Abstract
Despite considerable ongoing efforts at the epidemiological, genetic and molecular level, the etiology of bipolar disorder had not yet been elucidated. To study possible contributing components to the pathophysiology of this disorder, we have hypothesized that levels of enzymes inhibited by therapeutically relevent lithium ion concentrations in the brain of patients may differ from those in normal controls and may be involved in the etiology of the disorder. Three Li-inhibitable enzymes were studied in postmortem brain samples of bipolar patients and normal controls. The expression and function of the two enzymes that are obviously involved in signaling cascades, IMPase, involved in the second messenger system of the phosphatidylinositol cycle, and GSK-3, a mediator of an array of signaling cascades, were not found to be different in postmortem frontal and occipital cortex of bipolar patients and normal controls. Only PAP phosphatase protein levels, but not its mRNA levels or enzymatic activity, were foudn to be significantly decreased in frontal cortex of bipolar patients compared with normal controls.
Original language | English |
---|---|
Pages (from-to) | 433-442 |
Number of pages | 10 |
Journal | Journal of Psychiatric Research |
Volume | 37 |
Issue number | 5 |
DOIs | |
State | Published - 1 Jan 2003 |
Keywords
- Bipolar disorder
- Glycogen synthase kinase (GSK)-3
- Inositol monophasphatase (IMPas)
- Lithium
- Phosphoadenosine-phosphate (PAP) phosphatase
- Postmortem brain
ASJC Scopus subject areas
- Psychiatry and Mental health
- Biological Psychiatry