NEUROGENETIC IMPAIRMENTS OF BRAIN REWARD CIRCUITRY LINKS TO REWARD DEFICIENCY SYNDROME (RDS) AS EVIDENCED BY GENETIC ADDICTION RISK SCORE (GARS): A CASE STUDY

Abstract

ABSTRACT holistic approaches that will safely activate brain reward circuitry in the mesolimbic dopamine system. KEY WORDS able to describe lifetime RDS behaviors in a recovery addict (17 years sober) blindly by just assessing *Corresponding author: Email: [e-mail] ; Tel: [phone] [I] INTRODUCTION The brain’s mesolimbic reward system is a critical site for experiences of well-being. The reward center is where chemical messengers including serotonin, enkephalin, γ-aminobutyric second messenger proteins act in concert to provide a net release of DA in the nucleus accumbens (NAc). The idea that the synthesis, vesicular storage, metabolism, receptor formation, and catabolism of neurotransmitters are controlled by genes is well documented [1-3]. Most importantly, polymorphisms of reward genes can disrupt the neurochemical events that culminate in neuronal release of DA within the mesolimbic reward circuitry. A breakdown of these neuronal events in the “The Brain Reward Cascade” [4] will eventually lead to DA dysfunction. DA neurotransmission is essential for an individual to experience of pleasure (reward) and the reduction of stress. DA dysfunction then can result in a deficiency in reward and a predisposition to substance-seeking in an attempt to ameliorate hypodopaminergic function [5].