Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P08908 (5-HT1A)
 5,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Kleptomania is currently classified in psychiatric nomenclature as one of the impulse control disorders (DSM-IV, 1994). It is characterized by repeated failure to resist impulses to steal objects, not for personal use or monetary gain. The objects are therefore discarded, given away, or hoarded (ICD-10, 1992). This disorder is known since the early 18th century from the phenomenological and clinical viewpoints, yet is still debated with regard to therapeutic strategies and criminal liability. Although there are usually complications associated with the legal consequences of being caught and arrested, subjects continue to violate the law despite repeated arrests and convictions. In a 28-year old man suffering from kleptomania, years of psychodynamic psychotherapy were ineffective. Only when he was treated as suffering from an impulse control disorder or a variant of obsessive-compulsive disorder, was there significant improvement. The positive response to buspirone (5-HT1A) augmentation of fluvoxamine (SSRI) suggested that disturbed central serotonergic neurotransmission might play an important role in the pathogenesis of kleptomania. This concept is strengthened by the comorbidity of the syndrome with depression and by its compulsive traits. We stress that although kleptomaniacs cannot differentiate between right and wrong, testing shows that their sense of reality is intact, but they act under the influence of drives they cannot resist.
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PMID:[Kleptomania: phenomenological, clinical and legal aspects]. 941 15

Biological markers for depression are of great interest to aid in elucidating the causes of major depression. We assess currently available biological markers to query their validity for aiding in the diagnosis of major depression. We specifically focus on neurotrophic factors, serotonergic markers, biochemical markers, immunological markers, neuroimaging, neurophysiological findings, and neuropsychological markers. We delineate the most robust biological markers of major depression. These include decreased platelet imipramine binding, decreased 5-HT1A receptor expression, increase of soluble interleukin-2 receptor and interleukin-6 in serum, decreased brain-derived neurotrophic factor in serum, hypocholesterolemia, low blood folate levels, and impaired suppression of the dexamethasone suppression test. To date, however, none of these markers are sufficiently specific to contribute to the diagnosis of major depression. Thus, with regard to new diagnostic manuals such as DSM-V and ICD-11 which are currently assessing whether biological markers may be included in diagnostic criteria, no biological markers for major depression are currently available for inclusion in the diagnostic criteria.
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PMID:Consensus paper of the WFSBP Task Force on Biological Markers: biological markers in depression. 1962 59

Pindolol, a 5-HT1A autoreceptor antagonist, given in combination with selective serotonin reuptake inhibitors (SSRIs), may enhance and/or accelerate the therapeutic efficacy of SSRIs. Fifty patients, meeting ICD-10 criteria for major depressive disorder or bipolar depression, were enrolled in our randomized, placebo-controlled, double-blind trial. One group received paroxetine plus pindolol (2.5 mg t.i.d.), and the other group received paroxetine plus placebo. The proportion of patients with sustained response (>or=50% reduction of baseline HAM-D 17 score maintained until the endpoint; p=0.252) and the proportion of patients with remission (HAM-D 17 <or=8 at last visit; p=0.769) did not differ significantly between the two treatment groups. However, a significantly greater proportion of patients who were not previously treated with antidepressants (n=15; p=0.041) and of patients with bipolar depression (n=11; p=0.015) had a sustained response in the paroxetine plus pindolol group compared to the paroxetine plus placebo group; furthermore there was a trend for first episode depressed patients to have a greater response in the paroxetine plus pindolol group (n=12; p=0.071). Summarizing, the entire study population showed no antidepressive benefit from pindolol augmentation. Nevertheless patients with bipolar depression irrespective of previous treatments and duration of illness, and unipolar patients not previously treated demonstrated a significant benefit from pindolol augmentation.
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PMID:Paroxetine with pindolol augmentation: a double-blind, randomized, placebo-controlled study in depressed in-patients. 1805 9