2007
DOI: 10.1186/1471-244x-7-46
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Inflammation-related genes up-regulated in schizophrenia brains

Abstract: Background: Multiple studies have shown that brain gene expression is disturbed in subjects suffering from schizophrenia. However, disentangling disease effects from alterations caused by medication is a challenging task. The main goal of this study is to find transcriptional alterations in schizophrenia that are independent of neuroleptic treatment.

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Cited by 239 publications
(192 citation statements)
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“…But inflammation is not restricted to AD among neurodegenerative disorders and other common diseases of the CNS (Steinman, 2008). On the contrary, inflammatory mediators are commonly produced in Parkinson's disease (Tansey et al, 2008), multiple sclerosis (Sanders and De, 2007), schizophrenia (Saetre et al, 2007) or AIDS dementia complex (Vesce et al, 2007), to cite just some examples. Therefore, we could expect that the brain microenvironment in all these conditions will be especially conducive for cancer growth.…”
Section: Time (Days)mentioning
confidence: 99%
“…But inflammation is not restricted to AD among neurodegenerative disorders and other common diseases of the CNS (Steinman, 2008). On the contrary, inflammatory mediators are commonly produced in Parkinson's disease (Tansey et al, 2008), multiple sclerosis (Sanders and De, 2007), schizophrenia (Saetre et al, 2007) or AIDS dementia complex (Vesce et al, 2007), to cite just some examples. Therefore, we could expect that the brain microenvironment in all these conditions will be especially conducive for cancer growth.…”
Section: Time (Days)mentioning
confidence: 99%
“…5,6 Nonsteroidal anti-inflammatory drugs may restore this balance by inhibition of prostaglandin E 2 synthesis and regulating anti-inflammatory cytokine production, thereby increasing the T H 1/T H 2 cytokine ratio. [6][7][8] Second, NSAIDs may ameliorate symptoms through antagonizing dysfunction of the n-methyl-d-aspartate (NMDA) receptor, a key feature of a well-established neurochemical model of schizophrenia. 9,10 This action is possible because prostaglandins are intermediates in the postsynaptic signal transduction cascade of cells with NMDA-type glutamate receptors, and prostaglandins inhibit astrocytic reuptake of glutamate.…”
mentioning
confidence: 99%
“…Thus, increased expression of inflammatory genes in schizophrenic subjects may affect myelin producing cells, offering a possible link between the inflammatory and the myelin hypothesis of the disease (173).…”
Section: The Immunological Markersmentioning
confidence: 99%
“…A recent theory postulates that schizophrenia may primarily be a consequence of vascular inflammation in the brain. The theory proposes that abnormalities arise because genetically modulated inflammatory reactions damage the micro-vascular system in response to environmental agents such as infections, hypoxia, and physical trauma (172)(173).…”
Section: The Immunological Markersmentioning
confidence: 99%