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Metabolites
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Metabolomics Meets Neuropsychiatry
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Metabolomics Meets Neuropsychiatry

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Integrative Metabolomics".

Deadline for manuscript submissions: closed (15 December 2023) | Viewed by 4612

Special Issue Editors

Dr. Anurag Kuhad

E-Mail Website
Guest Editor
Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh 160014, India
Interests: Neuropharmacology; metabolic disorders; neurodegenerative diseases; diabetic complications; neuropathic pain; pharmacokinetics
Dr. Raghunath Singh

E-Mail Website
Guest Editor
Schizophrenia Division, Centre for Addiction and Mental Health, Toronto, ON M6J 1H4, Canada
Interests: neuropharmacology; schizophrenia; antipsychotics; gut-microbiota; metabolism

Special Issue Information

Dear Colleagues,

Neuropsychiatric disorders (NPDs) such as schizophrenia, depression, bipolar, anxiety, substance abuse, attention deficit hyperactivity disorder, etc. have complex pathophysiology limiting the understanding of pathomechanisms and the discovery of novel biomarkers and therapeutic alternatives. In recent years, metabolomics has emerged as a pivotal tool in bridging the gaps between NPDs and metabolic comorbidities. The study of metabolites-originated neurotransmitters, peptides, amino acids, lipids, and fatty acids in the targeted brain tissues, blood cells, and serum samples has significantly been employed in the clinical diagnosis of NPDs. In addition, emerging evidence suggesting the association of gut microbiota and gut-bacteria-derived metabolites with NPDs has also attracted the scientific community. The study of drug metabolites in body fluids has also been a valuable tool in assessing the ratios of therapeutic action and adverse effects.

This Special Issue, “Metabolomics Meets Neuropsychiatry,” will highlight the implications of targeted/untargeted metabolomic approaches in understanding the mechanisms behind NPDs, as well as the therapeutic and adverse effects of drugs and identifying novel biomarkers. We invite the submission of original research and review articles covering this area of research, as well as studies investigating the effects of pharmacological interventions on altering the metabolites (neurotransmitters, lipids, amino acids, etc.) in NPDs and associated metabolic disorders. Furthermore, studies investigating the desired/adverse effects of drugs and drug metabolites in treating NPDs are also encouraged for submission.

Dr. Anurag Kuhad
Dr. Raghunath Singh
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • metabolomics
  • neuropsychiatric disorders
  • schizophrenia
  • bipolar
  • depression
  • biomarker
  • drug discovery

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Published Papers (2 papers)

