downregulation of myelination, energy, and translational genes in Menkes disease brain.
...
...