This approach could be employed in general for the identification of the binding profile of any chromatin-associated protein. The use of the Biotag also demonstrated the advantage of a better comparison between the different factors and the possibility to analyze the binding activities of mutants or alternative splice variants, which could not be distinguished by specific antibodies. Cerebral white Dabrafenib matter hyperintensities are highintensity areas observed on T2-weighted MR images and indicate white matter damage. Although WMH may be related to ischemia caused by chronic microvascular disease and hypoperfusion, they commonly occur in patients with Alzheimer’s disease and mild cognitive impairment. In contrast to diseased populations, most studies on non-demented elderly participants indicate that increased WMH in deep and periventricular areas may also be associated with cognitive impairment. A clinicalanatomic correlation study indicated that regional WMH volumes may be associated with cognitive performance using smaller regions of interest. Catechol-O-methyltransferase, the postsynaptic enzyme that metabolizes released dopamine, is a critical enzyme in the metabolic degradation of dopamine in the prefrontal cortex. The human COMT gene, mapped to chromosome 22q11, contains a common functional polymorphism, in which valine is substituted for methionine at the 158/108 locus on the peptide sequence. The Val allele results in a substantial increase in enzyme activity, and may increase dopamine degradation and reduce dopamine signaling. Dopamine signaling, specifically in the prefrontal cortex, is implicated in cognitive functioning. Numerous studies have demonstrated the effect of this genetic variant on neural function related to cognitive and affective processing. Several studies have shown that Met homozygous people have increased frontal cortex signal-to-noise ratios and improved performance in prefrontal-dependent cognitive tasks, such as working memory, whereas those with highactivity Val alleles have relatively inferior performance and inefficient dorsolateral prefrontal function. Egan et al investigated the effect of the COMT Val158Met genotype in prefrontal-mediated cognition using the Wisconsin card sorting test in patients with schizophrenia, their unaffected siblings, and controls. They found that participants with a low-activity Met allele had considerably fewer preservative errors on the WCST than Val-allele carriers, and that the Met allele load consistently predicted a more efficient physiological response in the prefrontal cortex. They suggested that the COMT Val allele may impair prefrontal cognition and physiology because it increases prefrontal dopamine depletion. Zinkstok et al examined the relationship between COMT Val158Met polymorphism and brain anatomy in healthy young adults.