Ziprasidone in the treatment of delayed carbon monoxide encephalopathy

Hu, Ming-Chuan; Shiah, I‐Shin; Yeh, Chin‐Bin; Chen, Hsing-Kang; Chen, Chih-Kang

doi:10.1016/j.pnpbp.2006.01.019

Cited by 13 publications

(5 citation statements)

References 6 publications

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“…The results of Novak et al [37] suggest that variants in the NRXN3 gene could contribute to the degree of nicotine dependence in patients with schizophrenia, while another association study confirmed a role for NRXN3 in susceptibility to smoking behavior [38] . As an organic mental disorder, DEACMP shows psychotic symptoms including visual and auditory hallucinations, persecutory delusions, depression and cognitive impairments [39] . The meta-analysis of five GWAS identified a marker in the NRXN3 gene (rs17757879) that showed a consistent protective effect in Alzheimer’s disease [40] .…”

Section: Discussionmentioning

confidence: 99%

DNA Pooling Base Genome-Wide Association Study Identifies Variants at NRXN3 Associated with Delayed Encephalopathy after Acute Carbon Monoxide Poisoning

Zhang

et al. 2013

PLoS ONE

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Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is more characteristic of anoxic encephalopathy than of other types of anoxia. Those who have the same poisoning degree and are of similar age and gender have a greater risk of getting DEACMP. This has made it clear that there are obvious personal differences. Genetic factors may play a very important role. The authors performed a genome-wide association study involving pooling of DNA obtained from 175 patients and 244 matched acute carbon monoxide poisoning without delayed encephalopathy controls. The Illumina HumanHap 660 Chip array was used for DNA pools. Allele frequencies of all SNPs were compared between delayed encephalopathy after acute carbon monoxide poisoning and control groups and ranked. A total of 123 SNPs gave an OR >1.4. Of these, 46 mapped in or close to known genes. Forty-eight SNPs located in 19 genes were associated with DEACMP after correction for 5% FDR in the genome-wide association of pooled DNA. Two SNPs (rs11845632 and rs2196447) locate in the Neurexin 3 gene were selected for individual genotyping in all samples and another cohort consisted of 234 and 271 controls. There were significant differences in the genotype and allele frequencies of rs11845632 and rs2196447 between the DEACMP group and controls group (all P-values <0.05). This study describes a positive association between Neurexin 3 and controls in the Han Chinese population, and provides genetic evidence to support the susceptibility of DEACMP, which may be the resulting interaction of environmental and genetic factors.

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Section: Discussionmentioning

confidence: 99%

DNA Pooling Base Genome-Wide Association Study Identifies Variants at NRXN3 Associated with Delayed Encephalopathy after Acute Carbon Monoxide Poisoning

Zhang

et al. 2013

PLoS ONE

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“…Nevertheless, antipsychotics affect SREBP pathways variably, depending on the cell type and culturing conditions [ 2 ]. Indeed, while some antipsychotics are strong SREBP inducers, for others, such as ziprasidone, both an activatory and no effects are reported [ 4 , 6 , 7 , 46 , 47 ]. Therefore, we decided to compare three antipsychotics having different damaging potential in patients, olanzapine (high), risperidone (medium) and ziprasidone (low/null) [ 12 – 14 ], and to analyse their effects on SREBP pathways in the HepG2 hepatoma cell line, in the presence of physiological glucose concentrations.…”

Section: Resultsmentioning

confidence: 99%

Olanzapine, risperidone and ziprasidone differently affect lysosomal function and autophagy, reflecting their different metabolic risk in patients

Pozzi,

Vantaggiato,

Brivio

et al. 2024

Transl Psychiatry

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The metabolic effects induced by antipsychotics in vitro depend on their action on the trafficking and biosynthesis of sterols and lipids. Previous research showed that antipsychotics with different adverse effects in patients cause similar alterations in vitro, suggesting the low clinical usefulness of cellular studies. Moreover, the inhibition of peripheral AMPK was suggested as potential aetiopathogenic mechanisms of olanzapine, and different effects on autophagy were reported for several antipsychotics. We thus assessed, in clinically-relevant culture conditions, the aetiopathogenic mechanisms of olanzapine, risperidone and ziprasidone, antipsychotics with respectively high, medium, low metabolic risk in patients, finding relevant differences among them. We highlighted that: olanzapine impairs lysosomal function affecting autophagy and autophagosome clearance, and increasing intracellular lipids and sterols; ziprasidone activates AMPK increasing the autophagic flux and reducing intracellular lipids; risperidone increases lipid accumulation, while it does not affect lysosomal function. These in vitro differences align with their different impact on patients. We also provided evidence that metformin add-on improved autophagy in olanzapine-treated cells and reduced lipid accumulation induced by both risperidone and olanzapine in an AMPK-dependent way; metformin also increased the production of bile acids to eliminate cholesterol accumulations caused by olanzapine. These results have different clinical implications. We demonstrated that antipsychotics with different metabolic impacts on patients actually have different mechanisms of action, thus supporting the possibility of a personalised antipsychotic treatment. Moreover, we found that metformin can fully revert the phenotype caused by risperidone but not the one caused by olanzapine, that still activates SREBP2.

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“…A recent hypothesis indicated that an antioxidant such as caffeic acid phenethyl ester and anti-nitric oxide therapy may be valuable for neuroprotection against CO poisoning ( 8 ). Thus far, the majority of research studies ( 9 – 11 ) have focused on the treatment for delayed encephalopathy caused by CO poisoning, whereas few ( 12 ) have reported the emergency treatment for CO poisoning.…”

Section: Introductionmentioning

confidence: 99%

A novel effective chemical hemin for the treatment of acute carbon monoxide poisoning in mice

Shi

Wen

et al. 2017

Exp Ther Med

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There is no effective drug for the therapy of acute carbon monoxide (CO) poisoning. The purpose of the present study was to investigate the potential preventive and therapeutic effects of hemin on an animal model of acute CO poisoning and to provide a potential therapeutic candidate drug. A total of 80 Kunming mice were randomly divided into four groups, namely the air control, acute CO poisoning, hemin-treatment + CO and hemin-pretreatment + CO groups (n=20 each). Furthermore, the mortality rate of mice, blood carboxyhaemoglobin (HbCO) concentration and serum malondialdehyde (MDA) concentration were measured, and pathological changes of the hippocampal area were determined using histochemical staining. The mice with acute CO poisoning had a 50% mortality rate at 1 h, with an increase in blood HbCO, serum MDA levels and pathological impairments of the hippocampus. Furthermore, the mortality rate, blood HbCO and serum MDA levels of mice with pretreatment and treatment of hemin were decreased. Additionally, the pathological changes of the hippocampal area were improved in the hemin-treatment and hemin-pretreatment groups compared with the mice treated with CO. These results suggest that hemin is a novel effective chemical for the prevention and treatment of acute CO poisoning in mice. Therefore, the present study provides a novel method and experimental basis for the application of hemin in treating patients with acute CO poisoning.

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Ziprasidone in the treatment of delayed carbon monoxide encephalopathy

Cited by 13 publications

References 6 publications

DNA Pooling Base Genome-Wide Association Study Identifies Variants at NRXN3 Associated with Delayed Encephalopathy after Acute Carbon Monoxide Poisoning

DNA Pooling Base Genome-Wide Association Study Identifies Variants at NRXN3 Associated with Delayed Encephalopathy after Acute Carbon Monoxide Poisoning

Olanzapine, risperidone and ziprasidone differently affect lysosomal function and autophagy, reflecting their different metabolic risk in patients

A novel effective chemical hemin for the treatment of acute carbon monoxide poisoning in mice

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