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3 Psychiatric and Drug Addiction Disorders
Pages 39-54

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From page 39...
... In Session III the discussion centered on specific areas of psychiatric and drug addiction research where specific biomarkers are currently showing promise, as well as opportunities for further impact.
From page 40...
... A focus on biomarkers to follow working memory deficits involving prefrontal cortical circuits would seem more likely to succeed than searching for a biomarker of DSM-IV schizophrenia, which is a heterogeneous syndrome defined only by symptoms and course. To understand the change in emphasis, Hyman first traced the intellectual and historical underpinnings of the current diagnostic classification systems and then argued that excessive reliance on current, consensus diagnostic categories―especially for the purpose of biomarker research―may lead researchers down blind alleys.
From page 41...
... . The DSM diagnostic system facilitated epidemiology, clinical trials, and research on disease mechanisms by producing broad agreement on specific disease entities.
From page 42...
... . Finally, symptom clusters of certain psychiatric disorders, such as bipolar disorder and psychosis or bipolar disorder and rapid cycling, failed to cosegregate across generations (Craddock et al., 2005)
From page 43...
... With modern genomic and genetic tools, such as highdensity whole-genome association studies, which are beginning to yield results for other complex disorders, risk genes should be found for psychiatric disorders, assuming that large enough populations can be assembled for analysis (Altshuler and Daly, 2007)
From page 44...
... Those who possess these genes are more likely to experience a positive treatment response, according to convergent findings drawing on multiple methodologies: large clinical trials, human genotyping and imaging research, and animal models, said Dr. Husseini Manji, director of the Mood and Anxiety Disorders Program at the National Institute of Mental Health (NIMH)
From page 45...
... . That major clinical trial of nearly 4,000 patients was a multisite effectiveness study aimed at realworld patients rather than the rarefied and more homogeneous samples of patients used in most clinical trials according to strict inclusionary and exclusionary criteria.
From page 46...
... The transporter's role is, in part, to reduce the concentration of serotonin in the synaptic cleft. In addition to the SNP within the HTR2A gene, two other SNPs were found to be associated with a positive treatment response.
From page 47...
... Depression treatment does not take effect until several weeks after initiation of treatment. Neurogenesis is one proposed mechanism that may explain the slow time line in treatment response, based on the fact that in separate experiments with knockout mice, mice heterozygous for Bcl-2 more quickly developed a depression-like behavior known as learned helplessness after a series of repeated shocks (Yuan et al., 2007)
From page 48...
... More research needs to be performed to explore these intriguing findings, but what has been accomplished thus far points to the seminal role that genotype may play in treatment response. The field has managed to marshal clinical findings and animal models to launch potentially the first generation of genetic predictors of treatment response for a widespread, serious, and disabling disorder.
From page 49...
... It also found some improvement in subjects' performance on a test battery designed to assess neuropsychological functioning. The proof-of-concept clinical trial has galvanized efforts to conduct larger trials with nicotinic agonists.
From page 50...
... . Lewis explained that the findings provided the rationale for a clinical trial, now in progress, using a GABAA alpha2 selective agonist to treat the cognitive symptoms of schizophrenia and measuring gamma band activity during working memory tasks as one measure of the drug's effectiveness.
From page 51...
... Establishing temporal course is key to understanding addiction vulnerability because drugs with short- versus longer-term reinforcing effects are more likely to elicit frequent administration and thereby pose greater addiction potential. Cocaine, for example, exerts its reinforcing effects and exits the brain so swiftly that it is more prone to addiction than is the psychostimulant methylphenidate, which has longer pharmacodynamics in the brain.
From page 52...
... was found to exert profound effects on the structure and function of corticolimbic circuitry governing emotional regulation and cognitive control. The polymorphism affected the volume of gray matter of the cingulate gyrus and the amygdala.
From page 53...
... An example of the second role of genetics―that is, by drug metabolism and pharmacological response―comes directly from the addiction field. A large body of clinical studies, as well as preclinical research, has found that the dopamine D2 receptor is extremely important in regulating reinforcing responses to drugs of abuse.
From page 54...
... This study―and others soon to be published regarding cocaine distribution to the fetus from maternal use―raises the possibility of lifelong structural and functional effects on brain neurocircuitry as a result of fetal exposure to drugs of abuse.


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