Abstract:To investigate whether the dopaminergic system plays a role in the etiology of anorexia nervosa (AN) via the dopamine D2 receptor, we investigated association and transmission disequilibrium at seven single-nucleotide polymorphisms (SNPs) spanning about 75 kbp of the gene DRD2. We studied 191 probands with a DSM-IV diagnosis of AN, 457 parents and affected relatives with a DSM-IV eating disorder diagnosis, and 98 unrelated, female, normal weight controls. The À141 C/À insertion/deletion (À141 Indel), previousl… Show more
“…Complimenting these functional magnetic resonance imaging (fMRI) studies is a report of higher 11 C-raclopride binding potential in the ventral striatum in women who were recovered from AN, suggesting that DA activity is enhanced in this population [343], and significant relations between multiple DRD 2 polymorphisms and AN [344]. …”
This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette’s syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader–Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.
“…Complimenting these functional magnetic resonance imaging (fMRI) studies is a report of higher 11 C-raclopride binding potential in the ventral striatum in women who were recovered from AN, suggesting that DA activity is enhanced in this population [343], and significant relations between multiple DRD 2 polymorphisms and AN [344]. …”
This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette’s syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader–Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.
“…Reduced CSF DA metabolites occur in malnourished individuals with AN (60) and persist after recovery (92). Individuals with AN have altered frequency of functional polymorphisms of DA D2 receptor genes that might affect receptor transcription and translation efficiency (93). The anteroventral striatum (AVS) and dorsal caudate are components of limbic and executive-associative pathways (94)(95)(96).…”
“…Molecular genetics has demonstrated abnormalities of monoamine related genes in AN including polymorphism of serotonin (5 HT) and dopamine (DA) receptor genes, 5HT2a (Kaye, Bailer et al, 2005;Kaye, Frank et al, 2005) and D2 (Bergen et al, 2005). In particular these alterations in 5HT and DA receptor density have been shown to be concentrated in limbic system in AN (Kaye, 2008), a part of the brain integral to the regulation of emotion.…”
We reviewed the evidence for emotion-related disturbances in anorexia nervosa (AN) from behavioural, cognitive, biological and genetic domains of study. These domains were brought together within the framework of an integrative neuroscience model that emphasizes the role of emotion and feeling and their regulation, in brain organization. PsychInfo and Medline searches were performed to identify published peer-reviewed papers on AN within each domain. This review revealed evidence for 'Emotion', 'Thinking and Feeling' and 'Self-regulation' disturbances in AN that span non-conscious to conscious processes. An integrative neuroscience framework was then applied to develop a model of AN, from which hypotheses for empirical investigation are generated. We propose that AN reflects a core disturbance in emotion at the earliest time stage of information processing with subsequent effects on the later stages of thinking, feeling and self-regulation.
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