Biomarkers for Psychiatric Disorders
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Biomarkers hold immense promise for the early detection of disease. Unlike other disorders like diabetes and heart disease where a limited number of biological markers are at hand that allow the physician to come up with a reliable diagnosis, there are currently no such markers available for affective disorders. As in any other disease area a major goal is therefore the identification of early markers that can categorize subsets of subjects in a consistent manner. This will allow a more precise definition and categorization of affective disorders and in turn facilitate investigations of the pathogenesis of the diseases and enhance our ability for treatment.
This edited volume will not only address the area of affective disorders but also other brain disorders that are neurological in nature, including Multiple Sclerosis and Alzheimer Disease.
deficiencies in the DPFC of schizophrenic patients, where tissue concentrations of mRNA encoding GAD67, a GABA synthetic enzyme, are consistently reduced (Lewis et al., 2005). Taken together, impairment of cognitive capacity and working memory provide a characteristic and prominent biomarker for schizophrenia in susceptible individuals. 2.2.4 2.2.4 Theory of Mind TOM, also known as mentalization, is the ability to attribute mental states, beliefs, desires, and thoughts to explain and predict
(Xu, 2003) presented evidence that B2AR and B1AR form heterodymers when coexpressed in cultured cells. Moreover, the B2AR expression affects the internalization and ligand-binding characteristics of B1AR. The Beta1 adrenergic receptor gene (ADRB1) is located in 10q24-q26 (Yang-Feng, 1990), spans 1,714 bp, and is constituted by a single exon. Eighty polymorphisms are known so far, and a recently identified functional polymorphism in the B1AR G(1165)C leading to the amino acid variation Gly389Arg
genes were chosen for testing based upon prior knowledge of the biochemical pathways in which they occur. Far fewer than 100 genes are generally accepted as replicated BD associations. Two other recent reviews (Kato, 2007; Farmer et al., 2007) were much more conservative in accepting what is an established BD association. Indeed Kato states that, “To date, no causative gene or genetic risk factor has been identified for bipolar disorder or depression.” Several of the genes associated with
Gene expression analysis of peripheral blood leukocytes from discordant sib-pairs with schizophrenia and bipolar disorder reveals points of convergence between genetic and functional genomic approaches. Am J Med Genet B Neuropsychiatr Genet 136: 12–25 Millar JK, Wilson-Annan JC, Anderson S, Christie S, Taylor MS, Semple CA, Devon RS, Clair DM, Muir WJ, Blackwood DH, Porteous DJ (2000) Disruption of two novel genes by a translocation co-segregating with schizophrenia. Hum Mol Genet 9:
problem may be via the use of laser capture microdissection (LCM) to cut out individual cell types and analyze their gene expression separately. However, the use of LCM to harvest a significant number of cells for this purpose is labor intensive. Furthermore, dissection of individual cells from brain tissue will lead to sampling of some of the neuropil, which will also confound findings. Nevertheless, with the development of more automated techniques for LCM and increased precision, this method