Abstract
BackgroundTardive dyskinesia (TD) is a motor side effect that may arise after long-term treatment of antipsychotic drugs. Its etiology is not well understood, but a number of risk factors have been associated with TD. TD occurrence appears to be familial, thus suggesting a genetic component. We previously reported on an association between the SLC18A2 gene that codes for the vesicular monoamine transporter 2 (VMAT2) that packages monoamines including dopamine from the cytoplasm into synaptic vesicles (Zai et al, 2013). In the present study, we examined the dopamine transporter gene SLC6A3 by itself and in conjunction with SLC18A2 for possible association with TD.MethodsWe genotyped and analyzed the variable-number tandem repeat (VNTR) polymorphism in the 3’ untranslated region of the SLC6A3 gene in our European sample of 187 schizophrenia/schizoaffective disorder patients assessed for TD occurrence based on the Abnormal Involuntary Movement Scale (AIMS). We also explored the interaction between the VNTR and the TD-associated SLC18A2 marker rs363224.ResultsOur preliminary analysis did not show the SLC6A3 VNTR to be associated with TD occurrence or severity. There also appeared to be no significant interaction between SLC6A3 VNTR and SLC18A2 rs363224 in TD occurrence or severity (p>0.05).DiscussionOur findings did not support a major role of the dopamine transporter gene in TD risk or severity, but we will examine additional putative functional markers in this gene.
Highlights
Johannes Schneider-Thoma*,1, Stefan Leucht1 1Technical University of Munich. Despite intensive research it is unknown if treatment with antipsychotic drugs contributes to the reduced life-expectancy observed in patients with schizophrenia and other severe mental disorders
As randomized controlled trials (RCT) are considered the best evidence to examine causal relationship, we aimed to analyze mortality related to antipsychotics based on all placebo-controlled RCTs conducted so far
We addressed the effects of age, diagnostic field, gender, study duration, antipsychotic drug used, drug dose and polypharmacy with subgroup- and meta-regression-analyses
Summary
Neurological soft signs (NSS) represent minor neurological signs which indicate non-specific cerebral dysfunction. Numerous studies have confirmed their presence in schizophrenia across all stages of the disease. During the past years studies increasingly reported on fluctuations of the NSS scores. To shade further light on the question whether NSS represent a state or a trait component or both, a review of longitudinal studies on schizophrenia patients was performed, because only measurements at two or more points in time can answer the question at hand. Methods: A search of studies which had assessed NSS in adult schizophrenia patients and included at least one follow-up examination was undertaken. All expressed abnormally increased NSS, to different extents. Studies gave some hints at relationships between NSS and symptoms, i.e. negative and cognitive symptoms. Discussion: The reviewed studies confirmed the presence of abnormal, i.e. elevated NSS in patients diagnosed with schizophrenia.
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