Tumor Necrosis Factor-alpha (TNF-α) −238 G/A Polymorphism Is Associated with the Treatment Resistance and Attempted Suicide in Schizophrenia

Özdilli, Kürşat; Tuncel, Fatıma Ceren; Pehlıvan, Mustafa; Pehlıvan, Sacide

doi:10.1080/08820139.2020.1832115

Cited by 16 publications

(16 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some evidence shows that there is an association between schizophrenia and allele A or G of TNF-α − 308 G/A [ 242 ] as well as Hasan et al demonstrated that TNF-α − 238 G/A and − 308 G/A polymorphisms are not associated with schizophrenia but TNF-α − 238 G/A polymorphism may be related to treatment resistance and attempted suicide in patients with schizophrenia. In particular, the patients that carry the GG genotype of TNF-α − 238 G/A seem to have a higher risk of treatment resistance [ 243 ].…”

Section: Genetic Findingsmentioning

confidence: 99%

Linking Inflammation, Aberrant Glutamate-Dopamine Interaction, and Post-synaptic Changes: Translational Relevance for Schizophrenia and Antipsychotic Treatment: a Systematic Review

Bartolomeis¹,

Barone²,

Vellucci³

et al. 2022

Mol Neurobiol

View full text Add to dashboard Cite

Evidence from clinical, preclinical, and post-mortem studies supports the inflammatory/immune hypothesis of schizophrenia pathogenesis. Less evident is the link between the inflammatory background and two well-recognized functional and structural findings of schizophrenia pathophysiology: the dopamine-glutamate aberrant interaction and the alteration of dendritic spines architecture, both believed to be the “quantal” elements of cortical-subcortical dysfunctional network. In this systematic review, we tried to capture the major findings linking inflammation, aberrant glutamate-dopamine interaction, and post-synaptic changes under a direct and inverse translational perspective, a paramount picture that at present is lacking. The inflammatory effects on dopaminergic function appear to be bidirectional: the inflammation influences dopamine release, and dopamine acts as a regulator of discrete inflammatory processes involved in schizophrenia such as dysregulated interleukin and kynurenine pathways. Furthermore, the link between inflammation and glutamate is strongly supported by clinical studies aimed at exploring overactive microglia in schizophrenia patients and maternal immune activation models, indicating impaired glutamate regulation and reduced N-methyl-D-aspartate receptor (NMDAR) function. In addition, an inflammatory/immune-induced alteration of post-synaptic density scaffold proteins, crucial for downstream NMDAR signaling and synaptic efficacy, has been demonstrated. According to these findings, a significant increase in plasma inflammatory markers has been found in schizophrenia patients compared to healthy controls, associated with reduced cortical integrity and functional connectivity, relevant to the cognitive deficit of schizophrenia. Finally, the link between altered inflammatory/immune responses raises relevant questions regarding potential new therapeutic strategies specifically for those forms of schizophrenia that are resistant to canonical antipsychotics or unresponsive to clozapine.

show abstract

Section: Genetic Findingsmentioning

confidence: 99%

Linking Inflammation, Aberrant Glutamate-Dopamine Interaction, and Post-synaptic Changes: Translational Relevance for Schizophrenia and Antipsychotic Treatment: a Systematic Review

Bartolomeis¹,

Barone²,

Vellucci³

et al. 2022

Mol Neurobiol

View full text Add to dashboard Cite

show abstract

“…Lastly, rs1800629 and rs361525 (–238 G/A) polymorphisms have been the subject of one study in patients with schizophrenia with or without a history of SA. The distribution of rs361525 genotype, but not that of rs1800629, was significantly different in SAs compared to individuals with no history of SB ( 44 ).…”

Section: Resultsmentioning

confidence: 79%

Genetic variations related to inflammation in suicidal ideation and behavior: A systematic review

et al. 2022

View full text Add to dashboard Cite

Background/objectivesImmune-inflammatory changes have been found in all types of suicidal ideation and behavior (SIB), independently of associated mental disorders. Since several Single Nucleotide Polymorphisms (SNPs) affect the function of inflammation-related genes, we searched the literature for genetic variations potentially altering inflammatory processes in SIB.MethodsWe included studies that looked for associations between SIB and SNPs in genes related to inflammatory processes. Case reports, literature reviews, and animal studies were excluded. Articles were retrieved from PubMed and PsycINFO databases, Google Scholar and GreySource Index until September 17th, 2022. Quality was assessed using Q-Genie.ResultsWe analyzed 32 studies. SIB has been associated with eighteen SNPs located in genes encoding for interleukin-8 (rs4073), C-reactive protein (rs1130864), tumor necrosis factor α (rs1800629, rs361525, and rs1099724), tumor necrosis factor receptor 2 (rs1061622), transforming growth factor β-1 (rs1982073), acid phosphatase 1 (rs7419262, rs300774), interleukin-10 (rs1800896), interferon γ (rs2430561), amino-carboxy muconate semialdehyde decarboxylase (rs2121337), interleukin 7 (rs10448044, rs10448042), macrophage migration inhibitory factor (rs755622), interleukin 1-α (rs1800587), and interleukin 1-β (rs1143634 and rs16944. A genome-wide association study reported one association at the threshold of significance with the rs300774 SNP, located in the 2p25 region containing ACP1 gene.DiscussionThe studies included were methodologically and clinically diverse and of moderate quality. Their findings suggest that some inflammation-related SNPs could increase the likelihood of SIB but the evidence to date is insufficient. Further research using gene-gene (GxG) and gene-environment (GxE) approaches is warranted.Systematic review registration[https://www.crd.york.ac.uk], identifier [CRD42022296310].

show abstract

“…Then, the Structured Clinical Interview for DSM-IV Axis-I Disorders (SCID-I) was administered to verify the patients’ diagnosis. 20 , 21 The Positive and Negative Symptoms Scale (PANSS) 22 , 23 was applied for patients with SCZ, while the Hamilton Depression Rating Scale (HAM-D) 24 , 25 and the Young Mania Rating Scale 26 , 27 were for evaluating BD patients concerning the severity of symptoms. We assessed the impairment of insight in SCZ with the Schedule for Assessing the Three Components of Insight (SATCI).…”

Section: Methodsmentioning

confidence: 99%

Investigation of inflammation related gene polymorphism of the mannose-binding lectin 2 in schizophrenia and bipolar disorder

Yazar

Erol

Pehlıvan

2021

NSJ

Self Cite

View full text Add to dashboard Cite

show abstract

Tumor Necrosis Factor-alpha (TNF-α) −238 G/A Polymorphism Is Associated with the Treatment Resistance and Attempted Suicide in Schizophrenia

Cited by 16 publications

References 50 publications

Linking Inflammation, Aberrant Glutamate-Dopamine Interaction, and Post-synaptic Changes: Translational Relevance for Schizophrenia and Antipsychotic Treatment: a Systematic Review

Linking Inflammation, Aberrant Glutamate-Dopamine Interaction, and Post-synaptic Changes: Translational Relevance for Schizophrenia and Antipsychotic Treatment: a Systematic Review

Genetic variations related to inflammation in suicidal ideation and behavior: A systematic review

Investigation of inflammation related gene polymorphism of the mannose-binding lectin 2 in schizophrenia and bipolar disorder

Contact Info

Product

Resources

About