Pharmacogenetics of Antipsychotics

Objective: During the past decades, increasing efforts have been invested in studies to unravel the influence of genetic factors on antipsychotic (AP) dosage, treatment response, and occurrence of adverse effects. These studies aimed to improve clinical care by predicting outcome of treatment with A...

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Published inCanadian journal of psychiatry Vol. 59; no. 2; pp. 76 - 88
Main Authors Brandl, Eva J, Kennedy, James L, Müller, Daniel J
Format Journal Article
LanguageEnglish
Published Los Angeles, CA SAGE Publications 01.02.2014
SAGE PUBLICATIONS, INC
The Canadian Psychiatric Association
Subjects
Antipsychotic Agents - adverse effects
Antipsychotic Agents - pharmacokinetics
Antipsychotic Agents - therapeutic use
Antipsychotics
Brain - drug effects
Clinical medicine
Cytochrome P-450 Enzyme System - genetics
Dopamine - metabolism
Dose-Response Relationship, Drug
Drug therapy
Enzymes
Gene expression
Genetic Markers - genetics
Genetics
Grants
Humans
In Review
Influence
Medical research
Pharmacogenetics
Polymorphism, Genetic - genetics
Precision Medicine
Psychiatry
Psychotic Disorders - blood
Psychotic Disorders - drug therapy
Psychotic Disorders - genetics
Psychotic Disorders - psychology
Schizophrenia
Serotonin - metabolism
Studies
Treatment Outcome
serotonin
candidate gene
adverse effect
treatment response
cytochrome P450 system
antipsychotic
genome-wide association
dopamine
pharmacogenetic
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Abstract Objective: During the past decades, increasing efforts have been invested in studies to unravel the influence of genetic factors on antipsychotic (AP) dosage, treatment response, and occurrence of adverse effects. These studies aimed to improve clinical care by predicting outcome of treatment with APs and thus allowing for individualized treatment strategies. We highlight most important findings obtained through both candidate gene and genome-wide association studies, including pharmacokinetic and pharmacodynamic factors. Methods: We reviewed studies on pharmacogenetics of AP response and adverse effects published on PubMed until early 2012. Owing to the high number of published studies, we focused our review on findings that have been replicated in independent studies or are supported by meta-analyses. Results: Most robust findings were reported for associations between polymorphisms of the cytochrome P450 system, the dopamine and the serotonin transmitter systems, and dosage, treatment response, and adverse effects, such as AP-induced weight gain or tardive dyskinesia. These associations were either detected for specific medications or for classes of APs. Conclusion: First promising and robust results show that pharmacogenetics bear promise for a widespread use in future clinical practice. This will likely be achieved by developing algorithms that will include many genetic variants. However, further investigation is warranted to replicate and validate previous findings, as well as to identify new genetic variants involved in AP response and for replication of existing findings.
AbstractList During the past decades, increasing efforts have been invested in studies to unravel the influence of genetic factors on antipsychotic (AP) dosage, treatment response, and occurrence of adverse effects. These studies aimed to improve clinical care by predicting outcome of treatment with APs and thus allowing for individualized treatment strategies. We highlight most important findings obtained through both candidate gene and genome-wide association studies, including pharmacokinetic and pharmacodynamic factors. We reviewed studies on pharmacogenetics of AP response and adverse effects published on PubMed until early 2012. Owing to the high number of published studies, we focused our review on findings that have been replicated in independent studies or are supported by meta-analyses. Most robust findings were reported for associations between polymorphisms of the cytochrome P450 system, the dopamine and the serotonin transmitter systems, and dosage, treatment response, and adverse effects, such as AP-induced weight gain or tardive dyskinesia. These associations were either detected for specific medications or for classes of APs. First promising and robust results show that pharmacogenetics bear promise for a widespread use in future clinical practice. This will likely be achieved by developing algorithms that will include many genetic variants. However, further investigation is warranted to replicate and validate previous findings, as well as to identify new genetic variants involved in AP response and for replication of existing findings.