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Research

17 pages, 1190 KiB  
Article
Targeted Analysis of Plasma Polar Metabolites in Postmenopausal Depression
by Maria Fernanda Naufel, Amanda Paula Pedroso, Adriana Pereira de Souza, Valter Tadeu Boldarine, Lila Missae Oyama, Edson Guimarães Lo Turco, Helena Hachul, Eliane Beraldi Ribeiro and Mônica Marques Telles
Metabolites 2024, 14(5), 286; https://doi.org/10.3390/metabo14050286 - 16 May 2024
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Abstract
Depression will be the disease with the highest incidence worldwide by 2030. Data indicate that postmenopausal women have a higher incidence of mood disorders, and this high vulnerability seems to be related to hormonal changes and weight gain. Although research evaluating the profile [...] Read more.
Depression will be the disease with the highest incidence worldwide by 2030. Data indicate that postmenopausal women have a higher incidence of mood disorders, and this high vulnerability seems to be related to hormonal changes and weight gain. Although research evaluating the profile of metabolites in mood disorders is advancing, further research, maintaining consistent methodology, is necessary to reach a consensus. Therefore, the objective of the present study was to carry out an exploratory analysis of the plasma polar metabolites of pre- and postmenopausal women to explore whether the profile is affected by depression. The plasma analysis of 50 polar metabolites was carried out in a total of 67 postmenopausal women, aged between 50 and 65 years, either without depression (n = 25) or with depression symptoms (n = 42), which had spontaneous onset of menopause and were not in use of hormone replacement therapy, insulin, or antidepressants; and in 42 healthy premenopausal women (21 without depression and 21 with depression symptoms), aged between 40 and 50 years and who were not in use of contraceptives, insulin, or antidepressants. Ten metabolites were significantly affected by depression symptoms postmenopause, including adenosine (FDR = 3.778 × 10−14), guanosine (FDR = 3.001 × 10−14), proline (FDR = 1.430 × 10−6), citrulline (FDR = 0.0001), lysine (FDR = 0.0004), and carnitine (FDR = 0.0331), which were down-regulated, and dimethylglycine (FDR = 0.0022), glutathione (FDR = 0.0048), creatine (FDR = 0.0286), and methionine (FDR = 0.0484) that were up-regulated. In premenopausal women with depression, oxidized glutathione (FDR = 0.0137) was down-regulated, and dimethylglycine (FDR = 0.0406) and 4-hydroxyproline (FDR = 0.0433) were up-regulated. The present study provided new data concerning the consequences of depression on plasma polar metabolites before and after the establishment of menopause. The results demonstrated that the postmenopausal condition presented more alterations than the premenopausal period and may indicate future measures to treat the disturbances involved in both menopause and depression. Full article
(This article belongs to the Special Issue Metabolomics Meets Neuropsychiatry)
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17 pages, 964 KiB  
Article
Altered Sphingolipid Hydrolase Activities and Alpha-Synuclein Level in Late-Onset Schizophrenia
by Tatiana Usenko, Anastasia Bezrukova, Katerina Basharova, Galina Baydakova, Elena Shagimardanova, Nataliya Blatt, Albert Rizvanov, Oleg Limankin, Maxim Novitskiy, Natalia Shnayder, Artem Izyumchenko, Mikhail Nikolaev, Anna Zabotina, Anna Lavrinova, Darya Kulabukhova, Regina Nasyrova, Ekaterina Palchikova, Natalia Zalutskaya, Irina Miliukhina, Yury Barbitoff, Oleg Glotov, Andrey Glotov, Anastasia Taraskina, Nikolai Neznanov, Ekaterina Zakharova and Sofya Pchelinaadd Show full author list remove Hide full author list
Metabolites 2024, 14(1), 30; https://doi.org/10.3390/metabo14010030 - 31 Dec 2023
Cited by 2 | Viewed by 1911
Abstract
Recent data described that patients with lysosomal storage disorders (LSDs) may have clinical schizophrenia (SCZ) features. Disruption of lipid metabolism in SCZ pathogenesis was found. Clinical features of schizophrenia (SCZ) have been demonstrated in patients with several lysosomal storage disorders (LSDs). Taking into [...] Read more.
Recent data described that patients with lysosomal storage disorders (LSDs) may have clinical schizophrenia (SCZ) features. Disruption of lipid metabolism in SCZ pathogenesis was found. Clinical features of schizophrenia (SCZ) have been demonstrated in patients with several lysosomal storage disorders (LSDs). Taking into account the critical role of lysosomal function for neuronal cells’ lysosomal dysfunction could be proposed in SCZ pathogenesis. The current study analyzed lysosomal enzyme activities and the alpha-synuclein level in the blood of patients with late-onset SCZ. In total, 52 SCZ patients with late-onset SCZ, 180 sporadic Parkinson’s disease (sPD) patients, and 176 controls were recruited. The enzymatic activity of enzymes associated with mucopolysaccharidosis (alpha-L-Iduronidase (IDUA)), glycogenosis (acid alpha-glucosidase (GAA)) and sphingolipidosis (galactosylceramidase (GALC), glucocerebrosidase (GCase), alpha-galactosidase (GLA), acid sphingomyelinase (ASMase)) and concentration of lysosphingolipids (hexosylsphingosine (HexSph), globotriaosylsphingosine (LysoGb3), and lysosphingomyelin (LysoSM)) were measured using LC-MS/MS. The alpha-synuclein level was estimated in magnetically separated CD45+ blood cells using the enzyme-linked immunosorbent assay (ELISA). Additionally, NGS analysis of 11 LSDs genes was conducted in 21 early-onset SCZ patients and 23 controls using the gene panel PGRNseq-NDD. Decreased ASMase, increased GLA activities, and increased HexSpn, LysoGb3, and LysoSM concentrations along with an accumulation of the alpha-synuclein level were observed in late-onset SCZ patients in comparison to the controls (p < 0.05). Four rare deleterious variants among LSDs genes causing mucopolysaccharidosis type I (IDUA (rs532731688, rs74385837) and type III (HGSNAT (rs766835582)) and sphingolipidosis (metachromatic leukodystrophy (ARSA (rs201251634)) were identified in five patients from the group of early-onset SCZ patients but not in the controls. Our findings supported the role of sphingolipid metabolism in SCZ pathogenesis. Aberrant enzyme activities and compounds of sphingolipids associated with ceramide metabolism may lead to accumulation of alpha-synuclein and may be critical in SCZ pathogenesis. Full article
(This article belongs to the Special Issue Metabolomics Meets Neuropsychiatry)
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