Abstract
Original language | English |
---|---|
Article number | 402 |
Journal | Front. Pharmacol. |
Volume | 10 |
Issue number | APR |
DOIs | |
Publication status | Published - 2019 |
Keywords
- Genetic
- Neuroimaging
- Pharmacogenetic
- Pharmacogenomic
- Precision medicine
- Treatment resistant schizophrenia (TRS)
- clozapine
- brain dysfunction
- data base
- dopaminergic system
- early diagnosis
- GABAergic system
- glutamatergic synapse
- heredity
- human
- molecular imaging
- neuroimaging
- neurotransmission
- nuclear magnetic resonance imaging
- pathogenesis
- pharmacogenetics
- pharmacogenomics
- Review
- serotoninergic system
- treatment response
- treatment-resistant schizophrenia
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Treatment-resistant schizophrenia: Genetic and neuroimaging correlates : Frontiers in Pharmacology. / Vita, A.; Minelli, A.; Barlati, S.; Deste, G.; Giacopuzzi, E.; Valsecchi, P.; Turrina, C.; Gennarelli, M.
In: Front. Pharmacol., Vol. 10, No. APR, 402, 2019.Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - Treatment-resistant schizophrenia: Genetic and neuroimaging correlates
T2 - Frontiers in Pharmacology
AU - Vita, A.
AU - Minelli, A.
AU - Barlati, S.
AU - Deste, G.
AU - Giacopuzzi, E.
AU - Valsecchi, P.
AU - Turrina, C.
AU - Gennarelli, M.
N1 - Cited By :2 Export Date: 10 February 2020 Correspondence Address: Vita, A.; Department of Mental Health and Addiction Services, ASST Spedali CiviliItaly; email: antonio.vita@unibs.it Chemicals/CAS: clozapine, 5786-21-0 References: Ahmed, M., Cannon, D.M., Scanlon, C., Holleran, L., Schmidt, H., McFarland, J., Progressive brain atrophy and cortical thinning in schizophrenia after commencing clozapine treatment (2015) Neuropsychopharmacology, 40, pp. 2409-2417; Anderson, V.M., Goldstein, M.E., Kydd, R.R., Russell, B.R., Extensive gray matter volume reduction in treatment-resistant schizophrenia (2015) Int. J. Neuropsychopharmacol., 18, p. yv016; Andreasen, N.C., Carpenter, W.T., Kane, J.M., Lasser, R.A., Marder, S.R., Weinberger, D.R., Remission in schizophrenia: Proposed criteria and rationale for consensus (2005) Am. J. 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PY - 2019
Y1 - 2019
N2 - Schizophrenia is a severe neuropsychiatric disorder that affects approximately 0.5–1% of the population. Response to antipsychotic therapy is highly variable, and it is not currently possible to predict those patients who will or will not respond to antipsychotic medication. Furthermore, a high percentage of patients, approximately 30%, are classified as treatment-resistant (treatment-resistant schizophrenia; TRS). TRS is defined as a non-response to at least two trials of antipsychotic medication of adequate dose and duration. These patients are usually treated with clozapine, the only evidence-based pharmacotherapy for TRS. However, clozapine is associated with severe adverse events. For these reasons, there is an increasing interest to identify better targets for drug development of new compounds and to establish better biomarkers for existing medications. The ability of antipsychotics to improve psychotic symptoms is dependent on their antagonist and reverse agonist activities at different neuroreceptors, and some genetic association studies of TRS have focused on different pharmacodynamic factors. Some genetic studies have shown an association between antipsychotic response or TRS and neurodevelopment candidate genes, antipsychotic mechanisms of action (such as dopaminergic, serotonergic, GABAergic, and glutamatergic) or pharmacokinetic factors (i.e., differences in the cytochrome families). Moreover, there is a growing body of literature on the structural and functional neuroimaging research into TRS. Neuroimaging studies can help to uncover the underlying neurobiological reasons for such resistance and identify resistant patients earlier. Studies examining the neuropharmacological mechanisms of antipsychotics, including clozapine, can help to improve our knowledge of their action on the central nervous system, with further implications for the discovery of biomarkers and the development of new treatments. The identification of the underlying mechanisms of TRS is a major challenge for developing personalized medicine in the psychiatric field for schizophrenia treatment. The main goal of precision medicine is to use genetic and brain-imaging information to improve the safety, effectiveness, and health outcomes of patients via more efficiently targeted risk stratification, prevention, and tailored medication and treatment management approaches. The aim of this review is to summarize the state of art of pharmacogenetic, pharmacogenomic and neuroimaging studies in TRS. Copyright © 2019 Vita, Minelli, Barlati, Deste, Giacopuzzi, Valsecchi, Turrina and Gennarelli.
