Journal
TRENDS IN MOLECULAR MEDICINE
Volume 17, Issue 2, Pages 97-107Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2010.10.010
Keywords
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Funding
- Zucker Hillside Hospital/National Institute of Mental Health (NIMH) Advanced Center for Intervention and Services Research for the Study of Schizophrenia [P30 MH 074543, P30 MH090590]
- Center for Intervention Development and Applied Research [P50 MH080173]
- Feinstein Institute for Medical Research NSLIJHS General Clinical Research Center
- National Center for Research Resources (NCRR), National Institutes of Health (NIH) [M01 RR018535]
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Mechanisms underlying antipsychotic cardiometabolic adverse effects are incompletely understood. This hampers the identification of high-risk patients, low-risk antipsychotics and preventive/ameliorative treatments. Recent clinical, molecular and genetic data suggest that: (i) antipsychotic-naive samples provide the greatest power for mechanistic studies; (ii) weight and metabolic effects can be discordant, pointing to overlapping and distinct mechanisms; (iii) antipsychotics affect satiety and energy homeostasis signaling; (iv) the specific peptides mediating these effects are unknown but probably overlap with those involved in idiopathic obesity; and (v) single nucleotide polymorphisms in genes encoding known neurotransmitter receptors and metabolic proteins are promising pharmacogenomic targets for countering adverse affects. However, sophisticated molecular studies and genome-wide association studies, ideally in antipsychotic-naive/first episode samples, are needed to further advance the field.
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