About this Research Topic
About 30% of patients diagnosed with schizophrenia do not respond to conventional antipsychotic medications, a phenomenon known as Treatment Resistant Schizophrenia (TRS). TRS is receiving increasing attention, with a growing number of experimental reports and literature revisions published in recent years. However, the topic is far from being exhaustively examined and several issues, at multiple levels, still need more in-depth investigation and/or systematization. The scope of this Research Topic on TRS is to provide authors with a dedicated space on this emergent field for focused research, systematic revisions of previously published data, or expert opinions on selected topics regarding TRS. As a means for gaining a more comprehensive schematization of the matter, this Research Topic is intended to be structured along distinct subsections, the organization of which is explained in detail below. One overarching key aim of this Topic will be to address the improving systematization in TRS research. Therefore, much Editorial and Author work should be devoted to provide broad cross-references among expert contributions. As an overall result, this Research Topic will provide readers with a wide panel of interconnected contributions from top-experts in the field that could aid in the comprehension and management of this severe and common clinical condition.
The first subsection will aim at dissecting the neurobiology of TRS. Notably, TRS has been considered to have a proper neurobiology, as it has attributed to separate dopaminergic or non-dopaminergic dysfunctions, glutamate dysfunctions, altered connectomics, and more relevant neurodevelopmental alterations. Therefore, this group of contributions would aim at systematizing and broadening knowledge on the neurobiological basis of the disease, including: i) genetics of TRS; ii) putative aberrant structure and function of synaptic plasticity; iii) connectomics of TRS; iv) neuroimaging and imaging genetics of TRS. Contributions on neurological soft signs are also expected, since these are markers of neurodevelopmental anomalies with relevant association to non-response to antipsychotics.
The scope of the second subsection is to provide a more comprehensive description of the clinical course of the disease. One key contribution should be the identification of stringent operative criteria for the diagnosis of TRS, which is still an ambiguous field. Further contributions could deal with other relevant clinical issues, such as: identification of at risk population for TRS; unique psychopathology and clinical features of the disease; disease trajectories, including disability outcomes and how to prevent them; acquired resistance, the so-called supersensitivity psychosis.
The third subsection is aimed at emphasizing novel possible therapeutic approaches to schizophrenia, including: i) novel strategies with already marketed psychotropic agents, e.g. combination therapy, after-clozapine therapy, therapy in super-refractory patients; ii) novel putative pharmacological approaches, e.g. oxytocin or glutamate modulators; iii) non-pharmacological strategies, e.g.: somatic therapy for resistant auditory hallucinations or other psychotic symptoms; iv) strategies deriving from novel technologies, e.g. virtual reality for improvement of social cognition deficits and social withdrawal; mobile-based approaches to improve adherence; or use of social networks.
The first subsection will aim at dissecting the neurobiology of TRS. Notably, TRS has been considered to have a proper neurobiology, as it has attributed to separate dopaminergic or non-dopaminergic dysfunctions, glutamate dysfunctions, altered connectomics, and more relevant neurodevelopmental alterations. Therefore, this group of contributions would aim at systematizing and broadening knowledge on the neurobiological basis of the disease, including: i) genetics of TRS; ii) putative aberrant structure and function of synaptic plasticity; iii) connectomics of TRS; iv) neuroimaging and imaging genetics of TRS. Contributions on neurological soft signs are also expected, since these are markers of neurodevelopmental anomalies with relevant association to non-response to antipsychotics.
The scope of the second subsection is to provide a more comprehensive description of the clinical course of the disease. One key contribution should be the identification of stringent operative criteria for the diagnosis of TRS, which is still an ambiguous field. Further contributions could deal with other relevant clinical issues, such as: identification of at risk population for TRS; unique psychopathology and clinical features of the disease; disease trajectories, including disability outcomes and how to prevent them; acquired resistance, the so-called supersensitivity psychosis.
The third subsection is aimed at emphasizing novel possible therapeutic approaches to schizophrenia, including: i) novel strategies with already marketed psychotropic agents, e.g. combination therapy, after-clozapine therapy, therapy in super-refractory patients; ii) novel putative pharmacological approaches, e.g. oxytocin or glutamate modulators; iii) non-pharmacological strategies, e.g.: somatic therapy for resistant auditory hallucinations or other psychotic symptoms; iv) strategies deriving from novel technologies, e.g. virtual reality for improvement of social cognition deficits and social withdrawal; mobile-based approaches to improve adherence; or use of social networks.
Keywords: psychosis, antipsychotics, clozapine, remission, refractory
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