AB - Schizophrenia is a severe neuropsychiatric disorder that affects approximately 0.5–1% of the population. Response to antipsychotic therapy is highly variable, and it is not currently possible to predict those patients who will or will not respond to antipsychotic medication. Furthermore, a high percentage of patients, approximately 30%, are classified as treatment-resistant (treatment-resistant schizophrenia; TRS). TRS is defined as a non-response to at least two trials of antipsychotic medication of adequate dose and duration. These patients are usually treated with clozapine, the only evidence-based pharmacotherapy for TRS. However, clozapine is associated with severe adverse events. For these reasons, there is an increasing interest to identify better targets for drug development of new compounds and to establish better biomarkers for existing medications. The ability of antipsychotics to improve psychotic symptoms is dependent on their antagonist and reverse agonist activities at different neuroreceptors, and some genetic association studies of TRS have focused on different pharmacodynamic factors. Some genetic studies have shown an association between antipsychotic response or TRS and neurodevelopment candidate genes, antipsychotic mechanisms of action (such as dopaminergic, serotonergic, GABAergic, and glutamatergic) or pharmacokinetic factors (i.e., differences in the cytochrome families). Moreover, there is a growing body of literature on the structural and functional neuroimaging research into TRS. Neuroimaging studies can help to uncover the underlying neurobiological reasons for such resistance and identify resistant patients earlier. Studies examining the neuropharmacological mechanisms of antipsychotics, including clozapine, can help to improve our knowledge of their action on the central nervous system, with further implications for the discovery of biomarkers and the development of new treatments. The identification of the underlying mechanisms of TRS is a major challenge for developing personalized medicine in the psychiatric field for schizophrenia treatment. The main goal of precision medicine is to use genetic and brain-imaging information to improve the safety, effectiveness, and health outcomes of patients via more efficiently targeted risk stratification, prevention, and tailored medication and treatment management approaches. The aim of this review is to summarize the state of art of pharmacogenetic, pharmacogenomic and neuroimaging studies in TRS. Copyright © 2019 Vita, Minelli, Barlati, Deste, Giacopuzzi, Valsecchi, Turrina and Gennarelli.
KW - Genetic
KW - Neuroimaging
KW - Pharmacogenetic
KW - Pharmacogenomic
KW - Precision medicine
KW - Treatment resistant schizophrenia (TRS)
KW - clozapine
KW - brain dysfunction
KW - data base
KW - dopaminergic system
KW - early diagnosis
KW - GABAergic system
KW - glutamatergic synapse
KW - heredity
KW - human
KW - molecular imaging
KW - neuroimaging
KW - neurotransmission
KW - nuclear magnetic resonance imaging
KW - pathogenesis
KW - pharmacogenetics
KW - pharmacogenomics
KW - Review
KW - serotoninergic system
KW - treatment response
KW - treatment-resistant schizophrenia
U2 - 10.3389/fphar.2019.00402
DO - 10.3389/fphar.2019.00402
M3 - Article
VL - 10
JO - Front. Pharmacol.
JF - Front. Pharmacol.
SN - 1663-9812
IS - APR
M1 - 402
ER -