Apoptosis in subacute sclerosing panencephalitis: Possibility for treatment

Anlar, Banu; Beken, Serdar; Talim, Beril

doi:10.1016/j.mehy.2012.12.028

Cited by 2 publications

(2 citation statements)

References 9 publications

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“…In our study, to evaluate oxidant and antioxidant status in subacute sclerosing panencephalitis, we analyzed malondialdehyde, reduced glutathione, beta-carotene, retinol, alpha-tocopherol, and ascorbic acid levels in patients with subacute sclerosing panencephalitis. Neuronal death is mediated by apoptotic mechanisms triggered by the inflammatory cascade or oxidative stress: inflammatory cytokines and nitric oxide metabolites are elevated in the cerebrospinal fluid, especially in certain clinical phenotypes of subacute sclerosing panencephalitis, although patients’ cerebrospinal fluid did not increase the number of apoptotic neurons in the study of Anlar et al 22 Hayashi et al 23 neuropathologically examined 6 autopsy cases of subacute sclerosing panencephalitis. On the basis of their findings, they speculated in subacute sclerosing panencephalitis that apoptosis and oxidative stress to DNA could contribute to the early neuronal damage, whereas lipid peroxidation and disturbed glutamate transport could be related to the subsequent neurodegeneration.…”

Section: Discussionmentioning

confidence: 99%

Oxidant and Antioxidant Status in Children With Subacute Sclerosing Panencephalitis

et al. 2013

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We analyzed serum alpha-tocopherol, beta-carotene, retinol, and ascorbic acid levels and malondialdehyde and reduced glutathione concentrations on erythrocyte and cerebrospinal fluid in 30 patients with subacute sclerosing panencephalitis to evaluate oxidant and antioxidant status. Serum alpha-tocopherol, beta-carotene, retinol, ascorbic acid levels, and erythrocyte and cerebrospinal fluid reduced glutathione concentrations were decreased; however, erythrocyte and cerebrospinal fluid malondialdehyde levels were increased in the patients. Cerebrospinal fluid malondialdehyde levels were different between clinical stages of the disease (P < .05). Higher cerebrospinal fluid malondialdehyde level was associated with the more severe clinical stage. A positive correlation was found between cerebrospinal fluid malondialdehyde level and clinical stages (r = 0.42; P < .05) and between erythrocyte malondialdehyde level and clinical stages (r = 0.40; P < .05). Our findings showed presence of oxidative damage in subacute sclerosing panencephalitis and that antioxidants were increased as defense mechanisms of the organism against oxidative damage.

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Section: Discussionmentioning

confidence: 99%

Oxidant and Antioxidant Status in Children With Subacute Sclerosing Panencephalitis

et al. 2013

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“…12,13 Recently antiapoptotic drugs have also been suggested for subacute sclerosing panencephalitis. 14,15 However, the exact mechanism of neurodegeneration remains still unknown.…”

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confidence: 99%

Expression Patterns of Micro-RNAs 146a, 181a, and 155 in Subacute Sclerosing Panencephalitis

et al. 2014

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Subacute sclerosing panencephalitis is caused by persistent brain infection of mutated virus, showing inflammation, neurodegeneration, and demyelination. Although many factors are emphasized in the pathogenesis of subacute sclerosing panencephalitis, the exact mechanism of neurodegeneration remains unknown. Micro-RNAs are small, noncoding RNAs that regulate gene expression at the posttranscriptional levels. Micro-RNAs are essential for normal immune system development; besides they are also implicated in the pathogenesis of many chronic inflammatory disorders. The aim of this study is to investigate the expression patterns of micro-RNAs 146a, 181a, and 155 in peripheral blood mononuclear cells of patients with subacute sclerosing panencephalitis. We enrolled 39 patients with subacute sclerosing panencephalitis and 41 healthy controls. Quantitative analysis of micro-RNAs 146a, 181a, and 155 were performed using specific stem-loop primers followed by real-time polymerase chain reaction. All of 3 micro-RNAs were upregulated in subacute sclerosing panencephalitis patients. In addition, the level of micro-RNA 155 expression was higher in stage 3 patients. But, micro-RNA 146a and 181a expression levels showed no association or correlation with clinically relevant data. Alteration of peripheral blood mononuclear cell micro-RNAs in subacute sclerosing panencephalitis may shed new light on the pathogenesis of disease and may contribute to the aberrant systemic rise in mRNA levels in subacute sclerosing panencephalitis.

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Apoptosis in subacute sclerosing panencephalitis: Possibility for treatment

Cited by 2 publications

References 9 publications

Oxidant and Antioxidant Status in Children With Subacute Sclerosing Panencephalitis

Oxidant and Antioxidant Status in Children With Subacute Sclerosing Panencephalitis

Expression Patterns of Micro-RNAs 146a, 181a, and 155 in Subacute Sclerosing Panencephalitis

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