Howes et al (SEE ARTICLE) examined brain dopamine function in people with prodromal signs of psychosis. They found that, although not psychotic, these individuals showed dopamine overactivity in the striatum that was related to the severity of prodromal symptoms and impairment in verbal fluency.
Ernst et al (SEE ARTICLE) report findings from a postmortem brain study suggesting that a truncated form of the tropomyosin-related kinase B receptor is reduced in 9 different regions of the frontal cortex in suicide completers. They used a series of complementary techniques to validate and further explore these findings. A methylation analysis of the tropomyosin-related kinase B promoter suggested that epigenetic factors may account for the reduced activity of this gene in suicide completers.
Fakra et al (SEE ARTICLE) report that a common genetic polymorphism associated with increased negative feedback inhibition of serotonin neurons leads to decreased threat-related amygdala reactivity. Moreover, they demonstrate that through its effects on amygdala reactivity the polymorphism predicts 9.2% of variability in trait anxiety.
Reif et al (SEE ARTICLE) demonstrate that a repeat polymorphism in the regulatory region of the neuronal nitric oxide synthase gene is functional at the molecular level. Short variants of this repeat are associated with a wide range of impulsive behaviors, like aggression, adult attention-deficit/hyperactivity disorder, and cluster B personality disorder as well as impaired prefrontal functioning as measured by event-related potentials.
Marsh et al (SEE ARTICLE) used functional magnetic resonance imaging to investigate disturbances in neural systems that mediate the processes of self-regulatory control in women with bulimia nervosa. During correct responses on incongruent trials of the Simon task, patients did not activate frontostriatal circuits to the same degree as did control women. Functional abnormalities in these circuits may contribute to binge eating and other impulsive behaviors in women with bulimia nervosa.
Childhood separation anxiety disorder often precedes panic disorder. Battaglia et al (SEE ARTICLE) relied on hypersensitivity to CO2, common to both phenotypes, to investigate the nature of their continuity in a multivariate study of young twins of the Norwegian Institute of Health cohort. Shared genetic determinants appear to be the major underlying cause of continuity of childhood separation anxiety into adult panic disorder. Childhood parental loss in turn accounted for a significant additional proportion of the covariation.
In a case-control study of persons with chronic fatigue syndrome (CFS) and controls identified from a general population sample of 19 381 adult residents of Georgia, Heim et al (SEE ARTICLE) demonstrate that childhood trauma is an important risk factor for CFS. In addition, they demonstrate that neuroendocrine dysfunction, a hallmark feature of CFS, is associated with childhood trauma, possibly reflecting a biological correlate of vulnerability due to early developmental insults.
Small et al (SEE ARTICLE) studied middle-aged and older persons without dementia to determine whether known risk factors for Alzheimer disease are associated with 2-(1-{6-[(2-[F-18]fluoroethyl)(methyl)amino]-2-naphthyl}ethylidene)malononitrile (FDDNP)–positron emission tomography (PET) binding, an in vivo measure of brain amyloid plaques and tau tangles. Impaired cognitive status, older age, and inheritance of the apolipoprotein E-4 genetic risk for Alzheimer disease were associated with increased brain FDDNP-PET binding.
Epstein et al (SEE ARTICLE) show that polydrug-dependent individuals can provide data about their moods and activities in real time using handheld computers and that these data prospectively confirm some long-held beliefs about triggers of drug craving and use.
Fusar-Poli et al (SEE ARTICLE) used functional magnetic resonance imaging to investigate the effects of 2 main psychoactive constituents of Cannabis sativa (
9-tetrahydrocannabinol and cannabidiol) on regional brain function during emotional processing. The effects of cannabidiol on limbic regions underlie its anxiolytic effect, whereas the anxiogenic properties of 9-tetrahydrocannabinol are related to effects in other brain regions.
