Working memory and attention deficits in adolescent offspring of schizophrenia or bipolar patients: Comparing vulnerability markers

Dept of Psychiatry & Behavioral Neuroscience, Wayne State University SOM, Detroit, MI 48301, USA.
Progress in Neuro-Psychopharmacology and Biological Psychiatry (Impact Factor: 3.69). 07/2011; 35(5):1349-54. DOI: 10.1016/j.pnpbp.2011.04.009
Source: PubMed


Working memory deficits abound in schizophrenia and attention deficits have been documented in schizophrenia and bipolar disorder. Adolescent offspring of patients may inherit vulnerabilities in brain circuits that subserve these cognitive domains. Here we assess impairments in offspring of schizophrenia (SCZ-Offspring) or bipolar (BP-Offspring) patients compared to controls (HC) with no family history of mood or psychotic disorders to the second degree.
Three groups (n=100 subjects; range: 10-20 yrs) of HC, SCZ-Offspring and BP-Offspring gave informed consent. Working memory was assessed using a delayed spatial memory paradigm with two levels of delay (2s & 12s); sustained attention processing was assessed using the Continuous Performance Task-Identical Pairs version.
SCZ-Offspring (but not BP-Offspring) showed impairments in working memory (relative to HC) at the longer memory delay indicating a unique deficit. Both groups showed reduced sensitivity during attention but only BP-Offspring significantly differed from controls.
These results suggest unique (working memory/dorsal frontal cortex) and potentially overlapping (attention/fronto-striatal cortex) vulnerability pathways in adolescent offspring of patients with schizophrenia and bipolar disorder. Working memory and attention assessments in these offspring may assist in the clinical characterization of the adolescents vulnerable to SCZ or BP.

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    Frontiers in Psychiatry 05/2014; 5:50. DOI:10.3389/fpsyt.2014.00050
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    • "However, a number of studies using animal models of mania have observed increased levels of reactive oxygen species (ROS), a marker of mitochondrial dysfunction (Murphy, 2013). One study demonstrated increased lipid peroxidation, and a high number of free radical, superoxide in submitochondrial particles of the prefrontal cortex and hippocampus (Diwadkar et al., 2011). A second study showed that repeated amphetamine exposure, which induces manic symptomatology in animal models, increases levels of anti-oxidant enzymes, superoxide dismutase (SOD) and catalase (CAT), in regional specific manner, in the prefrontal cortex, hippocampus and striatum (Glahn et al., 2007). "
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