Copper, MS and schizophrenia
Type of Spiritual Experience
Cuprizone is a toxin that induces myelin damage by killing oligodendrocytes resulting in demyelination in both white and gray matter of the CNS. It is a copper chelator, and causes rapid demyelination and gliosis, or rapid proliferation of glia subtypes.
The key is not the chelator itself but the fact it causes copper imbalance.
A description of the experience
Neurobiol Dis. 2013 Nov;59:63-8. doi: 10.1016/j.nbd.2013.07.003. Epub 2013 Jul 16. Cuprizone short-term exposure: astrocytic IL-6 activation and behavioral changes relevant to psychosis. Tezuka T, Tamura M, Kondo MA, Sakaue M, Okada K, Takemoto K, Fukunari A, Miwa K, Ohzeki H, Kano S, Yasumatsu H, Sawa A, Kajii Y. Mitsubishi Tanabe Pharma Corporation, Yokohama, Japan.
A growing body of evidence suggests the involvement of inflammatory processes in the pathophysiology of schizophrenia.
Four- to 8-week exposure to cuprizone, a copper chelator, causes robust demyelination and has been used to build a model for multiple sclerosis.
In contrast, we report here the effects of 1-week cuprizone exposure in mice. This short-term cuprizone exposure elicits behavioral changes that include augmented responsiveness to methamphetamine and phencyclidine, as well as impaired working memory.
The cellular effects of 1-week cuprizone exposure differ substantially from the longer-term exposure; perturbation of astrocytes and microglia is induced without any sign of demyelination. Furthermore, the proinflammatory cytokine interleukin-6 was significantly up-regulated in glial fibrillary acidic protein (GFAP)-positive cells. We propose that this cuprizone short-term exposure may offer a model to study some aspects of biology relevant to schizophrenia and related conditions.
KEYWORDS: Astrocyte, Cytokine, Inflammation, Interleukin-6, Schizophrenia