Objective. The aim of this paper is the presentation of current experimental and clinical data on psychotropic drugs in patients with COVID-19 infection as well as the review of the literature from 2020–2022 on the effects of antidepressants, antipsychotics, mood stabilisers and other drugs on the occurrence and course of COVID-19 infection. Some of them exert the antiviral effect on SARS-CoV-2, some can diminish the risk, and some can act therapeutically on the infection. The most data on a favourable effect on infection concern fluvoxamine, a selective serotonin reuptake inhibitor (SSRI), while other antidepressant drugs can diminish the risk of intubation or death. SSRI drugs act therapeutically in post-covid depression. Antiviral effects of chlorpromazine and haloperidol were not confirmed in clinical observations. The use of long-acting injectable atypical antipsychotic drugs may decrease the risk of infection. Despite the evidence of antiviral action of lithium – against herpes in clinical studies and against coronaviruses in experimental papers, the current data on the effect of lithium on the occurrence and course of COVID-19 infection do not allow firm conclusions. Also, the data on the use of valproate is equivocal despite propitious theoretical premises. In the article, the potential of other drugs used in psychiatric therapeutics such as amantadine, disulfiram, hydroxyzine, cannabidiol, melatonin, and memantine was discussed.
Conclusions. Drugs acting therapeutically on the course of COVID-19 may include fluvoxamine and other antidepressants. A favourable effect of lithium on the occurrence and course of COVID-19 infection has not been unambiguously demonstrated despite previous numerous data on the drug’s antiviral activity.
Aim. The present study aims to analyse relationships between the way of pharmacological treatment (antipsychotic vs antipsychotic + antidepressant) and negative symptoms in a group of schizophrenia patients hospitalised for the first time 11 to 15 years ago. Depressive symptoms, social functioning, and quality of life were also scrutinised.
Methods. 56 patients were assessed one month after the hospitalisation (Time 1), and then as follows: 1 year later, 4–6, 7–11 and 11–15 years after Time 1. The following measures were used: Marder’s Negative Symptoms Factor Score (NSFS), Calgary Depression Scale for Schizophrenia (CDSS), Social Functioning (SFS) and WHOQoL – Bref scales.
Results. Most patients received antipsychotic medications throughout the whole observation period (85.7–94.6%). Out of them, 69.6–77.6% were treated with antipsychotics only and 22.9–32.4% with antipsychotics + antidepressants. There were no significant relationships between the mode of treatment and the frequency of negative symptoms or significant differences between the compared groups regarding the mean scores of the CDSS, SFS, and WHOQoL at any time point of the observation.
Conclusions. The way of treatment in terms of monotherapy (antipsychotics only) vs polytherapy (+ antidepressants) did not differentiate the frequency of negative symptoms and the levels of other clinical and psychosocial indicators of the course of the disease. The findings seem to reflect lack of satisfactory fulfilment of patients’ needs concerning relieving negative symptoms of schizophrenia.
Objectives. The aim of the study was to present the general rules and limitations of the proposed new system of classification of pharmacological substances used in psychiatry, i.e. Neuroscience-based Nomenclature (NbN).
Review of selected literature. Current literature on NbN and its possibilities in the classification of medicinal substances was reviewed. The currently used Anatomical Therapeutic Chemical (ATC) Classification and its limitations are presented. The structure of NbN is discussed and its practical use is described. The limitations of the NbN classification were also analysed.
Conclusions. Based on the current literature, we can conclude that the NbN classification of psychopharmaceuticals may turn out to be a breakthrough in this field. Due to its features, it is a system that is regularly updated. Thanks to the vast amount of information and the available mobile application, the NbN classification has a chance to enter everyday clinical practice.
Objectives. The aim of this article is to demonstrate the potential of cannabinoids such as tetrahydrocannabinol (THC) and cannabidiol (CBD) in neurodegenerative diseases.
Literature review. The endocannabinoid system was presented, including the CB1 and CB2 cannabinoid receptors, as well as endogenous cannabinoids, the most important of which is anandamide and enzymes for the synthesis and biodegradation of endocannabinoids.
Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and Amyotrophic Lateral Sclerosis (ALS), which define the progressive activity associated with the further loss of specific subpopulation of neurons and disorders of multiple brain neurotransmitters. These diseases also include pathological protein accumulation (such as tau proteins), impairment of the lysosomal system, excitotoxicity, oxidative stress, and inflammatory features of the nervous system. The endocannabinoid system can modulate phenomena with neurodegeneration. It is caused by the action of cannabinoid receptors – CB1, causing the normalization of glutamatergic transmission and autophagy, activation of CB2 receptors, limiting the weakening of action, and lowering the level of emission reduction – the independence of cannabinoid receptors. The article presents data on the beneficial effects of cannabinoids on the symptoms of neurodegenerative diseases obtained in experimental studies in animal models (AD, PD, HD, ALS), as well as in clinical studies (AD, PD, HD).
Conclusions. The results of research, mainly experimental and clinical, may indicate a beneficial effect of cannabinoids, reducing some of the symptoms of neurodegenerative diseases. These results are promising prerequisites for further research.
Objective. Schizophrenia is a neurodevelopmental disorder associated with deficits in cognition, affect, and social functioning. Despite its high heritability, there are known external risk factors, the presence of which substantially increases the likelihood of developing schizophrenia. Epigenetic modifications seem to play a key role in the multifactorial pathogenesis of the disease, linking genetic and environmental components through mechanisms that cause reversible changes in gene expression in response to specific external factors. DNA methylation is an example of such a mechanism. This work aims to review the current research regarding its potential role in the development, diagnosis, and treatment of schizophrenia.
Review of the literature. This article reviews the literature related to the issue of DNA methylation in schizophrenia. Articles in English have been selected from the PubMed database, using the following search terms: “DNA methylation,” “schizophrenia,” and “markers.” As the basis for further analysis, reviews devoted directly to epigenetic modifications, including DNA methylation, in schizophrenia, published between 2017 and 2022, were chosen from the results. A summary of the collected data is presented below.
Conclusions. Characteristic changes in the methylation pattern of specific genes appear in tissues collected from patients with schizophrenia or from corresponding animal models. The goal of further research should be to create a database of specific DNA methylation patterns, the presence of which could act as a biomarker or an indicator of the effectiveness of a therapeutic process. It is crucial to standardise the genome methylation analysis system and to validate other tissues to be used as substitutes for the brain tissue.