Proteomics in the Discovery of New Therapeutic Targets for Psychiatric Disease

Abstract

In terms of impact on and cost to society psychiatric disorders are among the most important health problems of today. Current estimates from the US suggest that the collective cost of psychiatric diseases could amount to one-third of the total health care budget with a cumulative lifetime prevalence of 30%. While undoubtedly improvements have been made in the diagnosis and treatment of at least the symptoms of mental illness, there has been frustratingly little progress in elucidating the molecular mechanisms. However, a fundamentally different approach to study molecular mechanisms of psychiatric diseases is emerging as a result of technological advances in expression profiling methods. This comprises the investigation of the expressed disease 'phenotypes', developing from the differential gene and protein expression in the central nervous system as a result of the complex interaction between genetic predisposition and environmental modulation. This paper will focus on proteomics, expression profiling at the protein level, reviewing some of the available tools and their application in the molecular analysis of psychiatric disease.

Traumatic Brain Injury: A Disease Process, Not an Event

“…Current estimates in the U.S. suggest that the collective cost of psychiatric diseases could be as high as one-third of the total health care budget (Voshol et al, 2003). It is therefore critical to note that psychiatric and psychological deficits are among the most disabling consequences of TBI (Table 5).…”

Extraction and proteomic analysis of proteins from normal and multiple sclerosis postmortem brain

“…In studies on the effects of postmortem time on protein expression patterns using proteomics on rodent brain, dihydropyrimidinase related protein-2 (DRP-2) was identified as a possible biomarker of postmortem time [13] and also temperature [14]. Another possible biomarker is nmyc downstream regulated gene 2 (NRDG-2), the levels of which appeared to change consistently as a function of time with postmortem interval in mouse brain [15].…”

Variability of healthy human proteome

“…Этот факт находит свое подтверждение в статье Voshol с соавт. [55]. Белок, идентифицированный как GFAP (glial fibrillary acidic protein), имел большой разброс концентраций как среди больных, так и среди здоровых лиц, и авторы пришли к выводу, что этот белок не может расцениваться как биомаркер.…”