Neurogenetics and gene therapy for reward deficiency syndrome: are we going to the Promised Land?

Abstract

Introduction: Addiction is a substantial health issue with limited treatment options approved by the FDA and as such currently available. The advent of neuroimaging techniques that link neurochemical and neurogenetic mechanisms to the reward circuitry brain function provides a framework for potential genomic-based therapies.

Areas Covered: Through candidate and genome-wide association studies approaches, many gene polymorphisms and clusters have been implicated in drug, food and behavioral dependence linked by the common rubric reward deficiency syndrome (RDS). The results of selective studies that include the role of epigenetics, noncoding micro RNAs in RDS behaviors especially drug abuse involving alcohol, opioids, cocaine, nicotine, pain and feeding are reviewed in this article. New targets for addiction treatment and relapse prevention, treatment alternatives such as gene therapy in animal models, and pharmacogenomics and nutrigenomics methods to manipulate transcription and gene expression are explored.

Expert Opinion: The recognition of the clinical benefit of early genetic testing to determine addiction risk stratification and dopaminergic agonistic, rather than antagonistic therapies are potentially the genomic-based wave of the future. In addition, further development, especially in gene transfer work and viral vector identification, could make gene therapy for RDS a possibility in the future.

Keywords:

• antisense
• gene therapy
• gene transfer
• hypodopaminergic
• neurogenetics
• neuroimaging
• reward deficiency syndrome

Acknowledgments

The authors appreciate the expert editorial assistance of Margaret A Madigan.

Declaration of interest:

K Blum is 100% owner of Synaptamine Inc. holding a number of nutrigenomic patents worldwide including genetic testing of RDS. Both K Blum and MS Gold are paid consultants of Rivermend. Kenneth Blum is the recipient of a grant from The Life Extension Foundation, Ft. Lauderdale, FL, USA to Path Foundation, NY, USA. Panayotis Thanos is the recipient of NIH grant R01HD70888–01A1. The preparation and review of the manuscript was supported in part by funds from the National Institutes of Health, NIAAA (R01–AA07112 and K05–AA00219) and the Medical Research Service of the US Department of Veterans Affairs (Marlene Oscar-Berman). Dr. Badgaiyan is supported by the National Institutes of Health grants 1R01NS073884 and 1R21MH073624, and VA Merit Review Awards CX000479 and CX000780. Marcelo Febo is the recipient of NIH DA019946 and is funded by the McKnight Brain Institute Foundation. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Notes

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