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Role of Tandem Mass Spectrometry in Diagnosis and Management of Inborn Errors of Metabolism
Published in P. Mereena Luke, K. R. Dhanya, Didier Rouxel, Nandakumar Kalarikkal, Sabu Thomas, Advanced Studies in Experimental and Clinical Medicine, 2021
Kannan Vaidyanathan, Sandhya Gopalakrishnan
The levels of expression of mitochondrial matrix proteins including isovaleryl coenzyme A dehydrogenase, agmatinase, and cytochrome b5 were downregulated in early stages of Wilson’s disease. As mitochondrial injuries progressed, expression levels of malate dehydrogenase 1, annexin A5, S-adenosylhomocysteine hydrolase, transferrin, and sulfite oxidase 1 were differentially regulated. S-adenosylhomocysteine hydrolase was under-expressed and is hypothesized to play a role in neurological pathology of Wilson’s disease. The study was done on a mouse model of Wilson’s disease (LEC rats) [57]. Shotgun proteomic analysis of Atp7b(-/-) mouse model of Wilson’s disease revealed increased expression of DNA repair machinery and nucleus-localized glutathione peroxidase (SeIH), and reduced expression ofligand-activated nuclear receptors FXR/NR1H4 and GR/NR3C1 and nuclear receptor-interacting partners [58]. Remodeling of RNA processing machinery may be involved in the pathogenesis of Wilson’s disease [59].
Agmatine-attenuated cognitive and social deficits in subchronic MK-801 model of schizophrenia in rats
Published in Psychiatry and Clinical Psychopharmacology, 2018
Gokhan Unal, Alpay Ates, Feyza Aricioglu
In spite of the given comprehensive pharmacological effects of agmatine, less is known about its role in schizophrenia. However, today, there is accumulating evidence that agmatine may have an effect on schizophrenia. The effect of agmatine has been examined in a limited number of studies in well-known PPI paradigm for schizophrenia in rodents. In the PPI model, agmatine has been shown to attenuate the disruptive effects of PCP [9]. Since agmatine does not produce extrapyramidal side effects, it has been suggested that it might be a therapeutic target for schizophrenia treatment. In the literature there are some conflicting reports indicating the effect of agmatine and it has been discussed that the alterations in data might be due to the levels of endogenous agmatine [9,19,28,29]. Agmatine mainly metabolized by a specific enzyme, agmatinase, into different polyamines, which can bind and block glutamatergic NMDA receptors. Both agmatine and polyamines, which are the end products of agmatine metabolism, interact with the glutamatergic system. Therefore, as postulated in previous studies, either agmatine and/or polyamines by being a part of hypofunction of NMDA receptors may cause schizophrenia [30]. In a post-mortem study, a positive correlation was shown between metabolism of agmatine and the age of disease onset and the duration of schizophrenia [31].
Evaluation of plasma agmatine level and its metabolic pathway in patients with bipolar disorder during manic episode and remission period
Published in International Journal of Psychiatry in Clinical Practice, 2019
Emine Yılmaz, M. Ramazan Şekeroğlu, Ekrem Yılmaz, Erdem Çokluk
The study has a number of limitations: The number of participants in the study could be increased. Agmatinase gene expression could have been helpful in determining the cause of agmatine level changes. In addition, studies performed on individuals with bipolar risk factors may be helpful in observing how agmatine levels may be affected by process changes. And also there are limited studies in the literature to explain the medication effects on agmatine levels or agmatine pathway.