During the past decades, increasing efforts have been invested in studies to unravel the influence of genetic factors on antipsychotic (AP) dosage, treatment response, and occurrence of adverse effects. These studies aimed to improve clinical care by predicting outcome of treatment with APs and thus allowing for individualized treatment strategies. We highlight most important findings obtained through both candidate gene and genome-wide association studies, including pharmacokinetic and pharmacodynamic factors. We reviewed studies on pharmacogenetics of AP response and adverse effects published on PubMed until early 2012. Owing to the high number of published studies, we focused our review on findings that have been replicated in independent studies or are supported by meta-analyses. Most robust findings were reported for associations between polymorphisms of the cytochrome P450 system, the dopamine and the serotonin transmitter systems, and dosage, treatment response, and adverse effects, such as AP-induced weight gain or tardive dyskinesia. These associations were either detected for specific medications or for classes of APs. First promising and robust results show that pharmacogenetics bear promise for a widespread use in future clinical practice. This will likely be achieved by developing algorithms that will include many genetic variants. However, further investigation is warranted to replicate and validate previous findings, as well as to identify new genetic variants involved in AP response and for replication of existing findings.
During the past decades, increasing efforts have been invested in studies to unravel the influence of genetic factors on antipsychotic (AP) dosage, treatment response, and occurrence of adverse effects. These studies aimed to improve clinical care by predicting outcome of treatment with APs and thus allowing for individualized treatment strategies. We highlight most important findings obtained through both candidate gene and genome-wide association studies, including pharmacokinetic and pharmacodynamic factors.OBJECTIVEDuring the past decades, increasing efforts have been invested in studies to unravel the influence of genetic factors on antipsychotic (AP) dosage, treatment response, and occurrence of adverse effects. These studies aimed to improve clinical care by predicting outcome of treatment with APs and thus allowing for individualized treatment strategies. We highlight most important findings obtained through both candidate gene and genome-wide association studies, including pharmacokinetic and pharmacodynamic factors.We reviewed studies on pharmacogenetics of AP response and adverse effects published on PubMed until early 2012. Owing to the high number of published studies, we focused our review on findings that have been replicated in independent studies or are supported by meta-analyses.METHODSWe reviewed studies on pharmacogenetics of AP response and adverse effects published on PubMed until early 2012. Owing to the high number of published studies, we focused our review on findings that have been replicated in independent studies or are supported by meta-analyses.Most robust findings were reported for associations between polymorphisms of the cytochrome P450 system, the dopamine and the serotonin transmitter systems, and dosage, treatment response, and adverse effects, such as AP-induced weight gain or tardive dyskinesia. These associations were either detected for specific medications or for classes of APs.RESULTSMost robust findings were reported for associations between polymorphisms of the cytochrome P450 system, the dopamine and the serotonin transmitter systems, and dosage, treatment response, and adverse effects, such as AP-induced weight gain or tardive dyskinesia. These associations were either detected for specific medications or for classes of APs.First promising and robust results show that pharmacogenetics bear promise for a widespread use in future clinical practice. This will likely be achieved by developing algorithms that will include many genetic variants. However, further investigation is warranted to replicate and validate previous findings, as well as to identify new genetic variants involved in AP response and for replication of existing findings.CONCLUSIONFirst promising and robust results show that pharmacogenetics bear promise for a widespread use in future clinical practice. This will likely be achieved by developing algorithms that will include many genetic variants. However, further investigation is warranted to replicate and validate previous findings, as well as to identify new genetic variants involved in AP response and for replication of existing findings.
