Antidepressant Drug Treatment (antidepressant + drug_treatment)

Distribution by Scientific Domains


Selected Abstracts


Platelet hyperactivity in clinical depression and the beneficial effect of antidepressant drug treatment: how strong is the evidence?

ACTA PSYCHIATRICA SCANDINAVICA, Issue 3 2004
R. Von Känel
Objective:, Platelet hyperactivity is thought to contribute to the increased coronary artery disease (CAD) risk in depression. This study reviewed the evidence for hyperactive platelets and for effects of antidepressant drug treatment on platelet ,stickiness' in clinical depression. Method:, By means of PubMed electronic library search, 34 studies in English were identified (1983,2003) and critically reviewed. Results:, In depression, flow cytometry studies allowing detection of subtle platelet activation states consistently found at least one platelet activation marker to be increased, while the bulk of platelet aggregation studies did not suggest increased platelet aggregability. Platelets seem to be more activated in depressed patients with CAD than in depressed individuals without CAD. The selective serotonin reuptake inhibitors normalized platelet hyperactivity in four studies. Conclusion:, Data on platelet activity in depression are inconclusive. To resolve this issue and its clinical implications, studies in larger sample sizes controlling for confounders of platelet functioning and prospectively designed are needed. [source]


Increased neurogenesis and brain-derived neurotrophic factor in neurokinin-1 receptor gene knockout mice

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2003
Sara Morcuende
Abstract It has previously been shown that chronic treatment with antidepressant drugs increases neurogenesis and levels of brain-derived neurotrophic factor in the hippocampus. These changes have been correlated with changes in learning and long-term potentiation and may contribute to the therapeutic efficacy of antidepressant drug treatment. Recently, antagonists at the neurokinin-1 receptor, the preferred receptor for the neuropeptide substance P, have been shown to have antidepressant activity. Mice with disruption of the neurokinin-1 receptor gene are remarkably similar both behaviourally and neurochemically to mice maintained chronically on antidepressant drugs. We demonstrate here that there is a significant elevation of neurogenesis but not cell survival in the hippocampus of neurokinin-1 receptor knockout mice. Neurogenesis can be increased in wild-type but not neurokinin-1 receptor knockout mice by chronic treatment with antidepressant drugs which preferentially target noradrenergic and serotonergic pathways. Hippocampal levels of brain-derived neurotrophic factor are also two-fold higher in neurokinin-1 receptor knockout mice, whereas cortical levels are similar. Finally, we examined hippocampus-dependent learning and memory but found no clear enhancement in neurokinin-1 receptor knockout mice. These data argue against a simple correlation between increased levels of neurogenesis or brain-derived neurotrophic factor and mnemonic processes in the absence of increased cell survival. They support the hypothesis that increased neurogenesis, perhaps accompanied by higher levels of brain-derived neurotrophic factor, may contribute to the efficacy of antidepressant drug therapy. [source]


Permutation tests for factorially designed neuroimaging experiments

HUMAN BRAIN MAPPING, Issue 3 2004
John Suckling
Abstract Permutation methods for analysis of functional neuroimaging data acquired as factorially designed experiments are described and validated. The F ratio was estimated for main effects and interactions at each voxel in standard space. Critical values corresponding to probability thresholds were derived from a null distribution sampled by appropriate permutation of observations. Spatially informed, cluster-level test statistics were generated by applying a preliminary probability threshold to the voxel F maps and then computing the sum of voxel statistics in each of the resulting three-dimensional clusters, i.e., cluster "mass." Using simulations comprising two between- or within-subject factors each with two or three levels, contaminated by Gaussian and non-normal noise, the voxel-wise permutation test was compared to the standard parametric F test and to the performance of the spatially informed statistic using receiver operating characteristic (ROC) curves. Validity of the permutation-testing algorithm and software is endorsed by almost identical performance of parametric and permutation tests of the voxel-level F statistic. Permutation testing of suprathreshold voxel cluster mass, however, was found to provide consistently superior sensitivity to detect simulated signals than either of the voxel-level tests. The methods are also illustrated by application to an experimental dataset designed to investigate effects of antidepressant drug treatment on brain activation by implicit sad facial affect perception in patients with major depression. Antidepressant drug effects in left amygdala and ventral striatum were detected by this software for an interaction between time (within-subject factor) and group (between-subject factor) in a representative two-way factorial design. Hum. Brain Mapping 22:193,205, 2004. © 2004 Wiley-Liss, Inc. [source]