King's College London

Research portal

The neurobiology of treatment-resistant schizophrenia: paths to antipsychotic resistance and a roadmap for future research

Research output: Contribution to journalReview article

Standard

The neurobiology of treatment-resistant schizophrenia : paths to antipsychotic resistance and a roadmap for future research. / Potkin, Steven G.; Kane, John M.; Correll, Christoph U.; Lindenmayer, Jean Pierre; Agid, Ofer; Marder, Stephen R.; Olfson, Mark; Howes, Oliver D.

In: NPJ SCHIZOPHRENIA, Vol. 6, No. 1, 1, 01.12.2020.

Research output: Contribution to journalReview article

Harvard

Potkin, SG, Kane, JM, Correll, CU, Lindenmayer, JP, Agid, O, Marder, SR, Olfson, M & Howes, OD 2020, 'The neurobiology of treatment-resistant schizophrenia: paths to antipsychotic resistance and a roadmap for future research', NPJ SCHIZOPHRENIA, vol. 6, no. 1, 1. https://doi.org/10.1038/s41537-019-0090-z

APA

Potkin, S. G., Kane, J. M., Correll, C. U., Lindenmayer, J. P., Agid, O., Marder, S. R., ... Howes, O. D. (2020). The neurobiology of treatment-resistant schizophrenia: paths to antipsychotic resistance and a roadmap for future research. NPJ SCHIZOPHRENIA, 6(1), [1]. https://doi.org/10.1038/s41537-019-0090-z

Vancouver

Potkin SG, Kane JM, Correll CU, Lindenmayer JP, Agid O, Marder SR et al. The neurobiology of treatment-resistant schizophrenia: paths to antipsychotic resistance and a roadmap for future research. NPJ SCHIZOPHRENIA. 2020 Dec 1;6(1). 1. https://doi.org/10.1038/s41537-019-0090-z

Author

Potkin, Steven G. ; Kane, John M. ; Correll, Christoph U. ; Lindenmayer, Jean Pierre ; Agid, Ofer ; Marder, Stephen R. ; Olfson, Mark ; Howes, Oliver D. / The neurobiology of treatment-resistant schizophrenia : paths to antipsychotic resistance and a roadmap for future research. In: NPJ SCHIZOPHRENIA. 2020 ; Vol. 6, No. 1.

Bibtex Download

@article{0480e84c461249a0802dd87244263e2c,
title = "The neurobiology of treatment-resistant schizophrenia: paths to antipsychotic resistance and a roadmap for future research",
abstract = "Treatment-resistant schizophrenia (TRS), the persistence of positive symptoms despite ≥2 trials of adequate dose and duration of antipsychotic medication with documented adherence, is a serious clinical problem with heterogeneous presentations. TRS can vary in its onset (at the first episode of psychosis or upon relapse), in its severity, and in the response to subsequent therapeutic interventions (i.e., clozapine, electroconvulsive therapy). The heterogeneity of TRS indicates that the underlying neurobiology of TRS may differ not only from treatment-responsive schizophrenia but also among patients with TRS. Several hypotheses have been proposed for the neurobiological mechanisms underlying TRS, including dopamine supersensitivity, hyperdopaminergic and normodopaminergic subtypes, glutamate dysregulation, inflammation and oxidative stress, and serotonin dysregulation. Research supporting these hypotheses is limited in part by variations in the criteria used to define TRS, as well as by the biological and clinical heterogeneity of TRS. Clinical trial designs for new treatments should be informed by this heterogeneity, and further clinical research is needed to more clearly understand the underlying neurobiology of TRS and to optimize treatment for patients with TRS.",
author = "Potkin, {Steven G.} and Kane, {John M.} and Correll, {Christoph U.} and Lindenmayer, {Jean Pierre} and Ofer Agid and Marder, {Stephen R.} and Mark Olfson and Howes, {Oliver D.}",
year = "2020",
month = "12",
day = "1",
doi = "10.1038/s41537-019-0090-z",
language = "English",
volume = "6",
journal = "NPJ SCHIZOPHRENIA",
issn = "2334-265X",
publisher = "Nature Publishing Group",
number = "1",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - The neurobiology of treatment-resistant schizophrenia

T2 - paths to antipsychotic resistance and a roadmap for future research

AU - Potkin, Steven G.

AU - Kane, John M.

AU - Correll, Christoph U.

AU - Lindenmayer, Jean Pierre

AU - Agid, Ofer

AU - Marder, Stephen R.

AU - Olfson, Mark

AU - Howes, Oliver D.

PY - 2020/12/1

Y1 - 2020/12/1

N2 - Treatment-resistant schizophrenia (TRS), the persistence of positive symptoms despite ≥2 trials of adequate dose and duration of antipsychotic medication with documented adherence, is a serious clinical problem with heterogeneous presentations. TRS can vary in its onset (at the first episode of psychosis or upon relapse), in its severity, and in the response to subsequent therapeutic interventions (i.e., clozapine, electroconvulsive therapy). The heterogeneity of TRS indicates that the underlying neurobiology of TRS may differ not only from treatment-responsive schizophrenia but also among patients with TRS. Several hypotheses have been proposed for the neurobiological mechanisms underlying TRS, including dopamine supersensitivity, hyperdopaminergic and normodopaminergic subtypes, glutamate dysregulation, inflammation and oxidative stress, and serotonin dysregulation. Research supporting these hypotheses is limited in part by variations in the criteria used to define TRS, as well as by the biological and clinical heterogeneity of TRS. Clinical trial designs for new treatments should be informed by this heterogeneity, and further clinical research is needed to more clearly understand the underlying neurobiology of TRS and to optimize treatment for patients with TRS.

AB - Treatment-resistant schizophrenia (TRS), the persistence of positive symptoms despite ≥2 trials of adequate dose and duration of antipsychotic medication with documented adherence, is a serious clinical problem with heterogeneous presentations. TRS can vary in its onset (at the first episode of psychosis or upon relapse), in its severity, and in the response to subsequent therapeutic interventions (i.e., clozapine, electroconvulsive therapy). The heterogeneity of TRS indicates that the underlying neurobiology of TRS may differ not only from treatment-responsive schizophrenia but also among patients with TRS. Several hypotheses have been proposed for the neurobiological mechanisms underlying TRS, including dopamine supersensitivity, hyperdopaminergic and normodopaminergic subtypes, glutamate dysregulation, inflammation and oxidative stress, and serotonin dysregulation. Research supporting these hypotheses is limited in part by variations in the criteria used to define TRS, as well as by the biological and clinical heterogeneity of TRS. Clinical trial designs for new treatments should be informed by this heterogeneity, and further clinical research is needed to more clearly understand the underlying neurobiology of TRS and to optimize treatment for patients with TRS.

UR - http://www.scopus.com/inward/record.url?scp=85077569967&partnerID=8YFLogxK

U2 - 10.1038/s41537-019-0090-z

DO - 10.1038/s41537-019-0090-z

M3 - Review article

AN - SCOPUS:85077569967

VL - 6

JO - NPJ SCHIZOPHRENIA

JF - NPJ SCHIZOPHRENIA

SN - 2334-265X

IS - 1

M1 - 1

ER -

View graph of relations

© 2018 King's College London | Strand | London WC2R 2LS | England | United Kingdom | Tel +44 (0)20 7836 5454