ABSTRACT
Individuals with 22q11.2 deletion syndrome (22q11.2DS) evince a 30% incidence of schizophrenia. We compared the white matter (WM) of 22q11.2DS patients without schizophrenia to a group of matched healthy controls using Tract-Based-Spatial-Statistics (TBSS). We found localized reduction of Fractional Anisotropy (FA) and Axial Diffusivity (AD; measure of axonal integrity) in WM underlying the left parietal lobe. No changes in Radial Diffusivity (RD; measure of myelin integrity) were observed. Of note, studies in chronic schizophrenia patients report reduced FA, no changes in AD, and increases in RD in WM. Our findings suggest different WM microstructural pathology in 22q11.2DS than in patients with schizophrenia.
Subject(s)
Brain/pathology , DiGeorge Syndrome/pathology , Nerve Fibers, Myelinated/pathology , Adolescent , Adult , Anisotropy , Brain Mapping , Case-Control Studies , Diffusion Tensor Imaging , Female , Humans , Male , Pilot Projects , Psychiatric Status Rating Scales , Young AdultABSTRACT
Of the anxiety disorders, panic disorder (PD) has been the most extensively studied from a genetic standpoint. Results of family studies have consistently demonstrated that PD runs in families, and twin studies indicate that genes contribute to this familiality. However, phenotypic and genetic complexity has made finding the specific genes involved in PD a challenge. There is still uncertainty about how best to define the phenotype for genetic studies and whether it is the clinical phenotype of PD or more latent psychologic and biologic traits that are inherited. To date, molecular genetic studies have suggested some chromosomal regions and genes that may contribute to risk, but none of these have been established. We review the genetic epidemiology of PD as well as recent molecular genetic studies of the disorder, and conclude with a discussion of promising strategies that attempt to uncover specific genetic loci involved in the etiology of PD.
