Uncovering associations between mental illness diagnosis, nitric oxide synthase gene variation, and peripheral nitric oxide concentration

McNeill, Rhiannon V.; Kehrwald, Christopher; Brum, Murielle; Knopf, Katrin; Brunkhorst-Kanaan, Nathalie; Etyemez, Semra; Koreny, Carolin; Bittner, Robert A.; Freudenberg, Florian; Herterich, Sabine; Reif, Andreas; Kittel‐Schneider, Sarah

doi:10.1016/j.bbi.2022.01.006

Cited by 15 publications

(13 citation statements)

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“…This finding is not surprising, considering the immense pain and fear children experience as a result of patterns of abandonment and abuse often lead to anger and impulsivity (Lobbestael et al, 2005). Studies have shown that NO signaling may be related to the pathogenesis of mental illness (McNeill et al, 2022). And NOS1AP genes is involved in physiological events that affect a variety of neurotransmitters including monoamine neurotransmitters, which have been shown to be associated with ASPD (Bortolato & Shih, 2011;Vincent, 2010).…”

Section: Discussionmentioning

confidence: 99%

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The influence of NOS1AP gene polymorphisms and childhood abuse on antisocial personality disorder in Chinese male violent inmates

Ouyang

Liu

et al. 2022

Personality & Mental Health

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Antisocial personality disorder (ASPD) is a common behavioral pattern that causes sufferers to ignore or violate the rights of others. Though its cause is still unclear, previous studies have shown that childhood maltreatment is closely related to ASPD. The NOS1AP gene is associated with various neuropsychiatric diseases, but a linkage between it and ASPD has not yet been discovered. This study recruited ASPD and non‐ASPD male subjects who had committed violent crimes from a prison in Nanjing, China. By comparing the two groups' genotypes, allele frequencies, and histories of childhood abuse, we explored the interaction between the NOS1AP gene and childhood maltreatment on the pathogenesis of ASPD. The results showed that polymorphism rs945713 in the NOS1AP gene was associated with ASPD and furthermore that this SNP may be involved in regulating the effect of childhood abuse on ASPD. This study found that childhood trauma increases the risk of ASPD in violent adult male inmates; for prisoners with ASPD, it is critical to pay attention to their childhood trauma and take early psychological intervention.

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Section: Discussionmentioning

confidence: 99%

“…Studies have shown that NO signaling may be related to the pathogenesis of mental illness (McNeill et al, 2022). And NOS1AP genes is involved in physiological events that affect a variety of neurotransmitters including monoamine neurotransmitters, which have been shown to be associated with ASPD (Bortolato & Shih, 2011; Vincent, 2010).…”

Section: Discussionmentioning

confidence: 99%

The influence of NOS1AP gene polymorphisms and childhood abuse on antisocial personality disorder in Chinese male violent inmates

Ouyang

Liu

et al. 2022

Personality & Mental Health

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“…As a practical contribution to the BPC 157/ketamine relation, we noted a considerable overlapping of gene overexpression as an apparent close connection between the ketamine and BPC 157 (the highest ketamine dose 30 mg/kg ip vs. lowest BPC 157 10 ng/kg ip dose) ( Figure 11 ). This was done with the genes’ expression analysis in brain tissue, using Nos1 [ 34 , 35 ], Nos2 [ 36 , 37 ], Nos3 [ 38 ], Plcg1 [ 39 , 40 ], Prkcg [ 41 , 42 ], Ptgs2 [ 43 ], and Ptk2 [ 44 , 45 ], all associated with schizophrenia presentation. We identified the similar overexpression of the genes in the healthy rats treated with the ketamine ( Nos1 , Nos2 , Plcg1 , Prkcg , Ptgs2 , and Ptk2 ) and in the BPC 157 ( Nos1 , Nos2 , Plcg1 , Prkcg , and Ptk2 ), thus a considerable overlapping of gene overexpression.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, to minimize at least partly the limitations known in the prime behavioral studies and to highlight a likely special point to explain how the dysfunction and its counteraction is causal to or the result of ketamine/BPC 157 interactions, a particular gene expression was carried out in the brain, providing their particular association with schizophrenia conditions. Analyzed [ 33 ] were Nos1 [ 34 , 35 ], Nos2 [ 36 , 37 ], Nos3 [ 38 ], phospholipase C, gamma 1 ( Plcg1 ) [ 39 , 40 ], protein kinase C gamma ( Prkcg ) [ 41 , 42 ], prostaglandin-endoperoxide synthase 2, cyclooxygenase (Cox)2 ( Ptgs2 ) [ 43 ], and protein tyrosine kinase 2 ( Ptk2 ) [ 44 , 45 ].…”

