China
Africa
Explore chapters and articles related to this topic
Study of Nutraceuticals in Cancer Treatment: An In Silico Approach
Published in Raj K. Keservani, Anil K. Sharma, Rajesh K. Kesharwani, Nutraceuticals and Dietary Supplements, 2020
Co-expression network figures are drawn using R package igraph. Only the top 20 genes with the highest correlations are shown in Figure 6.5. Co-expressed genes are C1QBP, COX10, CTDNEP1, EIF4A1, EIF5AL1, ELAC2, GEMIN4, METTL16, MYBBP1A, NDEL1, NUP88, PFAS, PITPNA, PLD2, RPA1, RPL26, SCO1, SENP3, TP53, TSR1, andYWHAE.
Unraveiling the correlation among neurodevelopmental and inflammatory biomarkers in patients with chronic schizophrenia
Published in Nordic Journal of Psychiatry, 2022
João V. Nani, Priscila G. C Almeida, Cristiano Noto, Rodrigo A. Bressan, Elisa Brietzke, Mirian A. F Hayashi
Nuclear distribution element like-1 (Ndel1) oligopeptidase is a cytosolic enzyme that cleaves small neuropeptides which were suggested to play several roles, including as endogenous antipsychotic and/or in neurogenesis/neuromodulation/neuroprotection [1,2]. Ndel1 also forms complexes with cytosolic cytoskeleton proteins, which are required for neurite outgrowth, neuronal migration and neurogenesis, suggesting its potential role in the susceptibility to develop psychiatric disorders, supporting the neurodevelopmental hypothesis of schizophrenia (SCZ) [3]. A significant lower Ndel1 activity was observed in antipsychotic-naïve first-episode psychosis (FEP) subjects compared with healthy controls (HCs), suggesting Ndel1 oligopeptidase activity as a potential biomarker of early stages and/or disease progression of SCZ [4]. Moreover, a linear correlation between decreases in Ndel1 activity and symptom amelioration following the treatment with risperidone was recently demonstrated by us in FEP individuals [4]. In line with this, chronic SCZ patients also show lower Ndel1 activity compared with HCs [5], as well as long-term treatment with typical or atypical antipsychotics decreased the Ndel1 activity in blood and brain of an animal model for SCZ studies [6]. We have also demonstrated a reduced Ndel1 activity in blood and brain of a transgenic animal model for SCZ studies, which presents abnormal dopaminergic signaling and disrupted neurodevelopment [2].
ACE activity in blood and brain axis in an animal model for schizophrenia: Effects of dopaminergic manipulation with antipsychotics and psychostimulants
Published in The World Journal of Biological Psychiatry, 2020
João V. Nani, Camila M. Yonamine, Diego Castro Musial, Caroline Dal Mas, Jair J. Mari, Mirian A. F. Hayashi
The molecular mechanism(s) underlying SCZ pathophysiology is still uncertain. Aiming to get insights into the(se) mechanism(s), we performed several studies based on enzyme activity measurements of selected members of a class of oligopeptidases that are generally involved in the maturation and degradation of hormone peptides and neuropeptides (Camargo et al. 1983; Camargo et al. 1984; Barrett and Rawlings 1992). Despite the limited number of studies in the field, recent evidences have emphasised the important role of these neuropeptidases in the pathophysiology of mental disorders (Maes et al. 1995; Breen et al. 2004; Arif et al. 2007; Deng et al. 2013; Fernández-Atucha et al. 2015; Prades et al. 2017). Our group has paid special attention to the oligopeptidase known as nuclear distribution element-like 1 (Ndel1) because of its dual role and unique functions, including the ability to bind and to form complex with the SCZ susceptibility gene product, known as DISC1 (disrupted-in-schizophrenia 1), and because of its ability to cleave neuropeptides such as NT and BK, which were reported to be crucial for response to antipsychotics and for neuron-generating division of neural progenitor cells, respectively (Borroto-Escuela et al. 2016; Feifel et al. 2016; Pillat et al. 2016). The formation of the Ndel1-DISC1 complex regulates neurite outgrowth and brain formation, and also negatively modulates Ndel1 oligopeptidase activity (Hayashi et al. 2005; Hayashi et al. 2010; Hayashi et al. 2015; Bradshaw and Hayashi 2017). Several studies consistently showed that Ndel1 expression and enzyme activity is down-regulated in SCZ patients compared to HCs paired by age and sex (Lipska et al. 2006; Gadelha et al. 2013; Gadelha et al. 2016). Interestingly, studies of our group with SHRs, an animal model presenting SCZ-like phenotypes, also allowed us to confirm the power of measuring Ndel1 activity in the blood to predict changes in the brain, and a good agreement of these data and the clinical data obtained from studies with chronic SCZ subjects was observed, which together strengthened the validity of using the SHR strain as an animal model for studying the molecular pathways underlying SCZ-like phenotypes (Nani et al. 2019). Therefore, with the aim of further assessment of ACE and the predictive validity of SHR as an animal model to evaluate new antipsychotic drugs targeting dopamine pathways, and at pharmacological validation before starting clinical trials, we continue to investigate SHRs as an animal model for studying SCZ-like phenotypes in response to pharmacotherapy with antipsychotics.