Objective: During the past decades, increasing efforts have been invested in studies to unravel the influence of genetic factors on antipsychotic (AP) dosage, treatment response, and occurrence of adverse effects. These studies aimed to improve clinical care by predicting outcome of treatment with APs and thus allowing for individualized treatment strategies. We highlight most important findings obtained through both candidate gene and genome-wide association studies, including pharmacokinetic and pharmacodynamic factors. Methods: We reviewed studies on pharmacogenetics of AP response and adverse effects published on PubMed until early 2012. Owing to the high number of published studies, we focused our review on findings that have been replicated in independent studies or are supported by meta-analyses. Results: Most robust findings were reported for associations between polymorphisms of the cytochrome P450 system, the dopamine and the serotonin transmitter systems, and dosage, treatment response, and adverse effects, such as AP-induced weight gain or tardive dyskinesia. These associations were either detected for specific medications or for classes of APs. Conclusion: First promising and robust results show that pharmacogenetics bear promise for a widespread use in future clinical practice. This will likely be achieved by developing algorithms that will include many genetic variants. However, further investigation is warranted to replicate and validate previous findings, as well as to identify new genetic variants involved in AP response and for replication of existing findings.
Author Kennedy, James L
Brandl, Eva J
Müller, Daniel J
AuthorAffiliation 3 Head, Pharmacogenetics Research Clinic, Neurogenetics Section, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, Ontario; Associate Professor, University of Toronto, Toronto, Ontario
1 Postdoctoral Research Fellow, Neurogenetics Section, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, Ontario
2 Head, Neurogenetics Section, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health (CAMH), Toronto, Ontario; Director, Neuroscience Research Department, Neuroscience Department, CAMH, Toronto, Ontario; l’Anson Professor of Psychiatry and Medical Science, University of Toronto, Toronto, Ontario
AuthorAffiliation_xml – name: 1 Postdoctoral Research Fellow, Neurogenetics Section, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, Ontario
– name: 2 Head, Neurogenetics Section, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health (CAMH), Toronto, Ontario; Director, Neuroscience Research Department, Neuroscience Department, CAMH, Toronto, Ontario; l’Anson Professor of Psychiatry and Medical Science, University of Toronto, Toronto, Ontario
– name: 3 Head, Pharmacogenetics Research Clinic, Neurogenetics Section, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, Ontario; Associate Professor, University of Toronto, Toronto, Ontario
Author_xml – sequence: 1
  givenname: Eva J
  surname: Brandl
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– sequence: 2
  givenname: James L
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  fullname: Kennedy, James L
– sequence: 3
  givenname: Daniel J
  surname: Müller
  fullname: Müller, Daniel J
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24881126$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright 2014 Canadian Psychiatric Association
Copyright Canadian Psychiatric Association Feb 2014
2014 Canadian Psychiatric Association 2014
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Issue 2
Keywords serotonin
candidate gene
adverse effect
treatment response
cytochrome P450 system
antipsychotic
genome-wide association
dopamine
pharmacogenetic
Language English
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Snippet Objective: During the past decades, increasing efforts have been invested in studies to unravel the influence of genetic factors on antipsychotic (AP) dosage,...
During the past decades, increasing efforts have been invested in studies to unravel the influence of genetic factors on antipsychotic (AP) dosage, treatment...
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StartPage 76
SubjectTerms Antipsychotic Agents - adverse effects
Antipsychotic Agents - pharmacokinetics
Antipsychotic Agents - therapeutic use
Antipsychotics
Brain - drug effects
Clinical medicine
Cytochrome P-450 Enzyme System - genetics
Dopamine - metabolism
Dose-Response Relationship, Drug
Drug therapy
Enzymes
Gene expression
Genetic Markers - genetics
Genetics
Grants
Humans
In Review
Influence
Medical research
Pharmacogenetics
Polymorphism, Genetic - genetics
Precision Medicine
Psychiatry
Psychotic Disorders - blood
Psychotic Disorders - drug therapy
Psychotic Disorders - genetics
Psychotic Disorders - psychology
Schizophrenia
Serotonin - metabolism
Studies
Treatment Outcome
Title Pharmacogenetics of Antipsychotics
URI https://journals.sagepub.com/doi/full/10.1177/070674371405900203
https://www.ncbi.nlm.nih.gov/pubmed/24881126
https://www.proquest.com/docview/1518931646
https://www.proquest.com/docview/1531952651
https://pubmed.ncbi.nlm.nih.gov/PMC4079237
Volume 59
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