Section: Introductionmentioning

confidence: 99%

BPC 157, L-NAME, L-Arginine, NO-Relation, in the Suited Rat Ketamine Models Resembling “Negative-Like” Symptoms of Schizophrenia

et al. 2022

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We attempted throughout the NO-system to achieve the particular counteraction of the ketamine-induced resembling “negative-like” schizophrenia symptoms in rats using pentadecapeptide BPC 157, and NO-agents, NG-nitro-L-arginine methylester (L-NAME), and/or L-arginine, triple application. This might be the find out the NO-system organized therapy (i.e., simultaneously implied NO-system blockade (L-NAME) vs. NO-system over-stimulation (L-arginine) vs. NO-system immobilization (L-NAME+L-arginine)). The ketamine regimen (intraperitoneally/kg) included: 3 mg (cognitive dysfunction, novel object recognition test), 30 mg (anxiogenic effect (open field test) and anhedonia (sucrose test)), and 8 mg/3 days (social withdrawal). Medication (mg/kg intraperitoneally) was L-NAME (5), L-arginine (100), and BPC 157 (0.01), alone and/or together, given immediately before ketamine (L-NAME, L-arginine, and combination) or given immediately after (BPC 157 and combinations). BPC 157 counteracted ketamine-cognition dysfunction, social withdrawal, and anhedonia, and exerted additional anxiolytic effect. L-NAME (antagonization, social withdrawal) and L-arginine (antagonization, cognitive dysfunction, anhedonia) both included worsening cognitive dysfunction, anhedonia, and anxiogenic effect (L-NAME), social withdrawal, and anxiogenic effect (L-arginine). Thus, ketamine-induced resembling “negative-like” schizophrenia symptoms were “L-NAME non-responsive, L-arginine responsive” (cognition dysfunction), “L-NAME responsive, L-arginine non-responsive” (social withdrawal), “L-NAME responsive, L-arginine responsive, opposite effect” (anhedonia) and “L-NAME responsive, L-arginine responsive, parallel effect” (both anxiogening). In cognition dysfunction, BPC 157 overwhelmed NO-agents effects. The mRNA expression studies in brain tissue evidenced considerable overlapping of gene overexpression in healthy rats treated with ketamine or BPC 157. With the BPC 157 therapy applied immediately after ketamine, the effect on Nos1, Nos2, Plcg1, Prkcg, and Ptgs2 (increased or decreased expression), appeared as a timely specific BPC 157 effect on ketamine-specific targets.

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“…Mental disorders remain among the top ten leading causes of burden worldwide, which makes research to establish causal pathways imperative for effective prevention and treatment [ 1 ]. In recent years, nitric oxide (NO) signaling has been implicated in the pathophysiology of several mental illnesses, such as schizophrenia and affective disorders, comprising bipolar disorder and major depressive disorder [ 2 ]. For example, in schizophrenia patients, NO metabolism is impaired in various organs, including the brain [ 3 , 4 , 5 ], and high NO levels are found in post-mortem samples of the prefrontal cortex and hippocampus [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Assessment of DDAH1 and DDAH2 Contributions to Psychiatric Disorders via In Silico Methods

Kozlova

Vaganova

Rodionov

et al. 2022

IJMS

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The contribution of nitric oxide synthases (NOSs) to the pathophysiology of several neuropsychiatric disorders is recognized, but the role of their regulators, dimethylarginine dimethylaminohydrolases (DDAHs), is less understood. This study’s objective was to estimate DDAH1 and DDAH2 associations with biological processes implicated in major psychiatric disorders using publicly accessible expression databases. Since co-expressed genes are more likely to be involved in the same biologic processes, we investigated co-expression patterns with DDAH1 and DDAH2 in the dorsolateral prefrontal cortex in psychiatric patients and control subjects. There were no significant differences in DDAH1 and DDAH2 expression levels in schizophrenia or bipolar disorder patients compared to controls. Meanwhile, the data suggest that in patients, DDAH1 and DDHA2 undergo a functional shift mirrored in changes in co-expressed gene patterns. This disarrangement appears in the loss of expression level correlations between DDAH1 or DDAH2 and genes associated with psychiatric disorders and reduced functional similarity of DDAH1 or DDAH2 co-expressed genes in the patient groups. Our findings evidence the possible involvement of DDAH1 and DDAH2 in neuropsychiatric disorder development, but the underlying mechanisms need experimental validation.

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Uncovering associations between mental illness diagnosis, nitric oxide synthase gene variation, and peripheral nitric oxide concentration

Cited by 15 publications

References 52 publications

The influence of NOS1AP gene polymorphisms and childhood abuse on antisocial personality disorder in Chinese male violent inmates

The influence of NOS1AP gene polymorphisms and childhood abuse on antisocial personality disorder in Chinese male violent inmates

BPC 157, L-NAME, L-Arginine, NO-Relation, in the Suited Rat Ketamine Models Resembling “Negative-Like” Symptoms of Schizophrenia

Assessment of DDAH1 and DDAH2 Contributions to Psychiatric Disorders via In Silico Methods

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